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Category Archives: Human Longevity

Link between dietary restriction, longevity examined – Mount Desert Islander

Posted: February 6, 2017 at 2:48 pm

BAR HARBOR Scientists at the MDI Biological Laboratory have published research which improves the understanding of the mechanisms by which the lifespan of roundworms can be lengthened by cutting back on calories.

It has been known for decades that drastically restricting certain nutrients without causing malnutrition prolongs health and lifespan in a wide range of species, but the molecular mechanisms underlying this effect have remained a mystery.

In a paper recently published in the journal Aging Cell, MDI Biological Laboratory scientist Aric Rogers shed light on an important genetic pathway underlying this process, raising the possibility that therapies can be developed that prolong the healthy years without having to suffer the consequences of a severely restricted diet.

Aric Rogers. PHOTO COURTESY OF THE MDI BIOLOGICAL LABORATORY

Its tantalizing to think that we might be able to activate a protective response to enhance our own health without resorting to extreme dietary regimes, Rogers said.

Rogers studies mechanisms important to the positive effects of dietary restriction in an intact organism the tiny roundworm, C. elegans as opposed to cells in a petri dish. This roundworm is an important model in aging research because it shares nearly half of its genes with humans and because of its short lifespan it lives for only two to three weeks which allows scientists to study many generations over a short period of time.

Arics identification of a molecular mechanism governing the life-prolonging effects of dietary restriction is a validation of our unique approach to research in aging and regenerative biology, said Kevin Strange, president of the laboratory. Our use of whole organisms as research models provides greater insight into the many factors controlling physiological processes than the use of cells alone.

The life-prolonging effects of dietary restriction, or calorie restriction, occur in just about every animal tested. They are thought to be an evolutionary adaptation to harsh environmental conditions. In the absence of enough food to eat, evolution has programmed organisms to switch from a growth mode to a survival mode so they can live long enough to reproduce when conditions improve.

The identification of a mechanism underlying the protective effect of dietary restriction could lead to therapies for age-related diseases, including Alzheimers and Parkinsons, that are associated with diminished cellular quality control. Alzheimers, for instance, is associated with the build-up of the toxic protein beta amyloid in the brain, and Parkinsons with a build-up of a toxic protein called alpha synuclein.

The link between aging and weakened cellular housekeeping functions raises the possibility that new drugs to prolong lifespan also could delay the onset of age-related degenerative diseases. Now that Rogers has identified a link, the next step is to investigate cause and effect by manipulating the genetic pathways that inhibit protein formation to see if the bodys ability to clear molecular clutter is improved.

We think therapies to activate these protective pathways could not only prolong lifespan but also delay the onset of age-related diseases, Rogers said. Most older people suffer from multiple chronic diseases. Anti-aging procedures applied to disease models almost always delay disease onset and improve outcomes, which suggests that disease-suppressing benefits may be accessed to extend healthy human lifespan.

The MDI Biological Laboratory, located in Bar Harbor, is an independent, nonprofit biomedical research institution focused on increasing healthy lifespan and increasing our natural ability to repair and regenerate tissues damaged by injury or disease. The institution develops solutions to complex human health problems through research, education and ventures that transform discoveries into cures. Visit mdibl.org.

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Genome Sequencing in Less than an Hour – Anti Aging News

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Posted on Feb. 1, 2017, 6 a.m. in Diagnostics Genetics in Disease

New sequencing machine will reportedly have the capability of sequencing an entire genome for less than $100, rather than the $1,000 it currently costs.

Illumina, a sequencing company, has debuted remarkable new machines, the NovaSeq 5000 and NovaSeq 6000, that one day will sequence an entire genome for thecost of under $100 and in fewer than 60 minutes as compared to the current one day. That $100 is only one-tenth the costthat was announced in 2014 by Illumina when it reached a milestone of a lower $1,000 per genome. Ten years ago, the costwas about $10 million.

When Illumina released their first machine in 2006, the cost was $300,000, but by last year, that price dropped to the above-stated $1,000. Previously, it had taken the Human Genome Project about $2.7 billion and 15 years to sequence the entire genome (minus only about one percent) from the DNA of a number ofvolunteers.

The human genome has an estimated 25,000 genes comprised of approximately three billion nucleotide base pairs. Affordable and quick sequencing will mean a revolution in the evaluation of human health and will enable far less costly and easier detection of rare diseases and link genetic variations with illness and health.

People are made up of extremely unique characteristics, so moving healthcare toward a more individualized approach will increase the knowledge and insight of known illnesses and allow for individually-tailored treatment options.

Although the NovaSeq does not yet have the capability of providing the stated inexpensive $100 sequencing, and the datagenerated in under an hour takes longer to beinterpreted, once this technology is adopted, the price will drop and the necessary time for the analysis of helpful data will decrease.

The projections are promising and exciting. The major advancement in this technology will have outstanding implications in research and also for the average person. The dramatic reduction in the cost will provide faster progress in clinical research for cancer and other genetically linked diseases.

Also, companies such as AncestryDNA and 23andMe that use sequencing machines, often ones from Illumina, cater to those people who want to learn more about their individual genomes.

The machine is currently owned by only six customers including the Broad Institute of MIT and Harvard, the Chan Zuckerberg BioHub, Human Longevity Inc. and Regeneron.

Illumina is regarded as the primary manufacturer of DNA sequencers with its market value of over $20 billion. It is also San Diego County's largest publicly-traded biotech company.

There is indeed a bright future for such next-generation sequencing devices.

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HMS 2017 Media Fellowships – Harvard Medical School (registration)

Posted: at 2:48 pm

Dear Journalist:

Harvard Medical Schools Media Fellowship program, now entering its 20th year, is accepting applications for its spring 2017 sessions. The fellowships bring together top health and science journalists and preeminent researchers and physician-scientists for a weeklong educational immersion on the HMS campus in Boston. The 2017 topics are:

How computation, math and big data are transforming basic discovery, diagnoses, clinical therapies and population health.

While scientists uncover the molecular aberrations that fuel cell atrophy and cell demise, evolutionary biologists ponder the limits of human longevity and frontline clinicians develop new therapies to stave off the degeneration and frailty of aging.

About the Media Fellowships During each weeklong session, media fellows spend time on the HMS campus and in our affiliated hospitals and institutes to gain a deeper understanding of the spectrum of research and state of the science in a particular area.

Reporters meet with a range of experts on a given topic, including basic scientists, translational investigators and practicing clinicians. Although reporters attend as a group, we try to work with each fellow to tailor the experience to individual interests within the broader theme. We will choose three fellows for each thematic track.

HMS will pay for participants lodging, meals and ground transportation, but fellows must cover their own travel costs to and from the Boston area.

These fellowships are offered as educational opportunities on a background basis. Over the past 19 years, HMS has hosted more than 100 reporters from print, online and broadcast news outlets. Reporters spend unsupervised time with faculty, researchers and physician-scientists from affiliated hospitals and various experts from other Harvard schools and institutes. Fellows often cultivate lasting relationships with scientists and generate a wealth of story ideas.

2017 Topics

Medicine by the Numbers April 24-28

Computation, information technology and the unprecedented amounts of data spewed out every second are transforming our lives. The massive amounts of data generated in research, medicine and other fields are also transforming our understanding of basic biomedical processes, our clinical decision making, diagnostic and treatment decisions and approaches to population health.

The marriage of previously disparate fields such as physics, computation, bioinformatics and information technology with medicine and biomedical science has generated novel ways to gauge risk, predict drug behavior and understand disease.

New data are flowing in from the genome, the proteome, the microbiome. This informationanalyzed and contextualized properlycan reframe the way we view basic biologic processes. It casts new light on how proteins network with each other in disease and health and it allows us to predict how drugs interact for therapeutic synergy or toxicity.

Computational and statistical analysis of genomic data also sharpens researchers ability to diagnose a person with an exceedingly rare disease or gauge an individuals risk of developing a common one. Neuroscientists are using data and algorithms to unravel how neurons in the brain communicate with one another. Cancer biologists use computation, biostatistics and bioinformatics to unravel the myriad complex links between the presence of genes and subsequent disease development. These are only some of the examples that illustrate the way bio-computation and information technology are starting to disrupt how we study the human body, how we think about science and how we practice medicine.

The Quest for Immortality: Rethinking an age-old question

May 15-19

Youth, aging, death and the quest for eternal life have been central themes in philosophy, literature, science and art since the dawn of humanity.

As scientists uncover the molecular aberrations that fuel cell atrophy and cell death, evolutionary biologists are pondering the limits of human longevity and frontline clinicians are developing new therapies to add more healthy years to peoples lives and stave off the degeneration and frailty that come with aging.

Today, we are closer than ever to developing treatments that halt the subtlest molecular shifts that can spark cellular degradation, loss of function and cell deaththe basis of degenerative diseases and aging. But are we any closer to stopping aging in its tracks or even reversing it?

According to scientists, slowing down the process of degeneration is an achievable goal, yet what are the proven strategies that frontline clinicians can use to slow down the march of aging? What does science tell us about the effects of diet, exercise and lifestyle on longevity? How far away are we from exercise in a pill that can halt DNA damage and boost cell repair?

On a societal scale, the graying of the population represents one of modern medicines greatest successes and one of its gravest challenges. With age, the risk for conditions such as cardiovascular disease, neurodegenerative disorders, cancer, bone loss and frailty rises precipitously. Researchers are trying to understand just why and how living longer precipitates changes that lead to aging and degeneration.

Caring for the old and frail can take a great economic toll on the health care system and a severe financial and personal toll on individual families who care for their aging relatives. How are health care policy experts and health care economists dealing with these challenges? How can we reconcile our desire for longer life with the need to remain healthy and independent longer?

According to some healthcare experts, the focus of our research and clinical efforts should be not so much to prolong life at all costs but to compress of morbidity. In other words, the focus should be on adding healthier, more independent and more productive years to ones life, rather than merely extending life.

These are just some of the questions, topics and themes that scientists and clinicians will explore with reporters during the five-day immersion. Journalists will also meet with scientists who can address the various micro- and macro-dimensions of aging, including basic researchers, frontline clinicians, geneticists, neurologists, geriatricians, public health experts, health care policy experts and bioethicists.

Application Process

By midnight on March 1, 2017, please email Ekaterina_pesheva@hms.harvard.edu the following:

In addition, please state that you have license from your editor, or usual freelance clients, to cover the topic broadly at some point in the future.

You are not obligated to cover Harvards work in the area, just the field as a whole.

We look forward to hearing from you or from someone you think would benefit from this experience.

Please contact me with any questions at ekaterina_pesheva@hms.harvard.edu or 617-432-0441.

Sincerely,

Ekaterina Pesheva

Director, Science Communications and Media Relations

Harvard Medical School

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Sprint 8 Exercises Increase Your "Fitness Hormone" Levels

Posted: January 23, 2017 at 7:50 am

A recent study published in the journal Mechanisms of Aging and Development confirms the "anti-aging" effect of high-intensity training.

Telomere shortening occurs as you age, however the factors involved are not entirely understood as of yet. The study was conducted to determine whether age-associated telomere shortening is related to habitual endurance exercise and maximal aerobic capacity.

The results suggest there's a direct association between reduced telomere shortening in your later years and high-intensity-type exercises.

The authors' state:

"The results of the present study provide evidence that leukocyte telomere length (LTL) is related to regular vigorous aerobic exercise and maximal aerobic exercise capacity with aging in healthy humans.

LTL is not influenced by aerobic exercise status among young subjects, presumably because TL is intact (i.e., already normal) in sedentary healthy young adults.

However, as LTL shortens with aging it appears that maintenance of aerobic fitness, produced by chronic strenuous exercise and reflected by higher VO2max, acts to preserve LTL.

Our results indicate that leukocyte telomere length (LTL) is preserved in healthy older adults who perform vigorous aerobic exercise and is positively related to maximal aerobic exercise capacity. This may represent a novel molecular mechanism underlying the "anti-aging" effects of maintaining high aerobic fitness."

But that's not all.

High-intensity interval-type training also boosts human growth hormone (HGH) production. A 2003 study published in the journal Sports Medicine found that "exercise intensity above lactate threshold and for a minimum of 10 minutes appears to elicit the greatest stimulus to the secretion of HGH."

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OLED – Wikipedia

Posted: January 10, 2017 at 2:45 am

An organic light-emitting diode (OLED) is a light-emitting diode (LED) in which the emissive electroluminescent layer is a film of organic compound that emits light in response to an electric current. This layer of organic semiconductor is situated between two electrodes; typically, at least one of these electrodes is transparent. OLEDs are used to create digital displays in devices such as television screens, computer monitors, portable systems such as mobile phones, handheld game consoles and PDAs. A major area of research is the development of white OLED devices for use in solid-state lighting applications.[1][2][3]

There are two main families of OLED: those based on small molecules and those employing polymers. Adding mobile ions to an OLED creates a light-emitting electrochemical cell (LEC) which has a slightly different mode of operation. OLED displays can use either passive-matrix (PMOLED) or active-matrix (AMOLED) addressing schemes. Passive matrix OLEDs (PMOLED) uses a simple control scheme in which you control each row (or line) in the display sequentially[4] whereas active-matrix OLEDs (AMOLED) require a thin-film transistor backplane to switch each individual pixel on or off, but allow for higher resolution and larger display sizes.

An OLED display works without a backlight; thus, it can display deep black levels and can be thinner and lighter than a liquid crystal display (LCD). In low ambient light conditions (such as a dark room), an OLED screen can achieve a higher contrast ratio than an LCD, regardless of whether the LCD uses cold cathode fluorescent lamps or an LED backlight.

Andr Bernanose and co-workers at the Nancy-Universit in France made the first observations of electroluminescence in organic materials in the early 1950s. They applied high alternating voltages in air to materials such as acridine orange, either deposited on or dissolved in cellulose or cellophane thin films. The proposed mechanism was either direct excitation of the dye molecules or excitation of electrons.[5][6][7][8]

In 1960 Martin Pope and some of his co-workers at New York University developed ohmic dark-injecting electrode contacts to organic crystals.[9][10][11] They further described the necessary energetic requirements (work functions) for hole and electron injecting electrode contacts. These contacts are the basis of charge injection in all modern OLED devices. Pope's group also first observed direct current (DC) electroluminescence under vacuum on a single pure crystal of anthracene and on anthracene crystals doped with tetracene in 1963[12] using a small area silver electrode at 400 volts. The proposed mechanism was field-accelerated electron excitation of molecular fluorescence.

Pope's group reported in 1965[13] that in the absence of an external electric field, the electroluminescence in anthracene crystals is caused by the recombination of a thermalized electron and hole, and that the conducting level of anthracene is higher in energy than the exciton energy level. Also in 1965, W. Helfrich and W. G. Schneider of the National Research Council in Canada produced double injection recombination electroluminescence for the first time in an anthracene single crystal using hole and electron injecting electrodes,[14] the forerunner of modern double-injection devices. In the same year, Dow Chemical researchers patented a method of preparing electroluminescent cells using high-voltage (5001500 V) AC-driven (1003000Hz) electrically insulated one millimetre thin layers of a melted phosphor consisting of ground anthracene powder, tetracene, and graphite powder.[15] Their proposed mechanism involved electronic excitation at the contacts between the graphite particles and the anthracene molecules.

Roger Partridge made the first observation of electroluminescence from polymer films at the National Physical Laboratory in the United Kingdom. The device consisted of a film of poly(N-vinylcarbazole) up to 2.2 micrometers thick located between two charge injecting electrodes. The results of the project were patented in 1975[16] and published in 1983.[17][18][19][20]

Hong Kong-born American physical chemist Ching W. Tang and his co-worker Steven Van Slyke at Eastman Kodak built the first practical OLED device in 1987.[21] This was a revolution for the technology. This device used a novel two-layer structure with separate hole transporting and electron transporting layers such that recombination and light emission occurred in the middle of the organic layer; this resulted in a reduction in operating voltage and improvements in efficiency.

Research into polymer electroluminescence culminated in 1990 with J. H. Burroughes et al. at the Cavendish Laboratory in Cambridge reporting a high efficiency green light-emitting polymer based device using 100nm thick films of poly(p-phenylene vinylene).[22]

Universal Display Corporation holds the majority of patents concerning the commercialization of OLEDs.[citation needed]

A typical OLED is composed of a layer of organic materials situated between two electrodes, the anode and cathode, all deposited on a substrate. The organic molecules are electrically conductive as a result of delocalization of pi electrons caused by conjugation over part or all of the molecule. These materials have conductivity levels ranging from insulators to conductors, and are therefore considered organic semiconductors. The highest occupied and lowest unoccupied molecular orbitals (HOMO and LUMO) of organic semiconductors are analogous to the valence and conduction bands of inorganic semiconductors.[23]

Originally, the most basic polymer OLEDs consisted of a single organic layer. One example was the first light-emitting device synthesised by J. H. Burroughes et al., which involved a single layer of poly(p-phenylene vinylene). However multilayer OLEDs can be fabricated with two or more layers in order to improve device efficiency. As well as conductive properties, different materials may be chosen to aid charge injection at electrodes by providing a more gradual electronic profile,[24] or block a charge from reaching the opposite electrode and being wasted.[25] Many modern OLEDs incorporate a simple bilayer structure, consisting of a conductive layer and an emissive layer. More recent developments in OLED architecture improves quantum efficiency (up to 19%) by using a graded heterojunction.[26] In the graded heterojunction architecture, the composition of hole and electron-transport materials varies continuously within the emissive layer with a dopant emitter. The graded heterojunction architecture combines the benefits of both conventional architectures by improving charge injection while simultaneously balancing charge transport within the emissive region.[27]

During operation, a voltage is applied across the OLED such that the anode is positive with respect to the cathode. Anodes are picked based upon the quality of their optical transparency, electrical conductivity, and chemical stability.[28] A current of electrons flows through the device from cathode to anode, as electrons are injected into the LUMO of the organic layer at the cathode and withdrawn from the HOMO at the anode. This latter process may also be described as the injection of electron holes into the HOMO. Electrostatic forces bring the electrons and the holes towards each other and they recombine forming an exciton, a bound state of the electron and hole. This happens closer to the emissive layer, because in organic semiconductors holes are generally more mobile than electrons. The decay of this excited state results in a relaxation of the energy levels of the electron, accompanied by emission of radiation whose frequency is in the visible region. The frequency of this radiation depends on the band gap of the material, in this case the difference in energy between the HOMO and LUMO.

As electrons and holes are fermions with half integer spin, an exciton may either be in a singlet state or a triplet state depending on how the spins of the electron and hole have been combined. Statistically three triplet excitons will be formed for each singlet exciton. Decay from triplet states (phosphorescence) is spin forbidden, increasing the timescale of the transition and limiting the internal efficiency of fluorescent devices. Phosphorescent organic light-emitting diodes make use of spinorbit interactions to facilitate intersystem crossing between singlet and triplet states, thus obtaining emission from both singlet and triplet states and improving the internal efficiency.

Indium tin oxide (ITO) is commonly used as the anode material. It is transparent to visible light and has a high work function which promotes injection of holes into the HOMO level of the organic layer. A typical conductive layer may consist of PEDOT:PSS[29] as the HOMO level of this material generally lies between the workfunction of ITO and the HOMO of other commonly used polymers, reducing the energy barriers for hole injection. Metals such as barium and calcium are often used for the cathode as they have low work functions which promote injection of electrons into the LUMO of the organic layer.[30] Such metals are reactive, so they require a capping layer of aluminium to avoid degradation.

Experimental research has proven that the properties of the anode, specifically the anode/hole transport layer (HTL) interface topography plays a major role in the efficiency, performance, and lifetime of organic light emitting diodes. Imperfections in the surface of the anode decrease anode-organic film interface adhesion, increase electrical resistance, and allow for more frequent formation of non-emissive dark spots in the OLED material adversely affecting lifetime. Mechanisms to decrease anode roughness for ITO/glass substrates include the use of thin films and self-assembled monolayers. Also, alternative substrates and anode materials are being considered to increase OLED performance and lifetime. Possible examples include single crystal sapphire substrates treated with gold (Au) film anodes yielding lower work functions, operating voltages, electrical resistance values, and increasing lifetime of OLEDs.[31]

Single carrier devices are typically used to study the kinetics and charge transport mechanisms of an organic material and can be useful when trying to study energy transfer processes. As current through the device is composed of only one type of charge carrier, either electrons or holes, recombination does not occur and no light is emitted. For example, electron only devices can be obtained by replacing ITO with a lower work function metal which increases the energy barrier of hole injection. Similarly, hole only devices can be made by using a cathode made solely of aluminium, resulting in an energy barrier too large for efficient electron injection.[32][33][34]

Efficient OLEDs using small molecules were first developed by Dr. Ching W. Tang et al.[21] at Eastman Kodak. The term OLED traditionally refers specifically to this type of device, though the term SM-OLED is also in use.[23]

Molecules commonly used in OLEDs include organometallic chelates (for example Alq3, used in the organic light-emitting device reported by Tang et al.), fluorescent and phosphorescent dyes and conjugated dendrimers. A number of materials are used for their charge transport properties, for example triphenylamine and derivatives are commonly used as materials for hole transport layers.[35] Fluorescent dyes can be chosen to obtain light emission at different wavelengths, and compounds such as perylene, rubrene and quinacridone derivatives are often used.[36] Alq3 has been used as a green emitter, electron transport material and as a host for yellow and red emitting dyes.

The production of small molecule devices and displays usually involves thermal evaporation in a vacuum. This makes the production process more expensive and of limited use for large-area devices, than other processing techniques. However, contrary to polymer-based devices, the vacuum deposition process enables the formation of well controlled, homogeneous films, and the construction of very complex multi-layer structures. This high flexibility in layer design, enabling distinct charge transport and charge blocking layers to be formed, is the main reason for the high efficiencies of the small molecule OLEDs.

Coherent emission from a laser dye-doped tandem SM-OLED device, excited in the pulsed regime, has been demonstrated.[37] The emission is nearly diffraction limited with a spectral width similar to that of broadband dye lasers.[38]

Researchers report luminescence from a single polymer molecule, representing the smallest possible organic light-emitting diode (OLED) device.[39] Scientists will be able to optimize substances to produce more powerful light emissions. Finally, this work is a first step towards making molecule-sized components that combine electronic and optical properties. Similar components could form the basis of a molecular computer.[40]

Polymer light-emitting diodes (PLED), also light-emitting polymers (LEP), involve an electroluminescent conductive polymer that emits light when connected to an external voltage. They are used as a thin film for full-spectrum colour displays. Polymer OLEDs are quite efficient and require a relatively small amount of power for the amount of light produced.

Vacuum deposition is not a suitable method for forming thin films of polymers. However, polymers can be processed in solution, and spin coating is a common method of depositing thin polymer films. This method is more suited to forming large-area films than thermal evaporation. No vacuum is required, and the emissive materials can also be applied on the substrate by a technique derived from commercial inkjet printing.[41][42] However, as the application of subsequent layers tends to dissolve those already present, formation of multilayer structures is difficult with these methods. The metal cathode may still need to be deposited by thermal evaporation in vacuum. An alternative method to vacuum deposition is to deposit a Langmuir-Blodgett film.

Typical polymers used in pleaded displays include derivatives of poly(p-phenylene vinylene) and polyfluorene. Substitution of side chains onto the polymer backbone may determine the colour of emitted light[43] or the stability and solubility of the polymer for performance and ease of processing.[44]

While unsubstituted poly(p-phenylene vinylene) (PPV) is typically insoluble, a number of PPVs and related poly(naphthalene vinylene)s (PNVs) that are soluble in organic solvents or water have been prepared via ring opening metathesis polymerization.[45][46][47] These water-soluble polymers or conjugated poly electrolytes (CPEs) also can be used as hole injection layers alone or in combination with nanoparticles like graphene.[48]

Phosphorescent organic light emitting diodes use the principle of electrophosphorescence to convert electrical energy in an OLED into light in a highly efficient manner,[50][51] with the internal quantum efficiencies of such devices approaching 100%.[52]

Typically, a polymer such as poly(N-vinylcarbazole) is used as a host material to which an organometallic complex is added as a dopant. Iridium complexes[51] such as Ir(mppy)3[49] are currently the focus of research, although complexes based on other heavy metals such as platinum[50] have also been used.

The heavy metal atom at the centre of these complexes exhibits strong spin-orbit coupling, facilitating intersystem crossing between singlet and triplet states. By using these phosphorescent materials, both singlet and triplet excitons will be able to decay radiatively, hence improving the internal quantum efficiency of the device compared to a standard pleaded where only the singlet states will contribute to emission of light.

Applications of OLEDs in solid state lighting require the achievement of high brightness with good CIE coordinates (for white emission). The use of macromolecular species like polyhedral oligomeric silsesquioxanes (POSS) in conjunction with the use of phosphorescent species such as Ir for printed OLEDs have exhibited brightnesses as high as 10,000cd/m2.[53]

Patternable organic light-emitting devices use a light or heat activated electroactive layer. A latent material (PEDOT-TMA) is included in this layer that, upon activation, becomes highly efficient as a hole injection layer. Using this process, light-emitting devices with arbitrary patterns can be prepared.[57]

Colour patterning can be accomplished by means of laser, such as radiation-induced sublimation transfer (RIST).[58]

Organic vapour jet printing (OVJP) uses an inert carrier gas, such as argon or nitrogen, to transport evaporated organic molecules (as in organic vapour phase deposition). The gas is expelled through a micrometre-sized nozzle or nozzle array close to the substrate as it is being translated. This allows printing arbitrary multilayer patterns without the use of solvents.

Conventional OLED displays are formed by vapor thermal evaporation (VTE) and are patterned by shadow-mask. A mechanical mask has openings allowing the vapor to pass only on the desired location.

Like ink jet material depositioning, inkjet etching (IJE) deposits precise amounts of solvent onto a substrate designed to selectively dissolve the substrate material and induce a structure or pattern. Inkjet etching of polymer layers in OLED's can be used to increase the overall out-coupling efficiency. In OLEDs, light produced from the emissive layers of the OLED is partially transmitted out of the device and partially trapped inside the device by total internal reflection (TIR). This trapped light is wave-guided along the interior of the device until it reaches an edge where it is dissipated by either absorption or emission. Inkjet etching can be used to selectively alter the polymeric layers of OLED structures to decrease overall TIR and increase out-coupling efficiency of the OLED. Compared to a non-etched polymer layer, the structured polymer layer in the OLED structure from the IJE process helps to decrease the TIR of the OLED device. IJE solvents are commonly organic instead of water based due to their non-acidic nature and ability to effectively dissolve materials at temperatures under the boiling point of water.[59]

For a high resolution display like a TV, a TFT backplane is necessary to drive the pixels correctly. Currently, low temperature polycrystalline silicon (LTPS) thin-film transistor (TFT) is used for commercial AMOLED displays. LTPS-TFT has variation of the performance in a display, so various compensation circuits have been reported.[60] Due to the size limitation of the excimer laser used for LTPS, the AMOLED size was limited. To cope with the hurdle related to the panel size, amorphous-silicon/microcrystalline-silicon backplanes have been reported with large display prototype demonstrations.[61]

Transfer-printing is an emerging technology to assemble large numbers of parallel OLED and AMOLED devices efficiently. It takes advantage of standard metal deposition, photolithography, and etching to create alignment marks commonly on glass or other device substrates. Thin polymer adhesive layers are applied to enhance resistance to particles and surface defects. Microscale ICs are transfer-printed onto the adhesive surface and then baked to fully cure adhesive layers. An additional photosensitive polymer layer is applied to the substrate to account for the topography caused by the printed ICs, reintroducing a flat surface. Photolithography and etching removes some polymer layers to uncover conductive pads on the ICs. Afterwards, the anode layer is applied to the device backplane to form bottom electrode. OLED layers are applied to the anode layer with conventional vapor deposition, and covered with a conductive metal electrode layer. As of 2011[update] transfer-printing was capable to print onto target substrates up to 500mm X 400mm. This size limit needs to expand for transfer-printing to become a common process for the fabrication of large OLED/AMOLED displays.[62]

The different manufacturing process of OLEDs lends itself to several advantages over flat panel displays made with LCD technology.

OLED technology is used in commercial applications such as displays for mobile phones and portable digital media players, car radios and digital cameras among others. Such portable applications favor the high light output of OLEDs for readability in sunlight and their low power drain. Portable displays are also used intermittently, so the lower lifespan of organic displays is less of an issue. Prototypes have been made of flexible and rollable displays which use OLEDs' unique characteristics. Applications in flexible signs and lighting are also being developed.[86]Philips Lighting have made OLED lighting samples under the brand name "Lumiblade" available online[87] and Novaled AG based in Dresden, Germany, introduced a line of OLED desk lamps called "Victory" in September, 2011.[88]

OLEDs have been used in most Motorola and Samsung color cell phones, as well as some HTC, LG and Sony Ericsson models.[89]Nokia has also introduced some OLED products including the N85 and the N86 8MP, both of which feature an AMOLED display. OLED technology can also be found in digital media players such as the Creative ZEN V, the iriver clix, the Zune HD and the Sony Walkman X Series.

The Google and HTC Nexus One smartphone includes an AMOLED screen, as does HTC's own Desire and Legend phones. However, due to supply shortages of the Samsung-produced displays, certain HTC models will use Sony's SLCD displays in the future,[90] while the Google and Samsung Nexus S smartphone will use "Super Clear LCD" instead in some countries.[91]

OLED displays were used in watches made by Fossil (JR-9465) and Diesel (DZ-7086).

Other manufacturers of OLED panels include Anwell Technologies Limited (Hong Kong),[92]AU Optronics (Taiwan),[93]Chimei Innolux Corporation (Taiwan),[94]LG (Korea),[95] and others.[96]

In 2009, Shearwater Research introduced the Predator as the first color OLED diving computer available with a user replaceable battery.[97][98]

DuPont stated in a press release in May 2010 that they can produce a 50-inch OLED TV in two minutes with a new printing technology. If this can be scaled up in terms of manufacturing, then the total cost of OLED TVs would be greatly reduced. DuPont also states that OLED TVs made with this less expensive technology can last up to 15 years if left on for a normal eight-hour day.[99][100]

The use of OLEDs may be subject to patents held by Universal Display Corporation, Eastman Kodak, DuPont, General Electric, Royal Philips Electronics, numerous universities and others.[101] There are by now thousands of patents associated with OLEDs, both from larger corporations and smaller technology companies.[23]

RIM, the maker of BlackBerry smartphones, uses OLED displays in their BlackBerry 10 devices.

A technical writer at the Sydney Herald thinks foldable OLED smartphones could be as much as a decade away because of the cost of producing them. There is a relatively high failure rate when producing these screens. As little as a speck of dust can ruin a screen during production. Creating a battery that can be folded is another hurdle.[102] However, Samsung has accelerated its plans to release a foldable display by the end of 2015[103]

Textiles incorporating OLEDs are an innovation in the fashion world and pose for a way to integrate lighting to bring inert objects to a whole new level of fashion. The hope is to combine the comfort and low cost properties of textile with the OLEDs properties of illumination and low energy consumption. Although this scenario of illuminated clothing is highly plausible, challenges are still a road block. Some issues include: the lifetime of the OLED, rigidness of flexible foil substrates, and the lack of research in making more fabric like photonic textiles.[104]

By 2004 Samsung, South Korea's largest conglomerate, was the world's largest OLED manufacturer, producing 40% of the OLED displays made in the world,[105] and as of 2010 has a 98% share of the global AMOLED market.[106] The company is leading the world of OLED industry, generating $100.2 million out of the total $475 million revenues in the global OLED market in 2006.[107] As of 2006, it held more than 600 American patents and more than 2800 international patents, making it the largest owner of AMOLED technology patents.[107]

Samsung SDI announced in 2005 the world's largest OLED TV at the time, at 21 inches (53cm).[108] This OLED featured the highest resolution at the time, of 6.22 million pixels. In addition, the company adopted active matrix based technology for its low power consumption and high-resolution qualities. This was exceeded in January 2008, when Samsung showcased the world's largest and thinnest OLED TV at the time, at 31inches (78cm) and 4.3mm.[109]

In May 2008, Samsung unveiled an ultra-thin 12.1inch (30cm) laptop OLED display concept, with a 1,280768 resolution with infinite contrast ratio.[110] According to Woo Jong Lee, Vice President of the Mobile Display Marketing Team at Samsung SDI, the company expected OLED displays to be used in notebook PCs as soon as 2010.[111]

In October 2008, Samsung showcased the world's thinnest OLED display, also the first to be "flappable" and bendable.[112] It measures just 0.05mm (thinner than paper), yet a Samsung staff member said that it is "technically possible to make the panel thinner".[112] To achieve this thickness, Samsung etched an OLED panel that uses a normal glass substrate. The drive circuit was formed by low-temperature polysilicon TFTs. Also, low-molecular organic EL materials were employed. The pixel count of the display is 480 272. The contrast ratio is 100,000:1, and the luminance is 200cd/m2. The colour reproduction range is 100% of the NTSC standard.

In the same month, Samsung unveiled what was then the world's largest OLED Television at 40-inch with a Full HD resolution of 1920 1080 pixels.[113] In the FPD International, Samsung stated that its 40-inch OLED Panel is the largest size currently possible. The panel has a contrast ratio of 1,000,000:1, a colour gamut of 107% NTSC, and a luminance of 200cd/m2 (peak luminance of 600cd/m2).

At the Consumer Electronics Show (CES) in January 2010, Samsung demonstrated a laptop computer with a large, transparent OLED display featuring up to 40% transparency[114] and an animated OLED display in a photo ID card.[115]

Samsung's latest AMOLED smartphones use their Super AMOLED trademark, with the Samsung Wave S8500 and Samsung i9000 Galaxy S being launched in June 2010. In January 2011 Samsung announced their Super AMOLED Plus displays, which offer several advances over the older Super AMOLED displays: real stripe matrix (50% more sub pixels), thinner form factor, brighter image and an 18% reduction in energy consumption.[116]

At CES 2012, Samsung introduced the first 55" TV screen that uses Super OLED technology.[117]

On January 8, 2013, at CES Samsung unveiled a unique curved 4K Ultra S9 OLED television, which they state provides an "IMAX-like experience" for viewers.[118]

On August 13, 2013, Samsung announced availability of a 55-inch curved OLED TV (model KN55S9C) in the US at a price point of $8999.99.[119]

On September 6, 2013, Samsung launched its 55-inch curved OLED TV (model KE55S9C) in the United Kingdom with John Lewis.[120]

Samsung introduced the Galaxy Round smartphone in the Korean market in October 2013. The device features a 1080p screen, measuring 5.7 inches (14cm), that curves on the vertical axis in a rounded case. The corporation has promoted the following advantages: A new feature called "Round Interaction" that allows users to look at information by tilting the handset on a flat surface with the screen off, and the feel of one continuous transition when the user switches between home screens.[121]

The Sony CLI PEG-VZ90 was released in 2004, being the first PDA to feature an OLED screen.[123] Other Sony products to feature OLED screens include the MZ-RH1 portable minidisc recorder, released in 2006[124] and the Walkman X Series.[125]

At the 2007 Las Vegas Consumer Electronics Show (CES), Sony showcased 11-inch (28cm, resolution 960540) and 27-inch (68.5cm), full HD resolution at 1920 1080 OLED TV models.[126] Both claimed 1,000,000:1 contrast ratios and total thicknesses (including bezels) of 5mm. In April 2007, Sony announced it would manufacture 1000 11-inch (28cm) OLED TVs per month for market testing purposes.[127] On October 1, 2007, Sony announced that the 11-inch (28cm) model, now called the XEL-1, would be released commercially;[122] the XEL-1 was first released in Japan in December 2007.[128]

In May 2007, Sony publicly unveiled a video of a 2.5-inch flexible OLED screen which is only 0.3 millimeters thick.[129] At the Display 2008 exhibition, Sony demonstrated a 0.2mm thick 3.5inch (9cm) display with a resolution of 320200 pixels and a 0.3mm thick 11inch (28cm) display with 960540 pixels resolution, one-tenth the thickness of the XEL-1.[130][131]

In July 2008, a Japanese government body said it would fund a joint project of leading firms, which is to develop a key technology to produce large, energy-saving organic displays. The project involves one laboratory and 10 companies including Sony Corp. NEDO said the project was aimed at developing a core technology to mass-produce 40inch or larger OLED displays in the late 2010s.[132]

In October 2008, Sony published results of research it carried out with the Max Planck Institute over the possibility of mass-market bending displays, which could replace rigid LCDs and plasma screens. Eventually, bendable, see-through displays could be stacked to produce 3D images with much greater contrast ratios and viewing angles than existing products.[133]

Sony exhibited a 24.5" (62cm) prototype OLED 3D television during the Consumer Electronics Show in January 2010.[134]

In January 2011, Sony announced the PlayStation Vita handheld game console (the successor to the PSP) will feature a 5-inch OLED screen.[135]

On February 17, 2011, Sony announced its 25" (63.5cm) OLED Professional Reference Monitor aimed at the Cinema and high end Drama Post Production market.[136]

On June 25, 2012, Sony and Panasonic announced a joint venture for creating low cost mass production OLED televisions by 2013.[137]

As of 2010, LG Electronics produced one model of OLED television, the 15inch 15EL9500[138] and had announced a 31" (78cm) OLED 3D television for March 2011.[139] On December 26, 2011, LG officially announced the "world's largest 55" OLED panel" and featured it at CES 2012.[140] In late 2012, LG announces the launch of the 55EM9600 OLED television in Australia.[141]

In January 2015, LG Display signed a long term agreement with Universal Display Corporation for the supply of OLED materials and the right to use their patented OLED emitters.[142]

Lumiotec is the first company in the world developing and selling, since January 2011, mass-produced OLED lighting panels with such brightness and long lifetime. Lumiotec is a joint venture of Mitsubishi Heavy Industries, ROHM, Toppan Printing, and Mitsui & Co. On June 1, 2011, Mitsubishi installed a 6-meter OLED 'sphere' in Tokyo's Science Museum.[143]

On January 6, 2011, Los Angeles based technology company Recom Group introduced the first small screen consumer application of the OLED at the Consumer Electronics Show in Las Vegas. This was a 2.8" (7cm) OLED display being used as a wearable video name tag.[144] At the Consumer Electronics Show in 2012, Recom Group introduced the world's first video mic flag incorporating three 2.8" (7cm) OLED displays on a standard broadcaster's mic flag. The video mic flag allowed video content and advertising to be shown on a broadcasters standard mic flag.[145]

BMW plans to use OLEDs in tail lights and interior lights in their future cars; however, OLEDs are currently too dim to be used for brake lights, headlights and indicators.[146]

Research by Andre De-Guerin suggests that some newer panels now use screen printed chips connected with a continuous backplane to get around the need for a single monolithic and fragile silicon TFT. This approach is known to be used by Samsung on some of their newer phones notably the S6, Note 4 and others. It is believed that the self-assembly method used avoids the need to destroy bad backplanes as they can be pre-sorted at the manufacturing stage and the bad ICs replaced by micro-manipulators or other methods; where this is not possible the bad area can be cut off and the backplane area thus salvaged recycled for smaller displays such as on smart watches.

In 2014, Mitsubishi Chemical Corporation (MCC), a subsidiary of the Mitsubishi Chemical Holdings developed an organic light-emitting diode (OLED) panel with a life of 30,000 hours, twice that of conventional OLED panels.[147]

The search for efficient OLED materials has been extensively supported by simulation methods. By now it is possible to calculate important properties completely computationally, independent of experimental input.[148][149] This allows cost-efficient pre-screening of materials, prior to expensive synthesis and experimental characterisation.

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Human Longevity, Inc. Hires Cynthia Collins, Healthcare …

Posted: January 6, 2017 at 10:44 pm

"We are extremely pleased to have Cindy join HLI as our new CEO. Her wide-ranging experience in leading and growing commercial operations for privately-held and publicly-traded life science businesses, will be invaluable to HLI," said Dr. Venter. "2017 will be a key year for HLI with the launch and expansion of many of our products including oncology, whole genome, HLI Knowledgebase, HLI Search, and the HLI Health Nucleus. Cindy's combination of innovative business leadership, coupled with commercialization and operations acumen in a variety of life science arenas, is the perfect skill set to bring our vision of high quality, genomic-powered products to the global marketplace."

Collins said, "HLI represents a tremendous opportunity to change healthcare and improve patient outcomes. I cannot imagine a more perfect union of my combined experience in diagnostics, therapeutics, and life sciences and in leading organizations through multiple phases of their life cycles to create value. I believe my capabilities and experience, combined with Dr. Venter's scientific success and vision, are highly complementary and will create a solid foundation for HLI's future."

Collins comes to HLI most recently from GE Healthcare where she was the CEO/ General Manager for the Cell Therapy and Purification and Analysis Businesses. Prior to that she was CEO of GE's Clarient Diagnostics, Inc., an in vitro diagnostics business. In her three years with GE, she restructured and refocused teams and investments for multiple strategic businesses and oversaw several strategic investments in Cell Therapy, which is a strategic growth play for GE.

Prior to joining GE, Collins was recruited by the board of directors of Genvec Inc. to be president and CEO. This publicly-traded biopharmaceutical company develops therapeutics and vaccines using adenovector technologies. Under Collins' tenure the company was able to get the first gene therapy product into clinical trial, advanced four major vaccine products for partnering and received the first approval in the US for a vaccine for Foot and Mouth Disease in cattle.

Prior to Genvec, Collins was the Group Vice President of the Cellular Analysis Business Group, a $1 billion business of Beckman Coulter, comprising 3 business units; Hematology, Flow Cytometry, and Hemostasis. Collins was recruited in to regain its market leadership positions in these businesses. In her 4 years there, prior to the acquisition of Beckman Coulter by Danaher, she was successful in growing these businesses and rebuilding the leadership team.

Collins was the President and CEO of Sequoia Pharmaceuticals, Inc. post Series B Financing. While there she recruited, and led the senior management team, developed the overall strategic plan, developed and met product development milestones and created innovative financing strategies which led to a successful Series C Financing. Under her tenure, the company succeeded in getting two new drugs through the IND process and in to clinical trials.

Before Sequoia, Collins was President of Clinical Microsensors, Inc. (now Genmark), which was a wholly owned subsidiary of Motorola, where she directed the development and commercialization of molecular diagnostics, microarray products. While there the company completed several clinical trials, and received FDA approval their Cystic Fibrosis assay and instrument platform.

Collins also has deep experience in running large business units in multinational corporations. She spent 17 years at Baxter Healthcare Corporation having arrived there from a start-up, Pandex Laboratories, which was acquired by Baxter. Her tenure at Baxter included Vice President and General Manager level positions for the Gene and Cell Therapy, Transfusion Therapies and BioScience divisions. Her career there culminated in being named President of the Oncology business, a global pharmaceutic business she built and led which had $150 million in sales, 900 employees in more than 100 countries, and a $25 million research and development budget.

Prior to Baxter Healthcare, Collins spent six years at Abbott Laboratories in a variety of operational positions.

Collins received her MBA from The University of Chicago, Booth School of Business and a Bachelor's of Science in Microbiology from the University of Illinois.

About Human Longevity, Inc.Human Longevity, Inc. (HLI) is the genomics-based, heath intelligence company creating the world's largest and most comprehensive database of whole genome, phenotype and clinical data. HLI is developing and applying large scale computing and machine learning to make novel discoveries to revolutionize the practice of medicine. HLI's business also includes the HLI Health Nucleus, a genomic powered clinical research center which uses whole genome sequence analysis, advanced clinical imaging and innovative machine learning, along with curated personal health information, to deliver the most complete picture of individual health. For more information, please visit http://www.humanlongevity.com or http://www.healthnucleus.com.

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/human-longevity-inc-hires-cynthia-collins-healthcare-industry-leader-as-new-chief-executive-officer-300385584.html

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Microbiome & Metabolome Human Longevity, Inc.

Posted: December 25, 2016 at 10:43 pm

Along with the genomic data gleaned from the sequencing complete human genomes, HLI will also be generating microbiome data for many of these individuals through its Biome Health division, under the leadership of Karen Nelson, Ph.D.

Nelson, who is also President of the J. Craig Venter Institute (JCVI), and her team led the first human microbiome study on the human gut which was published in the journal Science in 2006. Nelson and her team have gone on to publish numerous scientific papers on the microbiome. JCVI is also one of three large centers funded by the National Institutes of Health as part of its Human Microbiome Project (HMP) and has several federally funded projects focused on the human microbiome and disease underway.

There are 100 times more cells from bacteria, fungi, and viruses, in and on your body than there are human cells.

The microbiome consists of all of the microbes that live in and on the human body that contribute to the health and disease status of an individual. By better understanding a persons microbiome (gut, oral, skin, lung, and other body sites), the company anticipates developing improved probiotics, advanced diagnostics and therapeutic approaches to improve health and wellness.

Along with the microbiome data, HLI will capture and analyze metabolomic data from various cohorts. The metabolome includes the complete set of metabolites in a human genome. HLI has also signed an agreement with Metabolon Inc., a diagnostic products and services company located in Research Triangle Park, NC offering the biochemical profiling platform that will be used to capture this information from the HLI samples. Metabolomics is important because quantifying and understanding the full picture of circulating chemicals in the body can help researchers get a clearer picture of that individuals health status and map changes in the small molecules to end points of disease and gene mutations.

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Posted: December 11, 2016 at 7:43 am

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Human height – Wikipedia

Posted: December 10, 2016 at 1:44 pm

Human height or stature is the distance from the bottom of the feet to the top of the head in a human body, standing erect. It is measured using a stadiometer,[1] usually in centimetres when using the metric system,[2][3] or feet and inches when using the imperial system.[4][5]

When populations share genetic background and environmental factors, average height is frequently characteristic within the group. Exceptional height variation (around 20% deviation from average) within such a population is sometimes due to gigantism or dwarfism, which are medical conditions caused by specific genes or endocrine abnormalities.[6]

The development of human height can serve as an indicator of two key welfare components, namely nutritional quality and health.[7] In regions of poverty or warfare, environmental factors like chronic malnutrition during childhood or adolescence may result in delayed growth and/or marked reductions in adult stature even without the presence of any of these medical conditions.

The study of height is known as auxology.[8] Growth has long been recognized as a measure of the health of individuals, hence part of the reasoning for the use of growth charts. For individuals, as indicators of health problems, growth trends are tracked for significant deviations and growth is also monitored for significant deficiency from genetic expectations. Genetics is a major factor in determining the height of individuals, though it is far less influential in regard to differences among populations. Average height is relevant to the measurement of the health and wellness (standard of living and quality of life) of populations.[9]

Attributed as a significant reason for the trend of increasing height in parts of Europe are the egalitarian populations where proper medical care and adequate nutrition are relatively equally distributed.[10] Changes in diet (nutrition) and a general rise in quality of health care and standard of living are the cited factors in the Asian populations. Malnutrition including chronic undernutrition and acute malnutrition is known to have caused stunted growth in various populations.[11] This has been seen in North Korea, parts of Africa, certain historical Europe, and other populations.[12]Developing countries such as Guatemala have rates of stunting in children under 5 living as high as 82.2% in Totonicapn, and 49.8% nationwide.[13]

Height measurements are by nature subject to statistical sampling errors even for a single individual.[clarification needed] In a clinical situation, height measurements are seldom taken more often than once per office visit, which may mean sampling taking place a week to several months apart. The smooth 50th percentile male and female growth curves illustrated above are aggregate values from thousands of individuals sampled at ages from birth to age 20. In reality, a single individual's growth curve shows large upward and downward spikes, partly due to actual differences in growth velocity, and partly due to small measurement errors.

For example, a typical measurement error of plus or minus 0.5cm may completely nullify 0.5cm of actual growth resulting in either a "negative" 0.5cm growth (due to overestimation in the previous visit combined with underestimation in the latter), up to a 1.5cm growth (the first visit underestimating and the second visit overestimating) in the same elapsed time period between measurements. Note there is a discontinuity in the growth curves at age 2, which reflects the difference in recumbent length (with the child on his or her back), used in measuring infants and toddlers and standing height typically measured from age 2 onwards.

Height, like other phenotypic traits, is determined by a combination of genetics and environmental factors. A child's height based on parental heights is subject to regression toward the mean, therefore extremely tall or short parents will likely have correspondingly taller or shorter offspring, but their offspring will also likely be closer to average height than the parents themselves. Genetic potential and a number of hormones, minus illness, is a basic determinant for height. Other factors include the genetic response to external factors such as diet, exercise, environment, and life circumstances.

Humans grow fastest (other than in the womb) as infants and toddlers, rapidly declining from a maximum at birth to roughly age 2, tapering to a slowly declining rate, and then during the pubertal growth spurt, a rapid rise to a second maximum (at around 1112 years for female, and 1314 years for male), followed by a steady decline to zero. On average, female growth speed trails off to zero at about 15 or 16 years, whereas the male curve continues for approximately 3 more years, going to zero at about 1820. These are also critical periods where stressors such as malnutrition (or even severe child neglect) have the greatest effect.

Moreover, the health of a mother throughout her life, especially during her critical period and pregnancy, has a role. A healthier child and adult develops a body that is better able to provide optimal prenatal conditions.[12] The pregnant mother's health is important for herself but also for the fetus as gestation is itself a critical period for an embryo/fetus, though some problems affecting height during this period are resolved by catch-up growth assuming childhood conditions are good. Thus, there is a cumulative generation effect such that nutrition and health over generations influences the height of descendants to varying degrees.

The age of the mother also has some influence on her child's height. Studies in modern times have observed a gradual increase in height with maternal age, though these early studies suggest that trend is due to various socio-economic situations that select certain demographics as being more likely to have a first birth early in the mother's life.[14][15][16] These same studies show that children born to a young mother are more likely to have below-average educational and behavioural development, again suggesting an ultimate cause of resources and family status rather than a purely biological explanation.[15][16]

It has been observed that first-born males are shorter than later-born males.[17] However, more recently the reverse observation was made.[18] The study authors suggest that the cause may be socio-economic in nature.

The precise relationship between genetics and environment is complex and uncertain. Differences in human height is 60%80% heritable, according to several twin studies[19] and has been considered polygenic since the Mendelian-biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height.[20] The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.[21] In a separate study of body proportion using sitting-height ratio, it reports that these 697 variants can be partitioned into 3 specific classes, (1) variants that primarily determine leg length, (2) variants that primarily determine spine and head length, or (3) variants that affect overall body size. This gives insights into the biological mechanisms underlying how these 697 genetic variants affect overall height.[22]

The effect of environment on height is illustrated by studies performed by anthropologist Barry Bogin and coworkers of Guatemala Mayan children living in the United States. In the early 1970s, when Bogin first visited Guatemala, he observed that Mayan Indian men averaged only 157.5 centimetres (5ft 2in) in height and the women averaged 142.2 centimetres (4ft 8in). Bogin took another series of measurements after the Guatemalan Civil War, during which up to a million Guatemalans fled to the United States. He discovered that Maya refugees, who ranged from six to twelve years old, were significantly taller than their Guatemalan counterparts.[23] By 2000, the American Maya were 10.24cm (4.03in) taller than the Guatemalan Maya of the same age, largely due to better nutrition and health care.[24] Bogin also noted that American Maya children had relatively longer legs, averaging 7.02cm (2.76in) longer than the Guatemalan Maya (a significantly lower sitting height ratio).[24][25]

The Nilotic peoples of Sudan such as the Shilluk and Dinka have been described as some of the tallest in the world. Dinka Ruweng males investigated by Roberts in 195354 were on average 181.3 centimetres (5ft 1112in) tall, and Shilluk males averaged 182.6 centimetres (6ft 0in).[26] The Nilotic people are characterized as having long legs, narrow bodies and short trunks, an adaptation to hot weather.[27] However, male Dinka and Shilluk refugees measured in 1995 in Southwestern Ethiopia were on average only 1.764 m and 1.726 m tall, respectively. As the study points out, Nilotic people "may attain greater height if priviledged with favourable environmental conditions during early childhood and adolescence, allowing full expression of the genetic material."[28] Before fleeing, these refugees were subject to privation as a consequence of the succession of civil wars in their country from 1955 to the present. The tallest living married couple are ex-basketball players Yao Ming and Ye Li (both of China) who measure 228.6cm (7 ft 11 in) and 190.5cm (6 ft 3 in) respectively, giving a combined height of 419.1cm (13 ft 9 in). They married in Shanghai, China, on 6 August 2007.[29]

In Tibet, the khampas are known for their great height. Khampa males are on average 180cm tall (5ft 11 in).[30][31]

The people of the Dinaric Alps (mainly North Albanians and South Slavs) are on record as being the tallest in the world, with a male average height of 185.6cm (6ft 1.1 in) and female average height of 170.9cm (5ft 7.3 in).

Growth in stature, determined by its various factors, results from the lengthening of bones via cellular divisions chiefly regulated by somatotropin (human growth hormone (hGH)) secreted by the anterior pituitary gland. Somatotropin also stimulates the release of another growth inducing hormone Insulin-like growth factor 1 (IGF-1) mainly by the liver. Both hormones operate on most tissues of the body, have many other functions, and continue to be secreted throughout life; with peak levels coinciding with peak growth velocity, and gradually subsiding with age after adolescence. The bulk of secretion occurs in bursts (especially for adolescents) with the largest during sleep.

The majority of linear growth occurs as growth of cartilage at the epiphysis (ends) of the long bones which gradually ossify to form hard bone. The legs compose approximately half of adult human height, and leg length is a somewhat sexually dimorphic trait, with men having proportionately longer legs. Some of this growth occurs after the growth spurt of the long bones has ceased or slowed. The majority of growth during growth spurts is of the long bones. Additionally, the variation in height between populations and across time is largely due to changes in leg length. The remainder of height consists of the cranium. Height is sexually dimorphic and statistically it is more or less normally distributed, but with heavy tails.[citation needed] It has been shown that a log-normal distribution fits the data equally well, besides guaranteeing a non-negative lower confidence limit, which could otherwise attain a non-physical negative height value for arbitrarily large confidence levels.[32]

Most intra-population variance of height is genetic. Short stature and tall stature are usually not a health concern. If the degree of deviation from normal is significant, hereditary short stature is known as familial short stature and tall stature is known as familial tall stature. Confirmation that exceptional height is normal for a respective person can be ascertained from comparing stature of family members and analyzing growth trends for abrupt changes, among others. There are, however, various diseases and disorders that cause growth abnormalities.

Most notably, extreme height may be pathological, such as gigantism resulting from childhood hyperpituitarism, and dwarfism which has various causes. Rarely, no cause can be found for extreme height; very short persons may be termed as having idiopathic short stature. The United States Food and Drug Administration (FDA) in 2003 approved hGH treatment for those 2.25 standard deviations below the population mean (approximately the lowest 1.2% of the population). An even rarer occurrence, or at least less used term and recognized "problem", is idiopathic tall stature.

If not enough growth hormone is produced and/or secreted by the pituitary gland, then a patient with growth hormone deficiency can undergo treatment. This treatment involves the injection of pure growth hormone into thick tissue to promote growth.

Certain studies have shown that height is a factor in overall health while some suggest tallness is associated with better cardiovascular health and shortness with longevity.[33] Cancer risk has also been found to grow with height.[34]

Nonetheless, modern westernized interpretations of the relationship between height and health fail to account for the observed height variations worldwide.[35] Cavalli-Sforza and Cavalli-Sforza note that variations in height worldwide can be partly attributed to evolutionary pressures resulting from differing environments. These evolutionary pressures result in height related health implications. While tallness is an adaptive benefit in colder climates such as found in Europe, shortness helps dissipate body heat in warmer climatic regions.[35] Consequently, the relationships between health and height cannot be easily generalized since tallness and shortness can both provide health benefits in different environmental settings.

At the extreme end, being excessively tall can cause various medical problems, including cardiovascular problems, because of the increased load on the heart to supply the body with blood, and problems resulting from the increased time it takes the brain to communicate with the extremities. For example, Robert Wadlow, the tallest man known to verifiable history, developed trouble walking as his height increased throughout his life. In many of the pictures of the later portion of his life, Wadlow can be seen gripping something for support. Late in his life, although he died at age 22, he had to wear braces on his legs and walk with a cane; and he died after developing an infection in his legs because he was unable to feel the irritation and cutting caused by his leg braces.

Sources are in disagreement about the overall relationship between height and longevity. Samaras and Elrick, in the Western Journal of Medicine, demonstrate an inverse correlation between height and longevity in several mammals including humans.[33]

Women whose height is under 150cm (4ft 11in) may have a small pelvis, resulting in such complications during childbirth as shoulder dystocia.[36]

A study done in Sweden in 2005 has shown that there is a strong inverse correlation between height and suicide among Swedish men.[37]

A large body of human and animal evidence indicates that shorter, smaller bodies age slower, and have fewer chronic diseases and greater longevity. For example, a study found eight areas of support for the "smaller lives longer" thesis. These areas of evidence include studies involving longevity, life expectancy, centenarians, male vs. female longevity differences, mortality advantages of shorter people, survival findings, smaller body size due to calorie restriction, and within species body size differences. They all support the conclusion that smaller individuals live longer in healthy environments and with good nutrition. However, the difference in longevity is modest. Several human studies have found a loss of 0.5 year/centimeter of increased height (1.2 yr/inch). But these findings do not mean that all tall people die young. Many live to advanced ages and some become centenarians.[38]

There is a large body of research in psychology, economics, and human biology that has assessed the relationship between several seemingly innocuous physical features (e.g., body height) and occupational success.[39] The correlation between height and success was explored decades ago.[40][41] Shorter people are considered to have an advantage in certain sports (e.g., gymnastics, race car driving, etc.), whereas in many other sports taller people have a major advantage. In most occupational fields, body height is not relevant to how well people are able to perform, but nonetheless has been found to correlate with their success in several studies, although there may be other factors such as gender or socioeonomic status that explain this.[39][40][42][43]

A demonstration of the height-success association can be found in the realm of politics. In the United States presidential elections, the taller candidate won 22 out of 25 times in the 20th century.[44] Nevertheless, Ignatius Loyola, founder of the Jesuits, was 150cm (4ft 11in) and several prominent world leaders of the 20th century, such as Vladimir Lenin, Benito Mussolini, Nicolae Ceauescu and Joseph Stalin were of below average height. These examples, however, were all before modern forms of multi-media, i.e., television, which may further height discrimination in modern society. Further, growing evidence suggests that height may be a proxy for confidence, which is likewise strongly correlated with occupational success.[45]

In the eighteenth and nineteenth centuries, people of European descent in North America were far taller than those in Europe and were the tallest in the world.[10] The original indigenous population of Plains Native Americans was also among the tallest populations of the world at the time.[46]

In the late nineteenth century, the Netherlands was a land renowned for its short population, but today its population is among the world's tallest with young men averaging 183.8cm (6ft 0.4in) tall.[47]

According to a study by economist John Komlos and Francesco Cinnirella, in the first half of the 18th century, the average height of an English male was 165cm (5ft 5 in), and the average height of an Irish male was 168cm (5ft 6 in). The estimated mean height of English, German, and Scottish soldiers was 163.6cm 165.9cm (5ft 4.4 in 5ft 5.3 in) for the period as a whole, while that of Irish was 167.9cm (5ft 6.1 in). The average height of male slaves and convicts in North America was 171cm (5ft 7 in).[48]

American-born colonial soldiers of the late 1770s were on average more than 7.6cm (3 inches) taller than their English counterparts who served in Royal Marines at the same time.[49]

Average height of Americans and Europeans decreased during periods of rapid industrialization, possibly due to rapid population growth and increased economic inequality.[50] In early 19th century England, the difference between average height of English upper class youth (students of Sandhurst Military Academy) and English lower class youth (Marine Society boys) reached 22cm (8.7in), the highest that has been observed.[51]

Data derived from burials show that before 1850, the mean stature of males and females in Leiden, Netherlands was respectively 166.7cm (5ft 5.6 in) and 156.7cm (5ft 1.7 in). The average height of 19-year-old Dutch orphans in 1865 was 160cm (5ft 3 in).[52]

According to a study by J.W. Drukker and Vincent Tassenaar, the average height of Dutch decreased from 1830 to 1857, even while Dutch real GNP per capita was growing at an average rate of more than 0.5 percent per year. The worst decline were in urban areas that in 1847, the urban height penalty was 2.5cm (1in). Urban mortality was also much higher than rural regions. In 1829, the average urban and rural Dutchman was 164cm (5ft 4.6 in). By 1856, the average rural Dutchman was 162cm (5ft 3.8 in) and urban Dutchman was 158.5cm (5ft 2.4 in).[53]

A 2004 report citing a 2003 UNICEF study on the effects of malnutrition in North Korea, due to "successive famines," found young adult males to be significantly shorter.[specify] In contrast South Koreans "feasting on an increasingly Western-influenced diet," without famine, were growing taller. The height difference is minimal for Koreans over 40, who grew up at a time when economic conditions in the North were roughly comparable to those in the South, while height disparities are most acute for Koreans who grew up in the mid-1990s a demographic in which South Koreans are about 12cm (4.7in) taller than their North Korean counterparts as this was a period during which the North was affected by a harsh famine.[54] A study by South Korean anthropologists of North Korean children who had defected to China found that 18-year-old males were 5inches (13cm) shorter than South Koreans their age due to malnutrition.[55]

The tallest living man is Sultan Ksen of Turkey, at 251cm (8ft 3in). The tallest man in modern history was Robert Pershing Wadlow (19181940), from Illinois, in the United States, who was 272cm (8ft 11in) at the time of his death. The tallest woman in medical history was Zeng Jinlian of Hunan, China, who stood 248cm (8ft 112in) when she died at the age of 17. The shortest adult human on record was Chandra Bahadur Dangi of Nepal at 54.6cm (1ft 912in).

Adult height between populations often differs significantly. For example, the average height of women from the Czech Republic is greater than that of men from Malawi. This may be caused by genetic differences, childhood lifestyle differences (nutrition, sleep patterns, physical labor), or both.

Depending on sex, genetic and environmental factors, shrinkage of stature may begin in middle age in some individuals but tends to be universal in the extremely aged. This decrease in height is due to such factors as decreased height of inter-vertebral discs because of desiccation, atrophy of soft tissues and postural changes secondary to degenerative disease.

As with any statistical data, the accuracy of such data may be questionable for various reasons:

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Ageing – Wikipedia

Posted: December 7, 2016 at 7:57 am

Ageing, also spelled aging, is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing).

In humans, ageing represents the accumulation of changes in a human being over time,[1] encompassing physical, psychological, and social change. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases:[2] of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.

The causes of ageing are unknown; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA breaks, oxidised DNA and/or mitochondrial malfunctions)[3] may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA telomere shortening) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).

The discovery, in 1934, that calorie restriction can extend lifespan by 50% in rats has motivated research into delaying and preventing ageing.

Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age.[4] In contrast, many species can be considered immortal: for example, bacteria fission to produce daughter cells, strawberry plants grow runners to produce clones of themselves, and animals in the genus Hydra have a regenerative ability with which they avoid dying of old age.

Early life forms on Earth, starting at least 3.7 billion years ago,[5] were single-celled organisms. Such single-celled organisms (prokaryotes, protozoans, algae) multiply by fissioning into daughter cells, thus do not age and are innately immortal.[6][7]

Ageing and mortality of the individual organism became possible with the evolution of sexual reproduction,[8] which occurred with the emergence of the fungal/animal kingdoms approximately a billion years ago, and with the evolution of flowering plants 160 million years ago. The sexual organism could henceforth pass on some of its genetic material to produce new individuals and itself could become disposable with regards to the survival of its species.[8] This classic biological idea has however been perturbed recently by the discovery that the bacterium E. coli may split into distinguishable daughter cells, which opens the theoretical possibility of "age classes" among bacteria.[9]

Even within humans and other mortal species, there are cells with the potential for immortality: cancer cells which have lost the ability to die when maintained in cell culture such as the HeLa cell line,[10] and specific stem cells such as germ cells (producing ova and spermatozoa).[11] In artificial cloning, adult cells can be rejuvenated back to embryonic status and then used to grow a new tissue or animal without ageing.[12] Normal human cells however die after about 50 cell divisions in laboratory culture (the Hayflick Limit, discovered by Leonard Hayflick in 1961).[10]

A number of characteristic ageing symptoms are experienced by a majority or by a significant proportion of humans during their lifetimes.

Dementia becomes more common with age.[35] About 3% of people between the ages of 6574 have dementia, 19% between 75 and 84 and nearly half of those over 85 years of age.[36] The spectrum includes mild cognitive impairment and the neurodegenerative diseases of Alzheimer's disease, cerebrovascular disease, Parkinson's disease and Lou Gehrig's disease. Furthermore, many types of memory may decline with ageing, but not semantic memory or general knowledge such as vocabulary definitions, which typically increases or remains steady until late adulthood[37] (see Ageing brain). Intelligence may decline with age, though the rate may vary depending on the type and may in fact remain steady throughout most of the lifespan, dropping suddenly only as people near the end of their lives. Individual variations in rate of cognitive decline may therefore be explained in terms of people having different lengths of life.[38] There might be changes to the brain: after 20 years of age there may be a 10% reduction each decade in the total length of the brain's myelinated axons.[39][40]

Age can result in visual impairment, whereby non-verbal communication is reduced,[41] which can lead to isolation and possible depression. Macular degeneration causes vision loss and increases with age, affecting nearly 12% of those above the age of 80.[42] This degeneration is caused by systemic changes in the circulation of waste products and by growth of abnormal vessels around the retina.[43]

A distinction can be made between "proximal ageing" (age-based effects that come about because of factors in the recent past) and "distal ageing" (age-based differences that can be traced back to a cause early in person's life, such as childhood poliomyelitis).[38]

Ageing is among the greatest known risk factors for most human diseases.[2] Of the roughly 150,000 people who die each day across the globe, about two thirds100,000 per daydie from age-related causes. In industrialised nations, the proportion is higher, reaching 90%.[44][45][46]

At present, researchers are only just beginning to understand the biological basis of ageing even in relatively simple and short-lived organisms such as yeast.[47] Less still is known about mammalian ageing, in part due to the much longer lives in even small mammals such as the mouse (around 3 years). A primary model organism for studying ageing is the nematode C. elegans, thanks to its short lifespan of 23 weeks, the ability to easily perform genetic manipulations or suppress gene activity with RNA interference, and other factors.[48] Most known mutations and RNA interference targets that extend lifespan were first discovered in C. elegans.[49]

Factors that are proposed to influence biological ageing[50] fall into two main categories, programmed and damage-related. Programmed factors follow a biological timetable, perhaps a continuation of the one that regulates childhood growth and development. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defence responses. Damage-related factors include internal and environmental assaults to living organisms that induce cumulative damage at various levels.[51]

There are three main metabolic pathways which can influence the rate of ageing:

It is likely that most of these pathways affect ageing separately, because targeting them simultaneously leads to additive increases in lifespan.[53]

The rate of ageing varies substantially across different species, and this, to a large extent, is genetically based. For example, numerous perennial plants ranging from strawberries and potatoes to willow trees typically produce clones of themselves by vegetative reproduction and are thus potentially immortal, while annual plants such as wheat and watermelons die each year and reproduce by sexual reproduction. In 2008 it was discovered that inactivation of only two genes in the annual plant Arabidopsis thaliana leads to its conversion into a potentially immortal perennial plant.[54]

Clonal immortality apart, there are certain species whose individual lifespans stand out among Earth's life-forms, including the bristlecone pine at 5062 years[55] (however Hayflick states that the bristlecone pine has no cells older than 30 years), invertebrates like the hard clam (known as quahog in New England) at 508 years,[56] the Greenland shark at 400 years,[57] fish like the sturgeon and the rockfish, and the sea anemone[58] and lobster.[59][60] Such organisms are sometimes said to exhibit negligible senescence.[61] The genetic aspect has also been demonstrated in studies of human centenarians.

In laboratory settings, researchers have demonstrated that selected alterations in specific genes can extend lifespan quite substantially in yeast and roundworms, less so in fruit flies and less again in mice. Some of the targeted genes have homologues across species and in some cases have been associated with human longevity.[62]

Caloric restriction substantially affects lifespan in many animals, including the ability to delay or prevent many age-related diseases.[103] Typically, this involves caloric intake of 6070% of what an ad libitum animal would consume, while still maintaining proper nutrient intake.[103] In rodents, this has been shown to increase lifespan by up to 50%;[104] similar effects occur for yeast and Drosophila.[103] No lifespan data exist for humans on a calorie-restricted diet,[76] but several reports support protection from age-related diseases.[105][106] Two major ongoing studies on rhesus monkeys initially revealed disparate results; while one study, by the University of Wisconsin, showed that caloric restriction does extend lifespan,[107] the second study, by the National Institute on Ageing (NIA), found no effects of caloric restriction on longevity.[108] Both studies nevertheless showed improvement in a number of health parameters. Notwithstanding the similarly low calorie intake, the diet composition differed between the two studies (notably a high sucrose content in the Wisconsin study), and the monkeys have different origins (India, China), initially suggesting that genetics and dietary composition, not merely a decrease in calories, are factors in longevity.[76] However, in a comparative analysis in 2014, the Wisconsin researchers found that the allegedly non-starved NIA control monkeys in fact are moderately underweight when compared with other monkey populations, and argued this was due to the NIA's apportioned feeding protocol in contrast to Wisconsin's truly unrestricted ad libitum feeding protocol.[109] They conclude that moderate calorie restriction rather than extreme calorie restriction is sufficient to produce the observed health and longevity benefits in the studied rhesus monkeys.[110]

In his book How and Why We Age, Hayflick says that caloric restriction may not be effective in humans, citing data from the Baltimore Longitudinal Study of Aging which shows that being thin does not favour longevity.[need quotation to verify][111] Similarly, it is sometimes claimed that moderate obesity in later life may improve survival, but newer research has identified confounding factors such as weight loss due to terminal disease. Once these factors are accounted for, the optimal body weight above age 65 corresponds to a leaner body mass index of 23 to 27.[112]

Alternatively, the benefits of dietary restriction can also be found by changing the macro nutrient profile to reduce protein intake without any changes to calorie level, resulting in similar increases in longevity.[113][114] Dietary protein restriction not only inhibits mTOR activity but also IGF-1, two mechanisms implicated in ageing.[74] Specifically, reducing leucine intake is sufficient to inhibit mTOR activity, achievable through reducing animal food consumption.[115][116]

The Mediterranean diet is credited with lowering the risk of heart disease and early death.[117][118] The major contributors to mortality risk reduction appear to be a higher consumption of vegetables, fish, fruits, nuts and monounsaturated fatty acids, i.e., olive oil.[119]

The amount of sleep has an impact on mortality. People who live the longest report sleeping for six to seven hours each night.[120][121] Lack of sleep (<5 hours) more than doubles the risk of death from cardiovascular disease, but too much sleep (>9 hours) is associated with a doubling of the risk of death, though not primarily from cardiovascular disease.[122] Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality, though the cause is probably other factors such as depression and socioeconomic status, which would correlate statistically.[123] Sleep monitoring of hunter-gatherer tribes from Africa and from South America has shown similar sleep patterns across continents: their average sleeping duration is 6.4 hours (with a summer/winter difference of 1 hour), afternoon naps (siestas) are uncommon, and insomnia is very rare (tenfold less than in industrial societies).[124]

Physical exercise may increase life expectancy.[125] People who participate in moderate to high levels of physical exercise have a lower mortality rate compared to individuals who are not physically active.[126] Moderate levels of exercise have been correlated with preventing aging and improving quality of life by reducing inflammatory potential.[127] The majority of the benefits from exercise are achieved with around 3500 metabolic equivalent (MET) minutes per week.[128] For example, climbing stairs 10 minutes, vacuuming 15 minutes, gardening 20 minutes, running 20 minutes, and walking or bicycling for 25 minutes on a daily basis would together achieve about 3000 MET minutes a week.[128]

Avoidance of chronic stress (as opposed to acute stress) is associated with a slower loss of telomeres in most but not all studies,[129][130] and with decreased cortisol levels. A chronically high cortisol level compromises the immune system, causes cardiac damage/arterosclerosis and is associated with facial ageing, and the latter in turn is a marker for increased morbidity and mortality.[131][132] Stress can be countered by social connection, spirituality, and (for men more clearly than for women) married life, all of which are associated with longevity.[133][134][135]

The following drugs and interventions have been shown to retard or reverse the biological effects of ageing in animal models, but none has yet been proven to do so in humans.

Evidence in both animals and humans suggests that resveratrol may be a caloric restriction mimetic.[136]

As of 2015 metformin was under study for its potential effect on slowing ageing in the worm C.elegans and the cricket.[137] Its effect on otherwise healthy humans is unknown.[137]

Rapamycin was first shown to extend lifespan in eukaryotes in 2006 by Powers et al. who showed a dose-responsive effect of rapamycin on lifespan extension in yeast cells.[138] In a 2009 study, the lifespans of mice fed rapamycin were increased between 28 and 38% from the beginning of treatment, or 9 to 14% in total increased maximum lifespan. Of particular note, the treatment began in mice aged 20 months, the equivalent of 60 human years.[139] Rapamycin has subsequently been shown to extend mouse lifespan in several separate experiments,[140][141] and is now being tested for this purpose in nonhuman primates (the marmoset monkey).[142]

Cancer geneticist Ronald A. DePinho and his colleagues published research in mice where telomerase activity was first genetically removed. Then, after the mice had prematurely aged, they restored telomerase activity by reactivating the telomerase gene. As a result, the mice were rejuvenated: Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver, intestines and brain, recuperated from their degenerated state. "[The finding] offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working" says Ronald DePinho. However, activating telomerase in humans could potentially encourage the growth of tumours.[143]

Most known genetic interventions in C. elegans increase lifespan by 1.5 to 2.5-fold. As of 2009[update], the record for lifespan extension in C. elegans is a single-gene mutation which increases adult survival by tenfold.[49] The strong conservation of some of the mechanisms of ageing discovered in model organisms imply that they may be useful in the enhancement of human survival. However, the benefits may not be proportional; longevity gains are typically greater in C. elegans than fruit flies, and greater in fruit flies than in mammals. One explanation for this is that mammals, being much longer-lived, already have many traits which promote lifespan.[49]

Some research effort is directed to slow ageing and extend healthy lifespan.[144][145][146]

The US National Institute on Aging currently funds an intervention testing programme, whereby investigators nominate compounds (based on specific molecular ageing theories) to have evaluated with respect to their effects on lifespan and age-related biomarkers in outbred mice.[147] Previous age-related testing in mammals has proved largely irreproducible, because of small numbers of animals and lax mouse husbandry conditions.[citation needed] The intervention testing programme aims to address this by conducting parallel experiments at three internationally recognised mouse ageing-centres, the Barshop Institute at UTHSCSA, the University of Michigan at Ann Arbor and the Jackson Laboratory.

Several companies and organisations, such as Google Calico, Human Longevity, Craig Venter, Gero,[148]SENS Research Foundation, and Science for Life Extension in Russia,[149] declared stopping or delaying ageing as their goal.

Prizes for extending lifespan and slowing ageing in mammals exist. The Methuselah Foundation offers the Mprize. Recently, the $1 Million Palo Alto Longevity Prize was launched. It is a research incentive prize to encourage teams from all over the world to compete in an all-out effort to "hack the code" that regulates our health and lifespan. It was founded by Joon Yun.[150][151][152][153][154]

Different cultures express age in different ways. The age of an adult human is commonly measured in whole years since the day of birth. Arbitrary divisions set to mark periods of life may include: juvenile (via infancy, childhood, preadolescence, adolescence), early adulthood, middle adulthood, and late adulthood. More casual terms may include "teenagers," "tweens," "twentysomething", "thirtysomething", etc. as well as "vicenarian", "tricenarian", "quadragenarian", etc.

Most legal systems define a specific age for when an individual is allowed or obliged to do particular activities. These age specifications include voting age, drinking age, age of consent, age of majority, age of criminal responsibility, marriageable age, age of candidacy, and mandatory retirement age. Admission to a movie for instance, may depend on age according to a motion picture rating system. A bus fare might be discounted for the young or old. Each nation, government and non-governmental organisation has different ways of classifying age. In other words, chronological ageing may be distinguished from "social ageing" (cultural age-expectations of how people should act as they grow older) and "biological ageing" (an organism's physical state as it ages).[155]

In a UNFPA report about ageing in the 21st century, it highlighted the need to "Develop a new rights-based culture of ageing and a change of mindset and societal attitudes towards ageing and older persons, from welfare recipients to active, contributing members of society."[156] UNFPA said that this "requires, among others, working towards the development of international human rights instruments and their translation into national laws and regulations and affirmative measures that challenge age discrimination and recognise older people as autonomous subjects."[156] Older persons make contributions to society including caregiving and volunteering. For example, "A study of Bolivian migrants who [had] moved to Spain found that 69% left their children at home, usually with grandparents. In rural China, grandparents care for 38% of children aged under five whose parents have gone to work in cities."[156]

Population ageing is the increase in the number and proportion of older people in society. Population ageing has three possible causes: migration, longer life expectancy (decreased death rate) and decreased birth rate. Ageing has a significant impact on society. Young people tend to have fewer legal privileges (if they are below the age of majority), they are more likely to push for political and social change, to develop and adopt new technologies, and to need education. Older people have different requirements from society and government, and frequently have differing values as well, such as for property and pension rights.[157]

In the 21st century, one of the most significant population trends is ageing.[158] Currently, over 11% of the world's current population are people aged 60 and older and the United Nations Population Fund (UNFPA) estimates that by 2050 that number will rise to approximately 22%.[156] Ageing has occurred due to development which has enabled better nutrition, sanitation, health care, education and economic well-being. Consequently, fertility rates have continued to decline and life expectancy have risen. Life expectancy at birth is over 80 now in 33 countries. Ageing is a "global phenomenon," that is occurring fastest in developing countries, including those with large youth populations, and poses social and economic challenges to the work which can be overcome with "the right set of policies to equip individuals, families and societies to address these challenges and to reap its benefits."[159]

As life expectancy rises and birth rates decline in developed countries, the median age rises accordingly. According to the United Nations, this process is taking place in nearly every country in the world.[160] A rising median age can have significant social and economic implications, as the workforce gets progressively older and the number of old workers and retirees grows relative to the number of young workers. Older people generally incur more health-related costs than do younger people in the workplace and can also cost more in worker's compensation and pension liabilities.[161] In most developed countries an older workforce is somewhat inevitable. In the United States for instance, the Bureau of Labor Statistics estimates that one in four American workers will be 55 or older by 2020.[161]

Among the most urgent concerns of older persons worldwide is income security. This poses challenges for governments with ageing populations to ensure investments in pension systems continues in order to provide economic independence and reduce poverty in old age. These challenges vary for developing and developed countries. UNFPA stated that, "Sustainability of these systems is of particular concern, particularly in developed countries, while social protection and old-age pension coverage remain a challenge for developing countries, where a large proportion of the labour force is found in the informal sector."[156]

The global economic crisis has increased financial pressure to ensure economic security and access to health care in old age. In order to elevate this pressure "social protection floors must be implemented in order to guarantee income security and access to essential health and social services for all older persons and provide a safety net that contributes to the postponement of disability and prevention of impoverishment in old age."[156]

It has been argued that population ageing has undermined economic development.[162] Evidence suggests that pensions, while making a difference to the well-being of older persons, also benefit entire families especially in times of crisis when there may be a shortage or loss of employment within households. A study by the Australian Government in 2003 estimated that "women between the ages of 65 and 74 years contribute A$16 billion per year in unpaid caregiving and voluntary work. Similarly, men in the same age group contributed A$10 billion per year."[156]

Due to increasing share of the elderly in the population, health care expenditures will continue to grow relative to the economy in coming decades. This has been considered as a negative phenomenon and effective strategies like labour productivity enhancement should be considered to deal with negative consequences of ageing.[163]

In the field of sociology and mental health, ageing is seen in five different views: ageing as maturity, ageing as decline, ageing as a life-cycle event, ageing as generation, and ageing as survival.[164] Positive correlates with ageing often include economics, employment, marriage, children, education, and sense of control, as well as many others. The social science of ageing includes disengagement theory, activity theory, selectivity theory, and continuity theory. Retirement, a common transition faced by the elderly, may have both positive and negative consequences.[165] As cyborgs currently are on the rise some theorists argue there is a need to develop new definitions of ageing and for instance a bio-techno-social definition of ageing has been suggested.[166]

With age inevitable biological changes occur that increase the risk of illness and disability. UNFPA states that,[159]

"A life-cycle approach to health care one that starts early, continues through the reproductive years and lasts into old age is essential for the physical and emotional well-being of older persons, and, indeed, all people. Public policies and programmes should additionally address the needs of older impoverished people who cannot afford health care."

Many societies in Western Europe and Japan have ageing populations. While the effects on society are complex, there is a concern about the impact on health care demand. The large number of suggestions in the literature for specific interventions to cope with the expected increase in demand for long-term care in ageing societies can be organised under four headings: improve system performance; redesign service delivery; support informal caregivers; and shift demographic parameters.[167]

However, the annual growth in national health spending is not mainly due to increasing demand from ageing populations, but rather has been driven by rising incomes, costly new medical technology, a shortage of health care workers and informational asymmetries between providers and patients.[168] A number of health problems become more prevalent as people get older. These include mental health problems as well as physical health problems, especially dementia.

It has been estimated that population ageing only explains 0.2 percentage points of the annual growth rate in medical spending of 4.3% since 1970. In addition, certain reforms to the Medicare system in the United States decreased elderly spending on home health care by 12.5% per year between 1996 and 2000.[169]

Positive self-perception of health has been correlated with higher well-being and reduced mortality in the elderly.[170][171] Various reasons have been proposed for this association; people who are objectively healthy may naturally rate their health better than that of their ill counterparts, though this link has been observed even in studies which have controlled for socioeconomic status, psychological functioning and health status.[172] This finding is generally stronger for men than women,[171] though this relationship is not universal across all studies and may only be true in some circumstances.[172]

As people age, subjective health remains relatively stable, even though objective health worsens.[173] In fact, perceived health improves with age when objective health is controlled in the equation.[174] This phenomenon is known as the "paradox of ageing." This may be a result of social comparison;[175] for instance, the older people get, the more they may consider themselves in better health than their same-aged peers.[176] Elderly people often associate their functional and physical decline with the normal ageing process.[177][178]

The concept of successful ageing can be traced back to the 1950s and was popularised in the 1980s. Traditional definitions of successful ageing have emphasised absence of physical and cognitive disabilities.[179] In their 1987 article, Rowe and Kahn characterised successful ageing as involving three components: a) freedom from disease and disability, b) high cognitive and physical functioning, and c) social and productive engagement.[180]

The ancient Greek dramatist Euripides (5th century BC) describes the multiply-headed mythological monster Hydra as having a regenerative capacity which makes it immortal, which is the historical background to the name of the biological genus Hydra. The Book of Job (c. 6th century BC) describes human lifespan as inherently limited and makes a comparison with the innate immortality that a felled tree may have when undergoing vegetative regeneration.[181]

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