Science Simplified!

Comment

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 10:05am

Dead people tell no tales — but dead people’s microbes do.

Bacteria, fungi and worms living in the soil beneath a decomposing body can help reveal the time — and place — of death, scientists report December 10 in Science.

Researchers have tracked the comings and goings of cadaver microbes before, but the new study is the most comprehensive survey yet. For months, microbial ecologist Jessica Metcalf of the University of Colorado Boulder and colleagues tallied up microbes on and near dead mice and humans.

As bodies decayed, similar microbes cropped up like clockwork, even on different soil types and during different seasons of the year, the team found. The microbes were so predictable that researchers could estimate the time of death (within a few days) of a body that had been dead for about a month.

And because telltale microbes stayed in the soil long after a body had been moved, they could offer investigators clues about potential crime scenes, the team suggests.

 http://www.sciencemag.org/content/early/2015/12/09/science.aad2646

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:47am

The route followed by Hepatitis C to escape our Immune System :
A high proportion of hepatitis C-infected individuals develop chronic infections, suggesting that hepatitis C can subvert host antiviral responses.
The innate immune system, the body's first line of defence, is known to depend on the transcription factor nuclear factor κB (NF-κB). Its activation requires the ubiquitylation of upstream proteins including the adaptor protein NEMO (NF-κB essential modulator). Hepatitis C is one of many infectious pathogens that survive by inhibiting NF-κB signaling in host cells. Normally, the inflammatory cytokine tumor necrosis factor-α (TNF-α) induces antiviral innate immune responses by stimulating NF-κB through a cascade of signaling events. However patients with chronic hepatitis C infections have increased serum amounts of TNF-α, but have ineffective immune responses due to the inhibited NF-κB activation. The researchers hypothesized that the inhibition of TNF-α–induced NF-κB activation might be mediated by a viral protein expressed during hepatitis C infection. They used a luciferase reporter assay to screen which viral protein suppresses TNF-α–induced NF-κB activation and found that NS3 was sufficient to block NF-κB signaling in cells. Co-immunoprecipitation and immunofluorescence staining experiments showed that NS3 directly interacted with the linear ubiquitin chain assembly complex (LUBAC). More detailed domain mapping experiments showed that NS3 is bound to the ZnF-RBZ domain of HOIP (HOIL-1L–interacting protein; also known as RNF31), which is the same domain in LUBAC that binds to NEMO. To investigate the role of NS3 binding to HOIP, the researchers performed competitive coimmunoprecipitation experiments. They found that overexpression NS3 disrupted the interaction between HOIP and NEMO in a concentration-dependent manner. NS3 directly interacted with LUBAC, competed with NEMO for binding to LUBAC, and inhibited the LUBAC-mediated linear ubiquitylation of NEMO as well as the subsequent activation of NF-κB. The results highlight a novel immune evasion strategy adopted by hepatitis C to modulate host antiviral responses and enhance virus survival and persistence.
http://stke.sciencemag.org/content/8/403/ra118

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:38am

Arsenic release metabolically limited to permanently water-saturated soil
Scientists have solved the mystery of where the microbes responsible for releasing dangerous arsenic into groundwater in Southeast Asia get their food. Their findings, published Nature Geosciences, could guide future land management and future development. Groundwater in South and Southeast Asia commonly contains concentrations of arsenic 20 to 100 times greater than the World Health Organization's recommended limit, resulting in more than 100 million people being poisoned by drinking arsenic-laced water in Bangladesh, Cambodia, India, Myanmar, Vietnam and China. Arsenic is bound to iron oxide compounds in rocks from the Himalayas, and gets washed down the major rivers and deposited in the lowland basins and deltas. Scientists know that in the absence of oxygen, some bacteria living in those deposited sediments can use arsenic and iron oxide particles as an alternative means of respiration. When they do this, however, the microbes separate the arsenic and iron oxides and transfer the toxin into underlying groundwater. The mystery in this system, though, is an obvious source of energy that the microbes can tap to fuel the separation process.
The scientists hypothesized that bacteria residing in the shallow layers of seasonal wetlands were eating all of the digestible plant material during dry periods, when sediments are exposed to air and the microbes have access to oxygen. As a result, no food is left for the microbes when the floods returned, rendering them unable to cleave arsenic particles from iron oxides.
The same experiment repeated with samples taken from about 100 feet underground—the depth of most drinking wells in Asia—showed that bacteria living deep beneath permanent and seasonal wetlands are similarly limited and and do not release arsenic into groundwater under normal conditions. The careful sleuthing has identified the bacteria in the permanent wetlands as the primary culprit of arsenic release. The work suggests that, under normal conditions, microbes in seasonal wetlands don't pose a significant threat for adding arsenic to groundwater. But what if the conditions changed ?
To answer this question, the team conducted a second type of experiment, in which they simulated the conversion of a small, remote seasonal wetland into a permanent one by digging out a seasonal wetland plot and keeping it permanently filled with water. As predicted, this resulted in the release of arsenic. (The amount was small and transient and people were never threatened by the experiment.) The findings have large-scale implications for projecting changes in arsenic concentrations with land development in South and Southeast Asia and for the terrestrial carbon cycle.
http://www.nature.com/ngeo/journal/vaop/ncurrent/full/ngeo2589.html

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:32am

Pesticide In Milk Associated With Parkinson’s Disease: Exposure to a pineapple pesticide via milk intake has been linked to an increased incidence of Parkinson’s in Japanese men.
A pesticide used prior to the early 1980s and found in milk at that time may be associated with signs of Parkinson's disease in the brain, according to a study published in Neurology.
For the study, 449 Japanese-American men with an average age of 54 who participated in the Honolulu-Asia Aging Study were followed for more than 30 years and until death, after which autopsies were performed. Tests looked at whether participants had lost brain cells in the substantia nigra area of the brain, which occurs in Parkinson's disease and can start decades before any symptoms begin. Researchers also measured in 116 brains the amount of residue of a pesticide called heptachlor epoxide. The pesticide was found at very high levels in the milk supply in the early 1980s in Hawaii, where it was used in the pineapple industry. It was used to kill insects and was removed from use in the US around that time. The pesticide may also be found in well water. The study found that non-smokers who drank more than two cups of milk per day had 40 percent fewer brain cells in that area of the brain than people who drank less than two cups of milk per day. For those who were smokers at any point, there was no association between milk intake and loss of brain cells. Previous studies have shown that people who smoke have a lower risk of developing Parkinson's disease. Residues of heptachlor epoxide were found in 90 percent of people who drank the most milk, compared to 63 percent of those who did not drink any milk. Abbott noted that the researchers do not have evidence that the milk participants drank contained heptachlor epoxide. He also stated that the study does not show that the pesticide or milk intake cause Parkinson's disease; it only shows an association.
http://www.neurology.org/content/early/2015/12/09/WNL.0000000000002254

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:28am

Researchers have established that variation of a gene may help protect cancer patients from developing chemotherapy-induced cognitive impairment, commonly known as ‘chemofog’ or ‘chemobrain.’ Early-stage breast cancer patients who carry a specific variation of the brain derived neurotrophic factor (BDNF) gene are less likely to develop cognitive impairment after undergoing chemotherapy, according to the findings published in Neuro-Oncology. The BDNF gene is responsible for producing a protein that controls the growth and function of nerve cells in the brain and spinal cord. Studies have shown that a reduction in blood level of BDNF—due to variation in the BDNF gene—is associated with cognitive impairment in patients with Alzheimer’s disease and other neuropsychological disorders. The finding, from a recent study led by Associate Professor Alexandre Chan and PhD candidate Mr. Terence Ng from the National University of Singapore's (NUS) Department of Pharmacy, is the first time that the BDNF gene has been associated with cognitive changes in cancer patients.
The discovery can help researchers better understand the underlying mechanisms that lead to the development of this chemotherapy-induced side effect.
Background Brain-derived neurotrophic factor (BDNF), a neurotrophin that regulates neuronal function and development, is implicated in several neurodegenerative conditions. Preliminary data suggest that a reduction of BDNF concentrations may lead to postchemotherapy cognitive impairment. The researchers hypothesized that a single nucleotide polymorphism (rs6265) of the BDNF gene may predispose patients to cognitive impairment. This study was aimed to evaluate the effect of BDNF gene polymorphism on chemotherapy-associated cognitive impairment.
http://neuro-oncology.oxfordjournals.org/content/early/2015/08/18/n...

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:18am

The questions and problems climate meet threw at science...

Climate agreement reached by various Governments in Paris raises some interesting questions for scientists as to how we can achieve this: how much do we need to cut global greenhouse gas emissions? How quickly do we need to make those cuts? What else might we need to do to be able to keep warming to 1.5 °C – for example, would we need to develop technologies that actually remove CO2 from the atmosphere? If temperatures overshot 1.5 °C and then reduced to 1.5 °C, would sea level also overshoot and then reduce?

To answer these questions more precisely will require scientists to get an even more detailed understanding of how sensitive our climate is to CO2 and other greenhouse gases.

Key to this will be improving understanding of what we call ‘Earth system feedbacks’. These are natural feedback processes which could either increase or decrease the amount of warming we might expect in response to a given amount of greenhouse gases. For example, we know that there are stores of greenhouse gases ‘locked away’ under frozen ground (permafrost) in some parts of the world, such as northern  Russia. If that permafrost melts due to climate change, the gases would be released – which could further increase warming.

Scientists around the world are already working on providing answers to these questions by developing a new breed of ‘Earth System Models’ (essentially complex simulations of our planet run on powerful supercomputers), which take more of these feedback processes into account, and so will help inform planning of emissions to achieve the warming targets agreed in Paris.

Whether we limit warming to 2 °C or 1.5 °C, it’s clear we can expect some further change to our global climate over the coming decades. Research shows us that this will lead to some impacts and it’s vital that we understand in more detail what this means at a regional and local level.

For example, research tells us that some parts of the world can expect more extreme weather – including heat waves and increases in extreme rainfall. For those planning everything from future homes, to flood defences, to vital infrastructure, the detail on what to expect is essential.

Again, these are questions which science is already working to answer by harnessing new research and ever more powerful supercomputing technology. 

There’s still much more work to do in this area and it will be vital that the information generated by this research is presented in a way that allows everyone to make informed decisions about how we can become more resilient to our climate – whatever changes we can expect.

*There’s a lot of scientific debate about exactly what ‘pre-industrial levels’ means and how you would measure that, but here we use the average of temperatures during the period 1850-1899 as our representation.

- blog.metoffice.gov.uk

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 5:42am

Here is some interesting news: We all know that female mosquitoes spread diseases while having their meals. But you can avoid them in certain conditions. One of is to understand and follow their behaviour ...

A temperature-sensitive receptor prevents mosquitoes from being attracted to targets that are hotter than a potential host. Yes, true!

From warm summer days to cold winter nights, temperature is a ubiquitous sensory stimulus. All animals rely on their ability to detect environmental temperatures to avoid harm and to seek out more optimal conditions. Some animals, such as mosquitoes, also use their temperature sensors for a more nefarious purpose: to locate warm prey for a blood meal. Roman Corfas and Leslie Vosshall (e-Life) from Rockefeller University recently reported on the molecular basis of temperature-sensing behavior in Aedes aegypti, the mosquito that spreads yellow fever. They have shown how avoiding high temperatures can stop these insects from being attracted to targets that are too hot to represent a suitable host: in other words, while these mosquitoes like it hot, they don’t like it too hot.

Molecular receptors  guide the movements of some in the animal world like fruit flies and mosquitoes. In the malaria-spreading mosquito Anopheles gambiae, TRPA1 is expressed at the tips of the antennae. The tip of a mosquito antenna houses very sensitive thermoreceptors that could help drive host-seeking behavior.

Female mosquitoes normally prefer temperatures around 23°C. However, a puff of carbon dioxide (which could indicate that a metabolically active host is nearby) drives the mosquitoes to seek out temperatures that are closer to the body temperature of a mammal or bird (that is, between about 37°C and 43°C).  Corfas and Vosshall started by further characterizing this heat-seeking behavior. They found that mosquitoes were strongly attracted to a target when it was heated to temperatures above ambient, but only up to ~50°C. When it got hotter, this attraction declined strongly.

To probe the molecular mechanisms that might control this response, Corfas and Vosshall exploited genome-editing techniques to knock out the genes for GR19 and TRPA1 in A. aegypti. They found that mosquitoes lacking GR19 behaved like wild type mosquitoes and showed normal responses to heat. However, mosquitoes without TRPA1 continued to be attracted to the target even when its temperature reached potentially harmful levels (> 50°C).

The ability of animals to avoid high temperatures is commonly viewed from the perspective of damage avoidance. This response could also help a heat-seeking mosquito to choose among multiple potential targets.

As mosquito-borne illnesses kill more than a million people every year, interventions that can reduce the spread of such diseases are crucial. It is hoped that an increased understanding of how mosquitoes target their hosts can help accelerate the development of new control strategies.

Source: eLife Sciences

Comment by Dr. Krishna Kumari Challa on December 15, 2015 at 7:36am

We welcome climate pact to battle global warming at Paris.

The new accord, embraced by 195 nations, aims to cap warming to "well below" two degrees Celsius (3.6 degrees Fahrenheit) above pre-industrial levels, and to "pursue efforts" to limit the increase to 1.5C.

But according to scientists ... this ambitious temperature goal is not matched by an equally ambitious mitigation goal - the scientific term for the drawing-down of heat-trapping gases.

To have a two-thirds chance of limiting warming to two degrees, emissions would have to fall by 40-70 percent by mid-century, according to the Intergovernmental Panel on Climate Change (IPCC), the UN`s climate science body.

And to reach the 1.5C target also embraced in the newborn pact, those mid-century cuts would have to be even deeper: 70 to 95 percent.

Without these hard numbers -- dropped from an earlier draft -- the climate pact does not send a clear signal about the level and timing of emissions cuts.

Many scientists highlighted the imbalance created by boosting the ambition of the temperature target on the one hand, while removing the yardsticks against which progress toward that goal could be measured, on the other. How are we going to reach our objective unless we set out in the right direction? What matters more is how to get to the target.

Until governments accept this, we should restrain our optimism.

Scientific reality is unyielding. Stabilising greenhouse gases "in the second half of this century will require net carbon dioxide emissions to be reduced, in effect, to zero! scientists voiced concern about the fact that the new accord allows several years to pass before ramping up emissions reduction efforts.

We can`t wait until 2020 -- acting before then is essential, we have to be very pro-active, according to climate scientists.

Comment by Dr. Krishna Kumari Challa on December 13, 2015 at 11:13am

Comment by Dr. Krishna Kumari Challa on December 11, 2015 at 6:08am

There’s only so much brainpower to go around, and when the eyes hog it all, the ears suffer. When challenged with a tough visual task, people are less likely to perceive a tone, scientists report in the Dec. 9 Journal of Neuroscience. The results help explain what parents of screen-obsessed teenagers already know. For the study, people heard a tone while searching for a letter on a computer screen. When the letter was easy to find, participants were pretty good at identifying a tone. But when the search got harder, people were less likely to report hearing the sound, a phenomenon called inattentional deafness. Neural responses to the tone were blunted when people worked on a hard visual task, but not when the visual task was easy, researchers found. By showing that a demanding visual job can siphon resources away from hearing, the results suggest that perceptual overload can jump between senses.

• ‹ Previous
• 1
• …
• 859
• 860
• 861
• 862
• 863
• …
• 1047
• Next ›
• Page