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Category Archives: Microbiology

Siemens recalls microbiology testing panels: FDA

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Siemens recalls microbiology testing panels: FDA

dna impact: Javed Akhtar offers help to UP wonder kid

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Help has started to pour in for wonder kid Sushma Verma who has secured admission to M.Sc. (microbiology) at Lucknow University at the age of 13. She holds the record for being the youngest to complete High School (class X) in India at the age of seven.

dna had highlighted her plight and achievements in its edition on Thursday last. Her achievements deserve even more kudos as she has done it despite extreme deprivation.

Her father Tej Bahadur is a daily wage labourer and is barely able to run the household. Lucknow University (LU) procter Prof Manoj Dixit told dna that famous lyricist Javed Akhtar had come forward to help Sushma financially. He has sent a message through people he knows in Lucknow, he said.

Interestingly, neither Sushma nor her father have heard of Javed Akhtar. Neither do they know his son Farhan Akhtar or wife Shabana Azmi.

Besides, Rafat Sarosh, who works for Microsoft at Seattle, and Abhijit Patil, a microbiology teacher who runs a charitable foundation in Kolhapur (Maharashtra), have also offered to help Sushma. In his email to the Lucknow University, Rafat has mentioned that his father, an LU product, had gone through some very tough time, and total strangers came up and helped him. He said that if Sushmas fees is taken care of, he would be willing to give her Rs5,000 per month for other expenses. He has also offered to give her a laptop.

Prof Manoj Dixit said some LU teachers had also offered to help, and the LU authorities were also considering granting her fees waiver and hostel facility. We plan to collect about Rs5 lakh which should take care of her entire M.Sc. course, he said.

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dna impact: Javed Akhtar offers help to UP wonder kid

Research identifies how mouth cells resist Candida infection

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Public release date: 2-Sep-2013 [ | E-mail | Share ]

Contact: Benjamin Thompson b.thompson@sgm.ac.uk 44-758-468-9611 Society for General Microbiology

Candida albicans is a common fungus found living in, and on, many parts of the human body. Usually this species causes no harm to humans unless it can breach the body's immune defences, where can lead to serious illness or death. It is known as an opportunistic pathogen that can colonise and infect individuals with a compromised immune system. New research, presented today at the Society for General Microbiology's Autumn Conference, gives us a greater understanding of how mucosal surfaces in the body respond to C. albicans to prevent damage being done during infection.

Researchers from King's College London focused on oral epithelial cells, a mucosal layer of cells that line the mouth, providing a barrier against microbes. The group challenged oral epithelial cells grown in vitro with C. albicans, looking at gene expression six and 24 hours after infection.

The results showed that a molecular signalling pathway know as the 'PI3 Kinase pathway' is activated as soon as five minutes after the epithelial cells encounter C. albicans, before the fungus has time to become invasive. This pathway seems to be involved in priming epithelial cells to protect against future damage. Inhibiting the PI3 Kinase pathway increased the amount of damage caused by C. albicans and reduced the normal tissue healing response.

This finding makes the PI3 Kinase pathway an attractive target for new therapeutics against C. albicans. Dr David Moyes, who presented the work at the conference, hopes that by boosting the activity of the pathway it may be possible to reduce the fungus's ability to cause tissue damage.

He explains, "We are developing a complete picture of how C. albicans interacts with the epithelial cells that make up our mucosal surfaces and learning how they are able to discriminate between harmless and harmful microbes.

"Many of the symptoms of C. albicans infection, are caused by the body's incorrect or overactive response to cell damage. Developing therapies that act on the patient, not the microbe, provides an entirely novel way of treating an infection and the likelihood of resistance is much reduced."

Candida infections are the third most commonly acquired hospital blood-borne infection, resulting in 50,000 deaths annually. Over 75 per cent of fertile age women will suffer from at least one Candida infection and there are around 2 million cases of oral candidiasis each year among HIV/AIDS patients.

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Research identifies how mouth cells resist Candida infection

Stanford scientists show how antibiotics enable pathogenic gut infections

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Public release date: 1-Sep-2013 [ | E-mail | Share ]

Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center

STANFORD, Calif. A new study by researchers at the Stanford University School of Medicine could help pinpoint ways to counter the effects of the antibiotics-driven depletion of friendly, gut-dwelling bacteria.

A number of intestinal pathogens can cause problems after antibiotic administration, said Justin Sonnenburg, PhD, assistant professor of microbiology and immunology and the senior author of the study, to be published online Sept. 1 in Nature. Graduate students Katharine Ng and Jessica Ferreyra shared lead authorship.

"Antibiotics open the door for these pathogens to take hold. But how, exactly, that occurs hasn't been well understood," Sonnenburg said.

In the first 24 hours after administration of oral antibiotics, a spike in carbohydrate availability takes place in the gut, the study says. This transient nutrient surplus, combined with the reduction of friendly gut-dwelling bacteria due to antibiotics, permits at least two potentially deadly pathogens to get a toehold in that otherwise more forbidding environment.

In the past decade or so, much has been learned about the complex microbial ecosystem that resides in every healthy mammal's large intestine, including ours. The thousands of distinct bacterial strains that normally inhabit this challenging but nutrient-rich niche have adapted to it so well that we have difficulty living without them. They manufacture vitamins, provide critical training to our immune systems and even guide the development of our own tissues. Antibiotics decimate this gut-microbe ecosystem, which begins bouncing back within a few days but may take a month or more to regain its former numbers. And the ecosystem appears to suffer the permanent loss of some of its constituent bacterial strains.

It is thought that our commensal, or friendly, bacteria serve as a kind of lawn that, in commandeering the rich fertilizer that courses through our gut, outcompetes the less-well-behaved pathogenic "weeds." It has also been suggested that our commensal bugs secrete pathogen-killing factors. Another theory holds that the disruption of our inner microbial ecosystem somehow impairs our immune responsiveness.

"While these hypotheses are by no means mutually exclusive, our work specifically supports the suggestion that our resident microbes hold pathogens at bay by competing for nutrients," Sonnenburg said.

When that defense falters, as it does shortly after a course of antibiotics begins, marauding micro-organisms such as salmonella or Clostridium difficile can establish beachheads. Once they reach sufficient numbers, these two parasitic invaders can mount intentional campaigns to induce inflammation, a condition that impairs the restoration of our normal gut ecosystem but in which salmonella and C. difficile have learned to prosper.

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Stanford scientists show how antibiotics enable pathogenic gut infections

Stomach bacteria switch off human immune defences to cause disease

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Public release date: 1-Sep-2013 [ | E-mail | Share ]

Contact: Benjamin Thompson b.thompson@sgm.ac.uk 44-075-846-89611 Society for General Microbiology

Helicobacter pylori is a bacterium that establishes a life-long stomach infection in humans, which in some cases can lead to duodenal ulcers or stomach cancer. New research, presented at this week's Society for General Microbiology Autumn Conference, gives us a clearer understanding of how these bacteria can manipulate the human immune system to survive in the mucosal lining of the stomach.

Researchers from the University of Nottingham have shown that H. pylori is able to supress the body's normal production of 'human beta defensin 1' (hD1), an antimicrobial factor present in the stomach lining that helps prevent bacterial infection. By collecting stomach tissue biopsies from 54 patients at the Queens Medical Centre, Nottingham, the team showed that patients infected with H. pylori had ten times less hD1 than uninfected patients. Those with the lowest amount of hD1 had the most bacteria present in their stomach lining.

The most damaging strains of H. pylori make a molecular syringe called the cagT4SS, through which bacterial products are injected into cells of the stomach lining. In vitro work using human gastric epithelial cell lines showed that this activates chemical pathways to suppress hD1 production. These activated pathways are also involved in the stimulation of an inflammatory response, meaning that these H. pylori strains are able to survive and colonise more abundantly, while continuing to cause tissue damage over many decades. Previous research suggests that chronic inflammation of the stomach lining is strongly linked to gastric cancer.

It is estimated that half of the world's population have H. pylori in the mucosal lining of their stomach. For most people the infection is asymptomatic, although 1-2 per cent of those infected will develop gastric cancer. Survival rates for this disease remain low, as diagnosis is often very late, when the cancer is at an advanced stage.

Katie Cook, who is presenting this work says, "To identify people who are likely to suffer from stomach cancer we need to understand how H. pylori interacts with the cells of the stomach lining. Because our research is patient-focused we know that our findings are directly relevant.

"We hope to combine this work with that being carried out by our colleagues in order to develop a diagnostic test to predict the future risk of gastric cancer development."

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Stomach bacteria switch off human immune defences to cause disease

Science student wins three minute thesis comp

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A fundamental sciences PhD student used the movies Jurassic Park and the Hunger Games to explain complex microbiology and win Massey Universitys Three Minute Thesis competition.

Thomas Finn spoke for three minutes on his doctoral research at the finals event held at the Manawat campus last night.

He used the movies to communicate his research findings and explain the value of complex microbiology, and the use of new genetic sequencing tools.

Mr Finn says condensing his thesis - Understanding bacterial adaptation to aerobic and anaerobic environments through environmental evolution and whole genome analysis - into three-minutes was hard.

"It was tough, my supervisors and friends helped a lot. But once I had the idea of the Jurassic Park and Hunger Games, it just fell into place."

Mr Finn, from the Institute of Fundamental Sciences, won $1000 towards research costs and will represent Massey at the trans-Tasman competition in Sydney in October. He was also awarded the Peoples Choice and received a $500 book voucher.

Mirjam Guesgen, from the Institute of Veterinary, Animal and Biomedical Sciences, was runner-up with her presentation on whether lambs have empathy and won $500 towards her research.

The judges praised the finalists for the inspiring talks and for using humour to engage with the audience, and said picking a winner was difficult.

More than 60 students from a range of disciplines participated in Masseys third Three Minute Thesis competition, with the top ten presenting at the final event. An 80,000-word thesis would usually take nine hours to present.

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University of Akron geology and microbiology students conduct research in remote caves

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AKRON, Ohio -- Hazel Barton, an associate professor of microbiology and geology at the University of Akron, offers one of the most amazing field work experiences for students in the country, according to Popular Science.

Barton studies cave microbes, and students will often do their fieldwork in Brazilian caverns, accessible only by donning snakeproof boots and hacking through the Amazon with a machete, says the magazine, which named Bartons lab as one of the 10 most awesome college labs of 2013.

By analyzing rock samples and the microbes that live on them (many eat iron within the rock), they are learning how to better predict the formation of sinkholes and caves, says the article on popsci.com. Barton and her students also study the competition between various microbial species, looking for insights that could lead to new forms of antibiotics.

Bartons lab was awarded the same honor by the magazine in 2011 when she taught at Northern Kentucky University, UA officials said. She is internationally known for her discovery of antibiotic-resistant superbugs and co-starred in the 2001 IMAX film Journey Into Amazing Caves.

While Bartons campus-based lab at UA features microscopes and Petri dishes, students have followed her from Brazil to New Mexicos remote, virtually untouched Lechuguilla Cave, the university said. Barton and her team collect and study bacteria strains that live on sedimentary rock and minerals that have been around for at least four million years.

Popular Science searched for the coolest, strangest and most dangerous college labs. It looked for groundbreaking research, undergraduate access and sheer awesomeness.

Other college labs featured include an explosives program at Missouri University of Science and Technology, the Jet Propulsion laboratory at the California Institute of Technology, the National Wind Institute at Texas Tech University, where a high-impact gun fires two-by-fours at brick walls, and the IceCube Neutrino Facility at the South Pole operated by the University of Wisconsin-Madison.

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University of Akron geology and microbiology students conduct research in remote caves

Gene makes some HIV-infected patients more at risk for fungal disease

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Public release date: 27-Aug-2013 [ | E-mail | Share ]

Contact: Jim Sliwa jsliwa@asmusa.org 202-942-9297 American Society for Microbiology

HIV-infected people who carry a gene for a specific protein face a 20-fold greater risk of contracting cryptococcal disease, according to a study published in mBio, the online open-access journal of the American Society for Microbiology.

Cryptococcus neoformans is the most common cause of fungal meningitis among HIV-infected individuals. While the disease is a risk for everyone with HIV who has a very low level of CD4+ T cells, researchers have discovered that those with the gene for the protein FCGR3A 158V have an immune cell receptor that binds tightly to antibody-bound C. neoformans. Perversely, this tight binding by a vigilant immune system may mean the patient's own immune system strength becomes a weakness when facing the fungus.

"We found that this high affinity Fc receptor polymorphism was very highly overrepresented in the patients that got cryptococcal disease," says corresponding author Liise-anne Pirofski of the Albert Einstein College of Medicine & Montefiore Medical Center in The Bronx, New York. Patients with two copies of the high affinity Fc receptor gene had an almost 20-fold increased risk of contracting the disease.

"It's surprising that a receptor involved with a higher capacity to bind immune complexes would be associated with susceptibility in patients with HIV," says Pirofski, since phagocytosis of immune complexes is thought of as a mechanism for fighting invading microorganisms.

Differences among Fc gamma receptors (FCGR) have already been linked to cryptococcosis susceptibility among people who are not infected with HIV, but this new information sheds light on how these receptors could influence susceptibility in HIV patients, who are at elevated risk of developing cryptococcosis and are known to have high levels of antibodies to C. neoformans. FCGRs are proteins expressed on the outsides of different kinds of immune cells, including B lymphocytes, natural killer cells, macrophages, neutrophils, and mast cells. They bind to antibodies that have grabbed onto invading pathogens, then stimulate the immune cells to destroy the invaders.

The researchers performed PCR-based genotyping on banked samples from 164 men enrolled in the Multicenter AIDS Cohort Study (MACS), including 55 who were HIV-infected and developed cryptococcal disease, a control group of 54 who were HIV-infected and 55 who were HIV-uninfected. After correcting for a number of factors like demographics and T cell counts, they found a strong association between the gene for the high-affinity FCGR3A 158V allele and the risk of cryptococcal disease in HIV-infected men.

To figure out what that meant, they followed up with binding studies and showed that cells that express FCGR3A 158V bind more strongly to antibody-C. neoformans complexes. Greater affinity for the antibody-C. neoformans complex could increase the attachment of the fungus to monocytes or macrophages, which could in turn increase the numbers of fungi living and replicating inside immune cells. And there's also the possibility that these infected immune cells could act like a Trojan horse, delivering C. neoformans cells across the blood-brain barrier and allowing them to infect the brain. Pirofski says these possibilities are now under investigation.

C. neoformans is found all over the environment and studies show that nearly everyone is exposed to the fungus during their lifetime. However, the organism rarely causes disease in healthy people, but strikes most often in people with weakened immune systems. It is the main cause of fungal meningitis in people living with HIV, and causes devastating disease in those with profound CD4+ T cell deficiency.

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Gene makes some HIV-infected patients more at risk for fungal disease

13-year-old Sushma makes it to Lucknow University’s MSc Microbiology

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Thirteen-year-old child prodigy Sushma Verma has made it to the MSc Microbiology course at Lucknow University in the second merit list for postgraduate courses, which were announced Monday night.

At 13, she is busy preparing for MSc microbiology at LU

Sushma's father Tej Bahadur Verma said he locked the seat Tuesday itself by paying the fee online.

LU Vice-Chancellor Dr S B Nimse had recommended her name to the admission coordinator, saying "her age should not be a hurdle to all that she wants to achieve" while also adding that "proper procedures" would be followed for her application.

Even though he had time till Friday, an elated Tej Bahadur locked the seat Tuesday by paying the first installment of Rs 25,075. Bahadur, a daily wage earner, hopes to "somehow" manage to pay the fee of subsequent semesters.

Sushma, meanwhile, said she is happy as her wait is over. "I was hoping to get into Babasaheb Bhimrao Ambedkar (central) University as it is close by. After initial denial, they granted me admission and asked me to wait for an admission letter to be sent to my home, which hasn't come yet," Sushma said.

"So when I was selected at LU, I asked my father to lock the seat as I didn't want to risk losing an year," she said.

This year, Sushma completed her BSc in Zoology and Botany from an LU-affiliated college in three years. "The college was close by and my father would drop and pick me. LU campus is far and the every day commute may be troublesome but I'm looking forward to studying there," Sushma said.

Like other MSc Microbiology students, she has to report to the department on September 2.

Being a self-financed course, MSc Microbiology requires a minimum of 40 per cent seats to run. "We are certain the course will run but the picture will be clear only after the seats are locked for the second merit list," LU admission coordinator Prof N K Khare said. With a total of 30 seats, the course requires a minimum of 12 seats to run.

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13-year-old Sushma makes it to Lucknow University's MSc Microbiology


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