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Category Archives: Transhuman News

What drives killers like the Ottawa or Paris attackers?

Posted: January 16, 2015 at 4:44 pm

IMAGE:Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, January 15, 2015-Zehaf-Bibeau, the Islamist convert who recently killed a Canadian military reservist on duty in Ottawa, Canada, represents a type of attacker rarely discussed--a person so obsessed with an overvalued idea that it defines their identity and leads them to commit violence without regard for the consequences. Although it appears that the assailants in Paris had more ties with terrorist organizations, the individuals still fit the description of people acting on overvalued ideas. This emerging, and likely growing phenomenon is explored in the article, published in the Perspectives section of the journal, "Lone Wolf Killers: A Perspective on Overvalued Ideas," published in the peer-reviewed journal Violence and Gender, from Mary Ann Liebert, Inc., publishers.

The article is available free on the Violence and Gender website.

Author Matthew H. Logan, PhD, a 28-year veteran officer with the Royal Canadian Mounted Police (RCMP), as well as an RCMP Criminal Investigative Psychologist (ret.), Ontario, Canada, explains that these killers do not always work alone, stating that "in the future I believe we will see more 'packs' of these wolves as they unite on common beliefs and themes."

"The violence we witnessed in Paris just days ago shook the world," says Violence and Gender Editor-in-Chief Mary Ellen O'Toole, PhD, Forensic Behavioral Consultant and Senior FBI Profiler/Criminal Investigative Analyst (ret.). "It was coldblooded, purposeful, and seemingly without remorse, driven by a unique self-righteous ideation of the killers. Dr. Matt Logan explains the 'motivating mindset' of young male offenders, sometimes loners and sometimes part of a group, whose 'overvalued ideas' combined with their own psychopathology is what motivates them to engage in this type of terror. 'Overvalued ideas do not constitute mental illness,' according to Dr. Logan, which makes this senseless, savage violence seem even more chilling and despicable."

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About the Journal

Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other original content, the Journal critically examines biological, genetic, behavioral, psychological, racial, ethnic, and cultural factors as they relate to the gender of perpetrators of violence. Led by Editor-in-Chief Mary Ellen O'Toole, PhD, Forensic Behavioral Consultant and Senior FBI Profiler/Criminal Investigative Analyst (ret.), Violence and Gender explores the difficult issues that are vital to threat assessment and prevention of the epidemic of violence. Violence and Gender is published quarterly online with Open Access options and in print, and is the official journal of The Avielle Foundation. Tables of content and a sample issue may be viewed on the Violence and Gender website.

About the Publisher

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What drives killers like the Ottawa or Paris attackers?

Posted in Genetic Engineering | Comments Off on What drives killers like the Ottawa or Paris attackers?

New genetic clues found in fragile X syndrome

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Scientists have gained new insight into fragile X syndrome -- the most common cause of inherited intellectual disability -- by studying the case of a person without the disorder, but with two of its classic symptoms.

In patients with fragile X, a key gene is completely disabled, eliminating a protein that regulates electrical signals in the brain and causing a host of behavioral, neurological and physical symptoms. This patient, in contrast, had only a single error in this gene and exhibited only two classic traits of fragile X -- intellectual disability and seizures -- allowing the researchers to parse out a previously unknown role for the gene.

"This individual case has allowed us to separate two independent functions of the fragile X protein in the brain," said co-senior author Vitaly A. Klyachko, PhD, associate professor of cell biology and physiology at Washington University School of Medicine in St. Louis. "By finding the mutation, even in just one patient, and linking it to a partial set of traits, we have identified a distinct function that this gene is responsible for and that is likely impaired in all people with fragile X."

The research, appearing in the Proceedings of the National Academy of Sciences (PNAS) Online Early Edition in December and in the print issue Jan. 5, is by investigators at Washington University and Emory University School of Medicine in Atlanta.

In studying fragile X, researchers' focus long has been on the problems that occur when brain cells receive signals. Like radio transmitters and receivers, brain cells send and receive transmissions in fine tuned ways that separate the signals from the noise. Until recently, most fragile X research has focused on problems with overly sensitive receivers, those that allow in too much information. The new study suggests that fragile X likely also causes overactive transmitters that send out too much information.

"The mechanisms that researchers have long thought were the entirety of the problem with fragile X are obviously still very much in play," Klyachko said. "But this unique case has allowed us to see that something else is going on."

The finding also raises the possibility that drugs recently tested as treatments for fragile X may be ineffective, at least in part, because they only dialed down the brain's receivers, presumably leaving transmitters on overdrive.

Fragile X syndrome results from an inherited genetic error in a gene called FMR1. The error prevents the manufacture of a protein called FMRP. Loss of FMRP is known to affect how cells in the brain receive signals, dialing up the amount of information allowed in. The gene is on the X chromosome, so the syndrome affects males more often and more severely than females, who may be able to compensate for the genetic error if their second copy of FMR1 is normal.

Patients with fragile X have a range of symptoms. One of the mysteries of the syndrome is how loss of a single gene can lead to such a variety of effects in different patients. Some patients are profoundly intellectually disabled, unable to talk or communicate. Others are only mildly affected. Patients often experience seizures, anxiety and impulsive behavior. Typical physical symptoms include enlarged heads, flat feet and distinctive facial features. Almost one-third of patients with fragile X also show symptoms of autism spectrum disorders.

To gain insight into what else FMRP might do, the researchers plumbed genetic sequencing data from more than 900 males with intellectual disabilities but without classic fragile X syndrome. They looked for mutations in the FMR1 gene that might impair the protein but not eliminate it entirely. Even in this relatively large sample size, they only found one patient with abnormal FMRP, resulting from a change in a single letter of the gene's DNA code.

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Baylor College of Medicine scientist identify a novel precursor to neurodegeneration

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HOUSTON -- (Jan. 15, 2015) - Alteration of lipid metabolism in brain cells promotes the formation of lipid droplets that presage the loss of neurons, said researchers from Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital in a report that appears online in the journal Cell.

Neuroscience graduate student Lucy Liu, and Dr. Hugo Bellen, professor of molecular and human genetics, neuroscience, a Howard Hughes Medical Institute investigator and director of the Graduate Program in Developmental Biology at Baylor connected the presence of lipid droplet accumulation in the glia of specific mutants as a harbinger of neurodegeneration.

Fruit fly genetics

The Bellen lab uses fruit fly mutants of evolutionarily conserved genes that lead to neurodegeneration in human patients to dissect the molecular mechanisms that underlie the demise of neurons. The fruit flies carry mutations in genes that have human homologs that cause Leigh syndrome, Charcot-Marie-Tooth type 2A2 and ARSAL (autosomal recessive spastic ataxia with leukoencephalopathy). All of these mutations affect the function of the mitochondria, the powerhouse of the cell.

Lipid droplets and energy

Lipid droplets are organelles that serve as energy storage depots. They accumulate in the brain support cells (glia) when defects in the mitochondria of neurons lead to elevated levels of reactive oxygen species (ROS). Working with three independent fruit fly models and a mouse model, Liu et al., revealed a novel pathway leading to this accumulation through the inappropriate activation of two proteins: c-Jun-N-terminal Kinase (JNK) and Sterol Regulatory Element Binding Protein (SREBP). These lipid droplets accumulate in glial cells before signs of neurodegeneration appeared.

"This is the first documentation of lipid droplet accumulation in glial cell" said Liu, first author of the study. The authors show that elevated reactive oxygen species in the neurons promotes synthesis of lipids leading to the formation of lipid droplets in glia. This accumulation affects the glia's ability to support the neurons when the lipid droplets become peroxidated, completing a negative feedback loop.

Not enough for neurodegeneration

"ROS or lipid droplets alone do not lead to the rapid onset of neurodegeneration," said Bellen, senior author on the study. "The synergism of ROS with lipid droplets is key. Reducing one or the other delays neurodegeneration."

Upon further investigation, Liu and her colleagues showed that reducing many of the components of this pathway can delay neurodegeneration. For example, treatments with a blood-brain-barrier penetrating antioxidant delay the onset of neurodegeneration in flies and mice developed by their collaborator Dr. Albert Quintana at University of Washington in Seattle.

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Rare mutations do not explain 'missing heritability' in asthma

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Largest study to date of rare genetic variants and asthma risk finds few associations

Despite a strong suspected link between genetics and asthma, commonly found genetic mutations account for only a small part of the risk for developing the disease - a problem known as missing heritability.

Rare and low frequency genetic mutations have been thought to explain missing heritability, but it appears they are unlikely to play a major role, according to a new study led by scientists from the University of Chicago. Analyzing the coding regions of genomes of more than 11,000 individuals, they identified mutations in just three genes that were associated with asthma risk. Each was associated with risk in specific ethnicities. Their findings, published in Nature Communications on Jan. 16, suggest gaps in the current understanding of asthma genetics.

"Previous studies have likely overestimated the heritability of asthma," said study senior author Carole Ober, PhD, Blum-Riese Professor and chair of the Department of Human Genetics at the University of Chicago. "This could be because those estimates are based on correlations between family members that share environment as well as genes, which could inflate the heritability. Gene-environment interactions are not considered in these large scale association studies, and we know that these are particularly important in establishing individual risks for asthma."

Asthma affects more than 25 million adults and children of all ages and ethnicities in the US. Due to the widespread nature of the disease, most studies of its genetic underpinnings have focused on commonly occurring mutations, referred to as genetic variants. However, while numerous such variants have been identified, they are able to account for only a small proportion of the risk for inheriting or developing asthma. Rare mutations, found in less than five percent of the population, have been hypothesized to explain this disparity.

Graduate student Catherine Igartua led the analysis under the supervision of co-senior author Dan Nicolae, PhD, Professor in the Departments of Medicine, Statistics and Human Genetics. She evaluated nearly 33,000 rare or low frequency mutations in more than 11,000 individuals of a variety of ethnicities representing European, African and Latino backgrounds. She analyzed mutations jointly across subjects, using a technique that allowed them to study mutations common in one ethnicity, but rare in others.

Only mutations in the genes GRASP, GSDMB and MTHFR showed a statistical link to asthma risk. Mutations in the first two genes were found primarily in Latino individuals, and mutations in the last gene in those with African ancestry. These genes, involved in protein scaffolding, apoptosis regulation and vitamin B9 metabolism respectively, have as yet unknown roles in asthma. The rarity and ethnic-specificity of these genes is insufficient to account for the widespread prevalence of asthma.

Although rare mutations might not contribute much to population asthma risk, these genes still have the potential to serve as targets for therapeutic development. Ober points to the discovery of rare mutations in the LDL receptor that eventually led to the development of statins to treat high cholesterol. She also notes that it is possible, but unlikely, that there are mutations with large effects on asthma risk outside of their screen as it looked at approximate 60 percent of mutations in coding regions of the genome.

"It was assumed that there would be rare mutations with larger effect sizes than the common variants we have been studying," Ober said. "Surprisingly, we found that low frequency mutations explain only a very small amount of asthma risk."

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DNA: 67th Army Day observed on 15 January – Video

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DNA: 67th Army Day observed on 15 January
India on 15 January 2015 observed the 67th Army Day. Also watch: #39;Crane #39; Bedi vs Muffler man in Delhi polls!

By: Zee News

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DNA: 67th Army Day observed on 15 January - Video

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AW: *SOLO* Double DNA | FAQ Niki und Aveex – Video

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AW: *SOLO* Double DNA | FAQ Niki und Aveex
Bewerten und Kommentieren nicht vergessen meine Freunde 🙂 Skype fr Clanbewerbungen: SplizZ_ToFast GP-Erspieler: SplizZ_Lord ...

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AW: *SOLO* Double DNA | FAQ Niki und Aveex - Video

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COD Advanced Warfare – "MORS" DNA BOMB w/ EVERY GUN #14 – FEARS! (COD AW) – Video

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COD Advanced Warfare - "MORS" DNA BOMB w/ EVERY GUN #14 - FEARS! (COD AW)
Advanced Warfare - "MORS" DNA BOMB w/ EVERY GUN #15 - FEARS! (COD AW) DNA Bomb by: http://www.youtube.com/astroswifty Commentator: http://www.youtube.com/MrGunstreak ...

By: KARNAGE Clan

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COD Advanced Warfare - "MORS" DNA BOMB w/ EVERY GUN #14 - FEARS! (COD AW) - Video

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DNA: Zee Media Exclusive – Punsari, India’s No 1 village – Video

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DNA: Zee Media Exclusive - Punsari, India #39;s No 1 village
Zee Media Exclusive - Punsari, India #39;s No 1 village that offers Wi-Fi connectivity, has air-conditioned primary schools equipped with CCTV cameras. This dream village, Punsari, exists in Gujarat #39;s...

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DNA: Zee Media Exclusive - Punsari, India's No 1 village - Video

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DNA w/AK12 – Video

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DNA w/AK12
Une toute nouvelle video sur ma chaine ! Un gameplay en musique assez court.

By: RaGe ZirWorlz

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DNA w/AK12 - Video

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Two Wives: Dale’s DNA result – Video

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Two Wives: Dale #39;s DNA result
Janine dominates Dale #39;s DNA result because she don #39;t want Audrey to know the truth. Subscribe to ABS-CBN Entertainment channel! - http://bit.ly/ABS-CBNEntertainment Watch the full episodes...

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