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Comment by Dr. Krishna Kumari Challa on January 15, 2015 at 8:27am

Comment by Dr. Krishna Kumari Challa on January 15, 2015 at 8:27am

Global mobility: Science on the move

The big picture of global migration shows that scientists usually follow the research money — but culture can skew this pattern.

http://www.nature.com/news/global-mobility-science-on-the-move-1.11602

Comment by Dr. Krishna Kumari Challa on January 13, 2015 at 7:13am

Easter Island Extinction Blamed on Environment
Variation in Rapa Nui (Easter Island) land use indicates production and population peaks prior to European contact

Abstract

Many researchers believe that prehistoric Rapa Nui society collapsed because of centuries of unchecked population growth within a fragile environment. Recently, the notion of societal collapse has been questioned with the suggestion that extreme societal and demographic change occurred only after European contact in AD 1722. Establishing the veracity of demographic dynamics has been hindered by the lack of empirical evidence and the inability to establish a precise chronological framework. We use chronometric dates from hydrated obsidian artifacts recovered from habitation sites in regional study areas to evaluate regional land-use within Rapa Nui. The analysis suggests region-specific dynamics including precontact land use decline in some near-coastal and upland areas and postcontact increases and subsequent declines in other coastal locations. These temporal land-use patterns correlate with rainfall variation and soil quality, with poorer environmental locations declining earlier. This analysis confirms that the intensity of land use decreased substantially in some areas of the island before European contact.
http://www.pnas.org/content/early/2015/01/02/1420712112

Comment by Dr. Krishna Kumari Challa on January 8, 2015 at 6:52am

8th Science Communicators’ meet held at 102nd Indian Science Congress
http://www.dst.gov.in/whats_new/press-release15/pib_04-01-2015_2.html

Comment by Dr. Krishna Kumari Challa on January 7, 2015 at 9:37am

Feeling old? It might be from heavy metal.
High exposure to the toxic metal cadmium could prematurely age cells, potentially triggering a number of diseases as people age, according to a new study.
In a large national study, high exposure to cadmium was linked to shorter telomeres, "bits of DNA that act as caps" on chromosomes to help stabilize genes, said Ami Zota, a George Washington University assistant professor of environmental and occupational health who led the study. Shorten those caps too much, and cells weaken, leading to diseases.

Cadmium is used to make batteries.

The study is the largest to examine to examine links between cadmium and cell aging in people and suggests that exposure to the heavy metal could play a role in chronic illnesses, such as heart disease and kidney disease.

Cadmium is naturally occurring on Earth, but it is also produced to make batteries and coat iron and steel. People are exposed to cadmium through contaminated food, tobacco smoke and polluted air near industrial areas.
http://www.environmentalhealthnews.org/ehs/news/2015/jan/feeling-ol...

Comment by Dr. Krishna Kumari Challa on January 7, 2015 at 8:38am

https://www.youtube.com/channel/UCm4ZAOy6QTnN47cGI8PTnRQ

Comment by Dr. Krishna Kumari Challa on January 7, 2015 at 8:30am

Comment by Dr. Krishna Kumari Challa on January 6, 2015 at 8:08am

The loss of estrogen efficacy against cerebral ischemia in aged postmenopausal female mice
Physiological doses of E2 show neuroprotective effects in adult female mice but not in aged female mice.
ERα and ERβ expression in the cortex significantly decreased in the aged female mice.
Estrogen replacement treatment could not recover ERα and ERβ expression in the aged female mice.
Abstract

Estrogen has been shown to have neuroprotective effects in numerous experimental studies involving young and adult animals. However, several clinical trials have found that in aged postmenopausal women who received estrogen replacement therapy, there did not appear to be a reduction in the incidence of stroke. The aim of this study was to investigate the effects of physiological dosages of estrogen on aged female mice subjected to ischemia-reperfusion injury. Adult ovariectomized (OVX) female mice and 22-month-old female mice received daily subcutaneous injections of 100 μg/kg or 300 μg/kg 17β-estradiol (E2) at the back of the neck for four weeks, and the expression levels of estrogen receptor (ER) α and β in the cerebral cortex were determined using real-time PCR and Western blotting analyses. To mimic ischemic stroke, the mice received middle cerebral artery occlusion (MCAO) treatment for 1 h followed by a 24-h reperfusion period. The mice were then subjected to neurological deficit testing and infarct volume evaluation. The aged mice showed higher neurological deficit scores and larger infarct volumes compared with the adult mice. Both the lower and higher physiological dosages of E2 significantly improved the neurological test scores and decreased the infarct volume in the adult mice; however, E2 showed no neuroprotective effects in the aged mice. Furthermore, the protein expression of ERα and ERβ in the cerebral cortex was significantly decreased in the aged mice compared with the adult mice, and this decrease was not rescued by E2 treatment. These results indicate that the down-regulation of ERα and ERβ in the cerebral cortex may contribute to the loss of estrogen efficacy against ischemic injury in aged females and may point to new therapies for ischemic stroke in aged postmenopausal women.
http://www.sciencedirect.com/science/article/pii/S0304394013009981

Comment by Dr. Krishna Kumari Challa on January 2, 2015 at 7:35am

Comment by Dr. Krishna Kumari Challa on January 2, 2015 at 6:58am

Neuronal encoding of the switch from specific to generalized fear
Abstract:
Fear memories are crucial for survival. However, excessive generalization of such memories, characterized by a failure to discriminate dangerous from safe stimuli, is common in anxiety disorders. Neuronal encoding of the transition from cue-specific to generalized fear is poorly understood. We identified distinct neuronal populations in the lateral amygdala (LA) of rats that signaled generalized versus cue-specific associations and determined how their distributions switched during fear generalization. Notably, the same LA neurons that were cue specific before the behavioral shift to generalized fear lost their specificity afterwards, thereby tilting the balance of activity toward a greater proportion of generalizing neurons. Neuronal activity in the LA, but not the auditory cortex, was necessary for fear generalization. Furthermore, targeted activation of cAMP–PKA signaling in the LA increased neuronal excitability of LA neurons and led to generalized fear. These results provide a cellular basis in the amygdala for the alteration of emotional states from normal to pathological fear.
http://www.nature.com/neuro/journal/v18/n1/full/nn.3888.html

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