- Testosterone Decreases after Ingestion of Sugar
- Stress makes your hair go gray
- Huntington's disease deciphered
- Memories may be formed throughout the day, not just while sleeping
- Research uncovers clues to virus-cancer link
- Fish can learn despite small brains
- Magnetic bacteria found in Lonar lake
- Mayo researchers: Dramatic outcomes in prostate cancer study
Testosterone Decreases after Ingestion of SugarJune 14th, 2009
Men with low testosterone should have their hormone levels retested after they fast overnight because eating may transiently lower testosterone levels, a new study concludes.
In current guidelines for evaluating men with hypogonadism (low testosterone), The Endocrine Society recommends measuring blood levels of testosterone—the major male sex hormone—on two or more occasions in the morning, when testosterone is highest. However, no guidelines exist on when to draw a testosterone sample in relation to food intake, Hayes said.
Past research shows that a high level of insulin, the hormone primarily secreted after eating, is related to low testosterone levels. Like eating, glucose intake causes blood glucose (sugar) levels to rise, which stimulates secretion of insulin. Hayes and her colleagues examined the impact of a standard dose of glucose on testosterone levels in 74 men. The authors found that the glucose solution decreased blood levels of testosterone by as much as 25 percent.
Two hours after glucose administration, the testosterone level remained much lower than before the test in 73 of the 74 men, a statistically significant difference, the authors reported. Of the 66 men who had normal testosterone levels before the test, 10 (15 percent) became hypogonadal at one or more time points during the test.
The results did not differ by changes in insulin levels, according to the abstract. source
Stress makes your hair go grayJune 11th, 2009
Researchers have discovered that the kind of "genotoxic stress" that does damage to DNA depletes the melanocyte stem cells (MSCs) within hair follicles that are responsible for making those pigment-producing cells. Rather than dying off, when the going gets tough, those precious stem cells differentiate, forming fully mature melanocytes themselves.
Anything that can limit the stress might stop the graying from happening, the researchers said.
"The DNA in cells is under constant attack by exogenously- and endogenously-arising DNA-damaging agents such as mutagenic chemicals, ultraviolet light and ionizing radiation," said Emi Nishimura of Tokyo Medical and Dental University. "It is estimated that a single cell in mammals can encounter approximately 100,000 DNA damaging events per day."
Consequently, she explained, cells have elaborate ways to repair damaged DNA and prevent the lesions from being passed on to their daughter cells.
"Once stem cells are damaged irreversibly, the damaged stem cells need to be eliminated to maintain the quality of the stem cell pools," Nishimura continued. "We found that excessive genotoxic stress triggers differentiation of melanocyte stem cells." She says that differentiation might be a more sophisticated way to get rid of those cells than stimulating their death.
Nishimura's group earlier traced the loss of hair color to the gradual dying off of the stem cells that maintain a continuous supply of new melanocytes, giving hair its youthful color.
Now, they show in mice that irreparable DNA damage, as caused by ionizing radiation, is responsible. They further found that the "caretaker gene" known as ATM (for ataxia telangiectasia mutated) serves as a so-called stemness checkpoint, protecting against MSCs differentiation. That's why people with Ataxia-telangiectasia, an aging syndrome caused by a mutation in the ATM gene, go gray prematurely.
The findings lend support to the notion that genome instability is a significant factor underlying aging in general, the researchers said. They also support the "stem cell aging hypothesis," which proposes that DNA damage to long-lived stem cells can be a major cause for the symptoms that come with age.
In addition to the aging-associated stem cell depletion typically seen in melanocyte stem cells, qualitative and quantitative changes to other body stem cells have been reported in blood stem cells, cardiac muscle, and skeletal muscle, the researchers said. Stresses on stem cell pools and genome maintenance failures have also been implicated in the decline of tissue renewal capacity and the accelerated appearance of aging-related characteristics. source
My comment: The moral - say "NO" to stress. I just want to see how this is going to happen. Besides, as the article suppose, it's not so much up to the stress itself, as to DNA damaging. If a cell can have a DNA damaging experience 100 000 times a day, I won't bet that the stress of finishing a project is the biggest threat for the day. I think it's more a cumulative effect - like you're under stress, because of the project, you cannot find the time to have a lunch, you eat some junk food, you smoke too much (smoking kills you!), you get in a fight with your boss, you don't sleep enough, when you're done, you get desperately drunk. All this will affect the body, obviously, it will decrease the immune response, it will make you more vulnerable to all kinds of infection. And thus more reasons for DNA damaging. Not to mention the sun radiation and all other kinds of microwave emissions that fly around your head. Thus, if you want to have a beautiful hair (and healthy body) - say "No" to procrastination, stay positive, find time to eat and to rest and make sure you laugh enough.
Huntington's disease decipheredJune 14th, 2009
Researchers at the University of Illinois at Chicago College of Medicine have discovered how the mutated huntingtin gene acts on the nervous system to create the devastation of Huntington's disease.
The researchers were able to show that the mutated huntingtin gene activates a particular enzyme, called JNK3, which is expressed only in neurons and, further, to show what effect activation of that enzyme has on neuron function.
Huntington's disease is an adult onset neurodegenerative disease marked by progressive mental and physical deterioration. It has been known for more than a decade that everyone who develops the disease has mutations in a particular gene, called huntingtin.
"There are several puzzling aspects of this disease," said Brady, who is co-principal investigator on the study. "First, the mutation is there from day one. How is it that people are born with a perfectly functioning nervous system, despite the mutation, but as they grow up into their 30s and 40s they start to develop these debilitating symptoms? "
The second problem, according to Brady, is that the gene is expressed not just in the nervous system but in other parts of the body. However, the only part of the body that is affected is the nervous system.
Brady, Gerardo Morfini and their colleagues found that at extremely low concentrations, huntingtin was a potent inhibitor of axonal transport, the system within the neuron that shuttles proteins from the cell body where they are synthesized to the synaptic terminals where they are needed.A neuron's critical role in making connections may require it to make the cellular trunk, called an axon, between the cell body and the synaptic terminal to be very long. But even in the brain, axonal projections are very long compared to other cells. In addition to the challenge of distance, neurons are very complex cells with many specialized areas necessary to carry out synaptic connections, requiring a robust transport system.
"Inhibition of neuronal transport is enough to explain what is happening in Huntington's," said Brady. Loss of delivery of materials to the terminals results in loss of transmission of signals from the neuron. Loss of signal transmission causes the neurons to begin to die back, leading to reduced transmissions, more dying back and eventual neuronal cell death.
This mechanism also explains the late onset of the disease, Brady said. Activation of JNK3 reduces transport but does not eliminate it. Young neurons have a robust transport system, but transport gradually declines with age.Brady's group has also linked this pattern of progressive neurodegeneration -- marked by a loss of signaling between neurons, a slow dying back of neurons, and eventual neuron death -- to damage to the transport system in several other hereditary adult-onset neurodegenerative diseases and to Alzheimer's disease.source
My commentt: It's great that they understand the mechanism of this horrible disease (as well as all the other brain diseases - I mean, it's bad to have your body damaged, but to hurt you brain means to change you, to hurt you as a person, and that's really horrible) . But now, I think we have to start thinking how to fix the problem. That's all I can say.
Memories may be formed throughout the day, not just while sleepingJune 16th, 2009
Scientists have long thought that processes occurring during sleep were responsible for cementing the salient experiences of the day into long-term memories. Now, however, a study of scampering rats suggests that the mechanisms at work during sleep are also active while the animals are awake -- and that they encode events more accurately.
The finding has significant implications for understanding the way the brain learns and remembers, the researchers say. Among other things, it could offer insights into, and possible strategies for combating, post traumatic stress disorder.
The current study focused on the neural activity in a region of the brain known as the hippocampus, a horseshoe-shaped structure responsible for encoding all spatial and event memories of daily life. It is thought that the hippocampus rapidly encodes all experiences in highly plastic, or flexible, neural circuits within it and then, later, reactivates those neural representations of the experience that are deemed significant, allowing their patterns to be engrained in less-plastic hippocampal-neocortical circuits where they are stored as long-term memory.
"The accepted dogma has been that one learns something while awake - the process of rapid encoding -- and that later, while asleep, one replays the memory over and over again until it is cemented, or consolidated, in circuits throughout the brain," says the senior author of the study, Loren M. Frank, PhD, assistant professor of physiology and member of the W.M. Keck Center for Integrative Neuroscience at UCSF.
But this theory has not explained what happens if one does not sleep right after an experience, Frank notes.
However, until now, scientists have thought that awake replay of events was limited to the immediate past.
In the current study, Frank and first author Mattias P. Karlsson, PhD, a graduate student in Frank's lab, studied rats' neural replay in several settings - while they sniffed and explored two different places, one familiar, one novel -- and while they dozed in a rest box. In each case, the scientists recorded the activity of individual neurons in the hippocampus as they fired, one after the other, as the hippocampus "reflected" back on their experience in each place.
The first surprise was that in both awake settings there was a near constant replay of events that had taken place in the past - some 20 to 30 minutes earlier. These replay events were seen in peppered bursts of activity present during the brief pauses the animals made repeatedly during their exploration.
More surprisingly, the awake replay often involved events that had occurred in a different setting than the ones the animals were in during replay. In fact, 40 to 50 percent of the replays of past experience the animals had as they moved through the familiar place involved events they had experienced in the novel place.
"These findings suggest that elements of past experience are constantly being reactivated as we go about our daily lives, independent of incoming sensory information," says Frank.
Provocatively, the neural replay of past experiences detected in the animals while they slumbered was significantly less accurate than when they were awake. One possible explanation, says Frank, is that the replay during a sleep-like state may not be intended to be a perfect reenactment of what occurred. Evidence suggests that sleep is a time for making connections.source
My comment: This article is extremely interesting for many reasons. I recommend that you read it in its wholeness, since I had to cut it since it was so long. But it's worth the time to read it. Now, about memories. I don't exactly understand how the scientists knew what memories the mice replay in their brain, but I guess they just recorded the neural pathways what were activated when the mouse first saw the new environment and then saw the same neural pathways fire over and over again. In any case, it's pretty obvious people don't form memories only while they are sleeping. For example, people who take strong sedatives should miss the stages of sleep when there are dreams and other kinds of "replays" but they still form memories of their experiences. At least when I took sleeping pills, in the beginning, when I dozed off like immediately and woke up in the morning without dreams, I didn't have problems with my memories. Of course you could argue that I simply didn't remember my dreams, but there are different ways of sleeping - when you had dreams, you had the memory of time during the night, while if you didn't dream, you just fall asleep and then wake up - like after a surgery. There is no in-between period of time. And if there's not such period, there were no dreams in the meaning used in the research. Sure, they might mean that the replay wasn't conscious and that it didn't require any form of experiencing, but then what does it mean replay during the day?
Anyway, let's focus on what it is important. Obviously the daily chattering in our mind is not only annoying, it has some purpose. Especially when we're brought back to an even we experienced earlier and we try to make sense of it. If we trust this research (as well as few others, that I've already published), this remembering serves to form a long-lasting memory of the event. Thus, if we monitor and even control these experiences - like we don't allow in them bitter or fearful feelings in them, maybe, we'll evade forming long-lasting traumatic memories.
And in any case, I'm completely disgusted by the idea "we want to see if we can CONTROL this neural circuits and thus PREVENT traumatic memories from replaying". This is sick!
Research uncovers clues to virus-cancer linkJune 17th, 2009
In a series of recently-published articles, a research team from the University of North Carolina at Chapel Hill Lineberger Comprehensive Cancer Center has uncovered clues to the development of cancers in AIDS patients.
In an April article published in the journal PLoS Pathogens, Dirk Dittmer, Ph.D. associate professor of microbiology and immunology at UNC's School of Medicine, demonstrated that the Kaposi sarcoma associated herpesvirus (KSHV) is not only present in every tumor cell, but that the cells also transcribe microRNAs (miRNA) from the virus.
MicroRNAs are small molecules that regulate gene expression. Scientists have hypothesized that viruses can cause cancer through a mechanism where the viral genes take over the cell and induce cancerous growth through alteration of cell miRNA, since certain kinds of miRNA are responsible for putting the 'brakes' on uncontrolled cell growth.
Dittmer's team examined samples of tissue provided with the consent of Kaposi's sarcoma patients and found that specific miRNA biomarkers accurately identify stages of tumor progression. They found that certain miRNAs were lost as the tumors progressed, effectively accelerating the cancer's growth. More aggressive tumor stages expressed higher levels of KSHV miRNA.
In second study, published June 4 in the journal Blood, the team looked for the presence of tumor suppressor mRNAs in primary effusion lymphoma and Kaposi's Sarcoma.
His team found that several miRNAs known to suppress tumor activity were significantly less active in both types of cancer.Scientists believe that finding the mechanisms through which viruses take over cellular systems, resulting in cancer, is a promising strategy for cancer prevention and treatment, since it is much more feasible to block viral infection or develop specific inhibitors of the viral genes than try to inhibit all of the genetic changes within a cancer. source
Fish can learn despite small brainsTue Jun 16, 7:43 pm ET
LONDON (Reuters) – A small fish found in streams across Europe has a human-like ability to learn, British scientists reported Wednesday.
The nine-spined stickleback could be the first animal to exhibit a key humanstrategy that allows it to compare the behavior of others to its own experience and make choices that lead it to better food supplies.
"Small fish may have small brains but they still have some surprising cognitive abilities," said Jeremy Kendal of Durham University.
Kendal and colleagues from St. Andrews University found in tests that 75 percent of sticklebacks were clever enough to know from watching others that a feeder in a tank was rich in food, even though they had previously got little from it themselves.
Magnetic bacteria found in Lonar lake
NEW DELHI: Microbiologists in Maharashtra have found 'magnetic bacteria' in the ancient Lonar lake formed due to meteorite impact, a finding that might open a vista for searching extra-terrestrial life. The magnetotactic bacteria, which are object of interest of scientists from various fields world over, were isolated from the lake in Maharashtra's Buldana district which is the only impact crater formed in basaltic rock.
The bacteria are unique as they swim along geomagnetic field lines because they contain tiny magnetic crystals called magnetosomes, said Mahesh Chavadar, a microbiologist at the Yashwantrao Chavan College of Science in Karad.
The fact that the bacteria was found in the lake has thrown open doors for research on life outside universe. source
Mayo researchers: Dramatic outcomes in prostate cancer studyJune 19th, 2009
Two Mayo Clinic patients whose prostate cancer had been considered inoperable are now cancer free thanks in part to an experimental drug therapy that was used in combination with standardized hormone treatment and radiation therapy. The men were participating in a clinical trial of an immunotherapeutic agent called MDX-010 or ipilimumab. In these two cases, physicians say the approach initiated the death of a majority of cancer cells and caused the tumors to shrink dramatically, allowing surgery. In both cases, the aggressive tumors had grown well beyond the prostate into the abdominal areas.
The patients first received a type of hormone therapy called androgen ablation, which removes testosterone and usually causes some initial reduction in tumor size. Researchers then introduced a single dose of ipilimumab, an antibody, which builds on the anti-tumor action of the hormone and causes a much larger immune response, resulting in massive death of the tumor cells. Both men experienced consistent drops in their prostate specific antigen (PSA) counts over the following weeks until both were deemed eligible for surgery. Then, during surgery, came a greater surprise.
"The tumors had shrunk dramatically," says Michael Blute, M.D., Mayo urologist, co-investigator and surgeon, who operated on both men. "I had never seen anything like this before. "