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Comment by Dr. Krishna Kumari Challa on May 16, 2015 at 7:00am

Fascinating news: People take the drugs, their body breaks them down into different metabolites that are excreted, and the microbes take these different parts of the drug and put them back together in sewage treatment and recycling plants!

Wastewater treatment plants not only struggle removing pharmaceuticals, it seems some drugs actually increase after treatment. When researchers tested wastewater before and after treatment at a Milwaukee-area (USA) treatment plant, they found that two drugs—the anti-epileptic carbamazepine and antibiotic ofloxacin—came out at higher concentrations than they went in. The study suggests the microbes that clean our water may also piece some pharmaceuticals back together. Carbamazepine and ofloxacin on average increased by 80 percent and 120 percent, respectively, during the treatment process. Such drugs, and their metabolites (formed as part of the natural biochemical process of degrading and eliminating the compounds), get into the wastewater by people taking them and excreting them. Flushing drugs accounts for some of the levels too. “Microbes seem to be making pharmaceuticals out of what used to be pharmaceuticals".

The researchers have a clue as to how this might happen: microbes.

After removing the solids from incoming wastewater, treatment plants use microbes—tiny single-celled organisms—to decompose organic matter that comes in the sewage. Their best guess is that people take the drugs, their body breaks them down into different metabolites that are excreted, and the microbes take these different parts of the drug and put them back together!

Canadian researchers found carbamazepine more than doubled its initial medicinal load after treatment at a Peterborough, Ontario, plant.

These pharmaceuticals will act on hormones in our bodies.

http://www.environmentalhealthnews.org/ehs/news/2015/may/bacteria-m...

Comment by Dr. Krishna Kumari Challa on May 15, 2015 at 8:12am

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity
http://www.pnas.org/content/early/2015/05/06/1504239112
Brown fat is supposed to be the friendly kind of fat. But making the days longer with artificial light may turn brown fat into an enemy in the battle against obesity, a mouse study suggests.

Compared with mice experiencing normal light cycles, mice exposed to longer periods of light gained fat — not because they were eating more or moving less, but because their brown fat wasn't working efficiently. Brown fat in these mice converted fatty acids and glucose to heat more slowly than brown fat in mice experiencing normal days, researchers report May 11 in the Proceedings of the National Academy of Sciences.

Finding a way to boost brown fat's activity may combat the negative effects of extended time spent in artificial light, the scientists suggest.

Comment by Dr. Krishna Kumari Challa on May 15, 2015 at 7:34am

You Call It “Self-Exuberance”; I Call It “Bragging”

Miscalibrated Predictions of Emotional Responses to Self-Promotion

People engage in self-promotional behavior because they want others to hold favorable images of them. Self-promotion, however, entails a trade-off between conveying one’s positive attributes and being seen as bragging. We propose that people get this trade-off wrong because they erroneously project their own feelings onto their interaction partners. As a consequence, people overestimate the extent to which recipients of their self-promotion will feel proud of and happy for them, and underestimate the extent to which recipients will feel annoyed . Because people tend to promote themselves excessively when trying to make a favorable impression on others, such efforts often backfire, causing targets of self-promotion to view self-promoters as less likeable and as braggarts .

http://pss.sagepub.com/content/early/2015/05/07/0956797615573516.ab...

http://www.sciguru.org/newsitem/19053/bragging-backfires-study?utm_...

Comment by Dr. Krishna Kumari Challa on May 14, 2015 at 6:57am

Comment by Dr. Krishna Kumari Challa on May 12, 2015 at 8:32am

Cancer tricks the lymphatic system into spreading tumors...
Swollen lymph nodes are often the earliest sign of metastatic spread of cancer cells. Now cancer researchers and immunologists at Sweden's Karolinska Institutet have discovered how cancer cells can infiltrate the lymphatic system by 'disguising' themselves as immune cells (white blood cells). The researchers hope that this finding, which is published in the scientific journal Oncogene, will inform the development of new drugs.

The main reason why people die of cancer is that the cancer cells spread to form daughter tumours, or metastases, in vital organs, such as the lungs and liver. A route frequently used by cancer cells for dissemination is the lymphatic system. Upon entering lymphatic vessels, they migrate to nearby lymph nodes, which then swell up, and from there, to other organs via the blood. The details of how and why cancer cells use the lymphatic system for spread are, however, relatively unknown.

"It's not clear whether there are signals controlling this or whether it's just random," says principal investigator Jonas Fuxe, cancer researcher and Associate Professor at Karolinska Institutet's Department of Medical Biochemistry and Biophysics. "However, in recent years it has become evident that inflammation is a factor that can promote metastasis and that anti-inflammatory drugs may have a certain inhibitory effect on the spread of cancer."

The study is based on an interdisciplinary collaboration between cancer researchers and immunologists, which the researchers point out has has contributed to the new, exciting results. What they discovered was that an inflammatory factor known as TGF-beta (transforming growth factor-beta) can give cancer cells properties of immune cells by supplying the surface of the cancer cell with a receptor that normally only exists on the white blood cells that travel through the lymphatic system.

Equipped with this receptor, the cancer cells are able to recognise and migrate towards a gradient of a substance that is secreted from the lymphatic vessels and binds to the receptor. In this way, the cancer cells can effectively target lymphatic vessels and migrate on to lymph nodes, just like immune cells. According to the researchers, their results link inflammation and cancer in a novel way and make possible the development of new treatment models.

"With this discovery in our hands, we'd now like to try to find out which additional immune-cell properties cancer cells have and study how they affect the metastatic process," says Dr Fuxe. "The possibility of preventing or slowing down the spread of cancer cells via the lymphatic system is an attractive one, as it could reduce the risk of metastasis to other organs."
http://www.nature.com/onc/journal/vaop/ncurrent/abs/onc2015133a.html

Comment by Dr. Krishna Kumari Challa on May 9, 2015 at 8:32am

Are you planning to go to Mars? Then think again... for..the journey might damage your brain so much that when you reach Mars, you won't be able to enjoy your stay there. Why? Read on...

As NASA prepares for the first manned spaceflight to Mars, questions have surfaced concerning the potential for increased risks associated with exposure to the spectrum of highly energetic nuclei that comprise galactic cosmic rays. Animal models have revealed an unexpected sensitivity of mature neurons in the brain to charged particles found in space. Astronaut autonomy during long-term space travel is particularly critical as is the need to properly manage planned and unanticipated events, activities that could be compromised by accumulating particle traversals through the brain. Using mice subjected to space-relevant fluences of charged particles, researchers have shown that significant cortical- and hippocampal-based performance decrements 6 weeks after acute exposure. Animals manifesting cognitive decrements exhibited marked and persistent radiation-induced reductions in dendritic complexity and spine density along medial prefrontal cortical neurons known to mediate neurotransmission specifically interrogated by our behavioral tasks. Significant increases in postsynaptic density protein 95 (PSD-95) revealed major radiation-induced alterations in synaptic integrity. Impaired behavioral performance of individual animals correlated significantly with reduced spine density and trended with increased synaptic puncta, thereby providing quantitative measures of risk for developing cognitive decrements. Our data indicate an unexpected and unique susceptibility of the central nervous system to space radiation exposure, and argue that the underlying radiation sensitivity of delicate neuronal structure may well predispose astronauts to unintended mission-critical performance decrements and/or longer-term neurocognitive sequelae.

If humans are similarly susceptible, astronauts on voyages to Mars could suffer permanent cognitive impairment that could hinder their abilities to recall information and to think on their feet. Faster transits, new anti-radiation drugs and better spacecraft shielding should help. But until those solutions are developed, sending brain-damaged humans to Mars would be a dim-witted thing to do.

http://advances.sciencemag.org/content/1/4/e1400256

Comment by Dr. Krishna Kumari Challa on May 8, 2015 at 9:45am

Gram’s Stain Does Not Cross the Bacterial Cytoplasmic Membrane
http://pubs.acs.org/doi/abs/10.1021/acschembio.5b00042
Contrary to standard scientific texts, the purple dye called crystal violet, a main ingredient in gram staining, does not actually enter bacterial cells, researchers report April 27 in ACS Chemical Biology. Instead, the dye gets trapped in a tight package of sugar-filled polymers, called peptidoglycan, which envelops bacterial cells. The thickness and integrity of the sweet bacterial armor determines whether crystal violet leaves a cell purple or not. That royal shade, or lack of it, reveals a cell’s type of outer structure.
Abstract of the paper:
For well over a century, Hans Christian Gram’s famous staining protocol has been the standard go-to diagnostic for characterizing unknown bacteria. Despite continuous and ubiquitous use, we now demonstrate that the current understanding of the molecular mechanism for this differential stain is largely incorrect. Using the fully complementary time-resolved methods: second-harmonic light-scattering and bright-field transmission microscopy, we present a real-time and membrane specific quantitative characterization of the bacterial uptake of crystal-violet (CV), the dye used in Gram’s protocol. Our observations contradict the currently accepted mechanism which depicts that, for both Gram-negative and Gram-positive bacteria, CV readily traverses the peptidoglycan mesh (PM) and cytoplasmic membrane (CM) before equilibrating within the cytosol. We find that not only is CV unable to traverse the CM but, on the time-scale of the Gram-stain procedure, CV is kinetically trapped within the PM. Our results indicate that CV, rather than dyes which rapidly traverse the PM, is uniquely suited as the Gram stain.

Comment by Dr. Krishna Kumari Challa on May 8, 2015 at 9:36am

Scientists stumble across unknown stem-cell type ‘Region-selective’ pluripotent cells raise possibility of growing human organs in animals.

http://www.nature.com/news/scientists-stumble-across-unknown-stem-c...

Comment by Dr. Krishna Kumari Challa on May 5, 2015 at 9:47am

Comment by Dr. Krishna Kumari Challa on May 3, 2015 at 9:00am

Urinary tract infections (UTIs) are common, and widespread antibiotic resistance has led to urgent calls for new ways to combat them. Researchers at University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences report that an experimental drug that stabilizes a protein called HIF-1alpha protects human bladder cells and mice against a major UTI pathogen. The drug might eventually provide a therapeutic alternative or complement to standard antibiotic treatment.

The study is published April 30 by PLOS Pathogens.

HIF-1alpha is known to influence the innate immune response, the body’s first line of defense against intruding pathogens. Like many regulator proteins, HIF-1alpha is relatively short-lived. To increase HIF-1alpha levels, researchers have developed drugs that delay its breakdown. This same pathway has been the target for drugs now in advanced clinical trials for treatment of anemia.

In this study, Victor Nizet, MD, professor of pediatrics and pharmacy, and colleagues explored the use of HIF-1alpha-stabilizing drugs to boost the innate immune response to uropathogenic E.coli (UPEC) bacteria, a major cause of UTIs. In healthy human urinary tract cells, treatment with the drugs increased HIF-1alpha levels. Such cells were then more resistant to UPEC attachment, invasion and killing than human urinary tract cells with normal HIF-1alpha levels.

Using a mouse model of UTI, the researchers showed that administration of HIF-1alpha stabilizers directly into the bladder protected against UPEC infection. They also found that invasion of bladder cells, a critical early step in the infection process, was reduced in treated mice compared to untreated mice.

To verify the importance of HIF-1alpha in the defense against UPEC infection, the researchers studied mice with reduced HIF-1alpha levels. Exposed to UPEC, these mice were more susceptible to bladder infection, and pre-treatment with HIF-1alpha stabilizers made no difference. This demonstrates that the drugs combat UTIs through their effect on HIF-1alpha.

Finally, the researchers examined whether treatment with HIF-1alpha stabilizers would be beneficial against an established UTI. To do this, they infected mice with UPEC first and then administered the drugs into the bladder six hours later. The treated mice had a more than 10-fold reduction in bladder colonization with the bacteria, demonstrating that HIF-1alpha stabilization is beneficial even after the initial infection.

“The ultimate goal of this research will be to advance HIF-1alpha stabilizers toward clinical trials in humans, using versions of the drug that can be taken orally and reach the urinary tract,” Nizet said.
http://journals.plos.org/plospathogens/article?id=10.1371/journal.p...

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