Wednesday, 31 October 2012

Healing a Damaged Brain is still a grey area...

When cells in the brain are damaged and die, for instance by stroke, there will be no repair or scar formation for those cells. The brain tissue will undergo liquefactive necrosis, and a rim of gliosis will form around the damaged area. Apart from a small amount in the blood vessels, there is no collagen or fibroblasts in the brain. A scar is formed by fibroblasts producing collagen to repair an area, which will later contract. If scars did form in the brain, the contraction would cause even more damage.

Around the edge of necrosis, astrocytes proliferate. These cells extend processes, and form a delicate rim of gliosis around the margin of damage. The empty space left by brain tissue fills up with cerebrospinal fluid.
Brain injury will commonly be accompanied by acute swelling, which impairs function in brain tissue that remains alive. Resolution of swelling is an important factor for the individual's function to improve. The greatest factor in functional recovery after brain injury comes from the brain's ability to learn, called neuroplasticity. After injury, neuroplasticity allows intact areas of the brain to adapt and attempt to compensate for damaged parts of the brain. Although axons and the peripheral nervous system in the developing brain can regenerate, they cannot in the adult brain. This is partly because of factors produced by cells in the brain that inhibit this regeneration. Dendrites, however, will develop from intact axons, as part of the neuroplasticity process. After severe brain injury, improvement in function related to neuroplasticity is unlikely to occur without help from health professionals skilled in rehabilitation.
In 1990 Dr. Richard Neubauer proved that these idling neurons can exist for years. In a groundbreaking experiment Dr. Neubauer performed hyperbaric oxygen therapy on a woman paralyzed for 14 years after a stroke. He found that after just one treatment, blood flow increased in the idling neurons surrounding her damaged tissue.
Traditionally, Hyperbaric Oxygen Therapy (HBOT) has been used as a technique to heal chronic wounds by rebuilding tissue. Patients enter a chamber and are exposed to high volumes of oxygen at great pressure. HBOT overcomes “stunned” cells, allowing them to function more normally again. In addition, it was recently proven that HBOT primarily affects genes in our cells that code for growth and repair hormones that inhibit inflammation and cell death.
For stroke survivors, HBOT reactivates the idling neurons, stimulates growth of new blood vessels, prevents cell death, and improves neurological function. HBOT has also been shown to cause the release of stem cells from our bone marrow into our circulation, where they are distributed throughout the body.
In recent years HBOT therapy has gained popularity as a treatment method for various traumatic brain injuries. Dr. Paul Harch, in New Orleans, treated a diver demented from brain decompression sickness. Brain decompression sickness is the quintessential example of HBOT in stroke: tiny bubbles passing through tiny blood vessels, damaging the blood vessels and causing thousands to millions of tiny spherical strokes or wounds in the brain. In two months of treatment the diver had improved cognitive, neurological, brain blood flow, and quality of life.
Successful treatments with HBOT was seen in other divers, patients with chronic stroke syndromes, and veterans returning with traumatic brain injuries and post-traumatic stress disorder. The amount of benefit HBOT can provide a stroke survivor depends on many factors.
  • The size of the stroke 
  • The length of time since the stroke 
  • The area of the brain involved 
  • The type of stroke 
  • Whether or not the patient received a clot-dissolving drug

Existing evidence suggests that HBOT is the most beneficial when started as soon after stroke as possible.
There are risks associated with HBOT, similar to some diving disorders. Pressure changes can cause a "squeeze" or barotrauma in the tissues surrounding trapped air inside the body, such as the lungs, behind the eardrum, inside paranasal sinuses, or trapped underneath dental fillings. Breathing high-pressure oxygen may cause oxygen toxicity. Temporarily blurred vision can be caused by swelling of the lens, which usually resolves in two to four weeks.
Patients inside the chamber may notice discomfort inside their ears as a pressure difference develops between their middle ear and the chamber atmosphere. This can be relieved by the Valsalva maneuver or by "jaw wiggling". As the pressure increases further, mist may form in the air inside the chamber and the air may become warm. Increased pressure may also cause ear drums to rupture, resulting in severe pain. To reduce the pressure, a valve is opened to allow air out of the chamber. As the pressure falls, the patient’s ears may "squeak" as the pressure inside the ear equalizes with the chamber. The temperature in the chamber will fall. The speed of pressurization and de-pressurization can be adjusted to each patient's needs.

  • Patients should not undergo HBO therapy if they are taking or have recently taken the following drugs: Doxorubicin (Adriamycin) – A chemotherapeutic drug. Cisplatin – Also a chemotherapeutic drug. 
  • Disulfiram (Antabuse) – Used in the treatment of alcoholism. 
  • Mafenide acetate (Sulfamylon) – Suppresses bacterial infections in burn wounds 

Evidence in a 2005 systematic review of the evidence for HBOT in the treatment of stroke showed no benefit to the treatment, though the generalizability of the finding was limited due to the wide variety in stage and type of stroke, and the treatment given. Good quality studies were recommended to determine if HBOT provides any benefit in stroke. Another review that examined the effectiveness of HBOT in acute stroke. It found no evidence that HBOT improved clinical outcomes at 6 months, but further study was recommended.

Despite lack of evidence, research from health pioneer (and former ANH-USA board member) Dr. Paul G. Harch published in the Journal of Neurotrauma indicates that hyperbaric oxygen therapy, or HBOT, is able to dramatically help veterans with post-concussion syndrome (a form of traumatic brain injury) and post-traumatic stress disorder (PTSD). Dr. Harch is an associate clinical professor of medicine at Louisiana State University in New Orleans.
Since January 2007, ANH-USA has been bringing attention to a project to have veterans treated with HBOT. In HBOT, the patient is put in a hyperbaric oxygen chamber, which saturates the tissues with twelve times more oxygen than can be absorbed by breathing. This greatly enhances the body’s own healing process.
According to Dr. Harch’s new study, even three years after the vets sustained brain injury, one month of HBOT was able to induce improvements in brain blood flow, cognition, symptoms, and quality of life, while the veterans experienced fewer suicidal thoughts. Specifically, improvements were seen in 92% of vets experiencing short-term memory problems, 87% of those complaining of headaches, 93% of those with cognitive deficits, 75% with sleep disruption, and 93% with depression. There were also improvements in irritability, mood swings, impulsivity, balance, motor function, IQ, and blood flow in the brain, as well as the reduction in PTSD symptoms and suicidal thoughts. And there was a reduction in—or complete elimination of—psychoactive and narcotic prescription medication usage in 64% of those previously prescribed the medication.

Besides the uses of a Hyperbaric chamber to avoid decompression sickness, there are people on both sides of the fence who are either promoting or debunking the healing properties of pressurised oxygen supply. The risks of Hyperbaric Oxygen Therapy might be too much for those whose medication counteracts the healing effects. Other illnesses such as Cardiac disease or Emphysema with CO2 retention have negative results with HBOT. This narrow field of users and complications of oxygen toxicity reduces its chances of being a confirmed method of healing. Despite the debunking or the lack of FDA approval there is a growing acceptance for people with cerebral palsy, stroke victims,encephalitis or PTSD not to mention a few other illnesses who claim to have success.
Oxygen therapy in this pressurized configuration might not be the ideal cure, but perhaps oxygenating the blood supply could offer an alternative. Only recently scientists created micro-particles into fat which oxygenates the blood safely without embolisms. If the goal of HBOT is to oxygenate the blood, it could theoretically be a sound method to minimalize the risk of oxygen toxicity by way of micro-particles. Curing brain damage is relatively a new science, while trials are still carrying on, there will be critics from both sides that will argue their cases. In this case I am hopeful there will be several different methods including micro particles that will establish neural repairs of any kind...

Tuesday, 30 October 2012

Aphrodisiacs, chemical desire for women.

An aphrodisiac is a substance that increases sexual desire. The name comes from Aphrodite, the Greek goddess of sexuality and love. Throughout history, many foods, drinks, and behaviors have had a reputation for making sex more attainable and/or pleasurable. However, from a historical and scientific standpoint, the alleged results may have been mainly due to mere belief by their users that they would be effective (i.e., the placebo effect). As well as the obvious of obtaining a high number of sexual encounters for gratification, married couples may have in one time or another experience situations of low libido.
Female sexual arousal disorder (FSAD), commonly referred to as frigidity, is a disorder characterized by a persistent or recurrent inability to attain sexual arousal or to maintain arousal until the completion of a sexual activity. The diagnosis can also refer to an inadequate lubrication-swelling response normally present during arousal and sexual activity. The condition should be distinguished from a general loss of interest in sexual activity and from other sexual dysfunctions, such as the orgasmic disorder (anorgasmia) and hypoactive sexual desire disorder, which is characterized as a lack or absence of sexual fantasies and desire for sexual activity for some period of time. Although female sexual dysfunction is currently a contested diagnostic, pharmaceutical companies are beginning to promote products to treat FSD, often involving low doses of testosterone.
Intrinsa is a testosterone patch by Procter and Gamble designed to treat Female Sexual Dysfunction.
FSD covers at least four different conditions: problems with desire, arousal, achieving orgasm, and genital pain. The patch aims to increase libido in women. Doctors have used a range of other treatments for women, including various hormones, antidepressants, and male impotence drugs like Viagra, Levitra, and Cialis. According to a P and G survey on female health 30 million women are naturally menopausal, 3 million are distressed by their lack of sexual desire, and 20% of 25 million women who are surgically menopausal are distressed.
A drug like Intrinsa works by releasing the hormone testosterone through the skin into the bloodstream. In women, testosterone is naturally produced by the ovaries and the adrenal gland. However, levels of the hormone decline with age, sometimes dramatically so after the menopause or after a hysterectomy. Testosterone therapy is systemic and needs to be applied over a period of weeks or months to have a noticeable effect.
In P and G's studies over six months of surgically menopausal women, those who received a placebo said satisfying sexual activity increased by an average of 19%, vs. a 73% increase for Intrinsa patch users.
Alkyl nitrites (poppers), have a history of use as a sexual enhancement aid, going back about fifty years. According to the text "Isobutyl nitrite and Related Compounds", many researchers agree that the alkyl nitrite may be a true aphrodisiac in the sense of promoting and enhancing sexual response. Although common toxic effects is headaches, reported by 43% of users on at least one occasion. However, most of the users most of the time do not have headaches. In a survey of 255 experienced users, 10% had experienced nasal irritation at least once and five percent had experienced nausea or temporary loss of erection. These negative effects were usually associated with "overuse" or with certain brands, perhaps reflecting a product quality or storage problem.
Many people report aphrodisiac-like effects from ergot-dervived drugs, which is likely due to their enhancement of the excitatory neurotransmitter dopamine in the brain. Raising dopamine levels is known to increase sexual arousal, but there appear to be other mechanisms operating as well. Cabergoline is especially interesting, as it allows men to have multiple orgasms, like women, because it blocks the release of the orgasm-inhibiting hormone prolactin. Prolactin levels naturally increase with age in men, and this is often partially responsible for age-associated impotence. With cabergoline some men are able to have numerous multiple orgasms in rapid succession. In one study with cabergoline, 60 healthy males, between the ages of 22 and 31, normally needed a break of 19 minutes between lovemaking sessions.
However, after taking cabergoline, they were able to have several orgasms within a few minutes. Medical psychologist Manfred Schedlowski, who was involved in the trials at Essen in Germany, said the drug raised the libido to enable the male to orgasm again more quickly. Cabergoline was reported to have no side effects on men during the tests, although a more recent study found that the drug is associated with an increased risk of heart failure. There may be another drawback as well. There is evidence that the release of prolactin, which surges during orgasm, promotes the growth of new neurons in the brain a process called neurogenesis.
Now, researchers at Monash University, led by Professor Susan Davis of the Women's Health Group, are testing the effectiveness of a testosterone-based 'as required', rather than ongoing, treatment for anorgasmia (a type of sexual dysfunction, in which a person can not orgasm). "We anticipate the treatment will work like Viagra for women. Rather than a long-term, therapy-based approach, this drug can be taken when a woman anticipates sexual activity," Professor Davis said. "We have previously shown that for women with low sexual interest, testosterone therapy not only improves sexual desire and arousal, but also enhances a woman’s ability to reach orgasm." The treatment would be administered in droplet sized doses via the nostrils and will be effective from two hours after it is administered, for up to six hours. With both neurological and vascular effects, it is anticipated the drug will be effective in the context of sexual activity, but will have no ill-effects if the activity doesn't take place.
Professor Davis said sexual dysfunction had important health implications for women. "Through previous research, we have shown that women under 50, who are not experiencing sexual pleasure will still participate in sexual activity on average five times per month, primarily to maintain relationship harmony," Professor Davis said. "Further, we have shown that women who report poor sexual functioning have lower wellbeing, despite not being depressed. Doctors have little to offer women who are experiencing anorgasmia, and this could be a breakthrough study for women who currently are frustrated by the lack of any treatment option." The researchers are hoping to recruit pre-menopausal women from Melbourne, Sydney, Perth and Adelaide to take part in the trial. Participants must be aged 18 to 49 and have experienced anorgasmia.
Sexually-enhancing properties of hydergine and yohimbine, as well as Hormone supplementation with testosterone can increase sex drive and performance in both men and women. These drugs and other pharmacological agents that assist with erectile dysfunction have vastly improved many people’s sex lives. In many cases drugs, some more them others have side effects which would probably be more harmful in the long run. Although clinical trials are in progress, it seems that its early days for a safe Aphrodisiac. The prospect of obtaining a legal drug that will cause sexual desire maybe more fantastic then the adverts that promote aftershaves and other beauty products. Drugs with secondary functions, that happen to enhance sexual libido can often be a ploy for the drug companies to re-market their product. Despite trials and research in the female libido, sexual dysfunction can effect as many as 1 in 4 women. Using a chemical solution to solve this problem might be the    last resort for what can be misinterpreted, as an off day for someone. In most cases the natural method of romance and gentle persuading is still the best solution. Going beyond natural Aphrodisiacs into the chemical realm, just seems like using a ruthie. A line that no one should cross...

Monday, 29 October 2012

The science of Hurricanes, let's try weather hacking

The two essential ingredients in every hurricane are warm water and moist warm air. That’s why hurricanes begin in the tropics. Hurricane season in the Atlantic begins June 1st and ends November 30th. The Eastern Pacific hurricane season begins May 15th and also ends November 30th. Most Atlantic hurricanes start to take shape when thunderstorms along the west coast of Africa drift out over warm ocean waters that are at least 80 degrees Fahrenheit (27 degrees Celsius), where they encounter converging winds from around the equator.
Hurricanes start when warm, moist air from the ocean surface begins to rise rapidly, where it encounters cooler air that causes the warm water vapor to condense and to form storm clouds and drops of rain. The condensation also releases latent heat, which warms the cool air above, causing it to rise and make way for more warm humid air from the ocean below. As this cycle continues, more warm moist air is drawn into the developing storm and more heat is transferred from the surface of the ocean to the atmosphere.
This continuing heat exchange creates a wind pattern that spirals around a relatively calm center, or eye, like water swirling down a drain. Converging winds near the surface of the water collide, pushing more water vapor upward, increasing the circulation of warm air, and accelerating the speed of the wind. At the same time, strong winds blowing steadily at higher altitudes pull the rising warm air away from the storm’s center and send it swirling into the hurricane’s classic cyclone pattern. High-pressure air at high altitudes, usually above 30,000 feet (9,000 meters), also pull heat away from the storm’s center and cool the rising air. As high-pressure air is drawn into the low-pressure center of the storm, the speed of the wind continues to increase. As the storm builds from thunderstorm to hurricane, it passes through three distinct stages based on wind speed:
  • Tropical depression—wind speeds of less than 38 miles per hour (61.15 kilometers per hour)
  • Tropical storm—wind speeds of 39 mph to 73 mph (62.76 kph to 117.48 kph)
  • Hurricane—wind speeds greater than 74 mph (119.09 kph)
This year, cyclone activity has continued longer than expected in the Atlantic, unperturbed by El Niño, which spawns high-level winds that stream eastward and can disrupt the swirling motion that gives a developing storm its power.
There was a strong indication that El Niño would form in time to suppress the peak of the hurricane season and El Niño just hasn't formed yet. The main reason for the recent abundance of cyclones is that since 1995, the Atlantic Ocean basin has been in the warm phase of a cyclical climate pattern called the Atlantic Multidecadal Oscillation, with hotter-than-average surface temperatures throughout the tropics and subtropics.
This pattern lasts for about 25-40 years, and comes with more hurricanes than its "cool" phase.
Warm water helps hurricanes form and fuels their strength.
In addition, in the past few years there has also been a strong West African monsoon, which creates disturbances in the eastern Atlantic that can turn into cyclones (the generic name for hurricanes and tropical storms).
There's also been relatively weak wind shear in the tropical Atlantic where cyclones form. Wind shear is a difference in wind speed or direction between the low and high atmosphere, which tears apart developing storms. Wind shear is the main way El Niño hampers cyclone formation. One thing that likely isn't to blame for the increase in hurricanes in recent years is global warming. Many climate models suggest that increased temperatures could actually lead to fewer, but stronger, hurricanes worldwide.
An average hurricane season has six hurricanes, but also about 25 hurricane days. The cyclones this year haven't been as strong as usual, with only one major hurricane, defined as Category 3 or stronger on the Saffir-Simpson scale.
 Better technology also allows us to detect more hurricanes than in the past. In recent decades satellites have significantly increased the detection of tropical storms that last less than 36 hours. This year there have been three tropical storms that lasted less than 1.5 days: tropical storms Helene, Joyce and Patty. These storms might have been missed in the pre-satellite era, and indeed, some storms actually could have been, meaning more seasons may have been as busy as this one has been. But regardless of what the hurricane season forecast is, people who live near the Atlantic or the Gulf of Mexico need to be prepared for storms.
While scientists agree on the mechanics of hurricane formation, and they agree that hurricanes are becoming more frequent and severe, that’s where consensus ends. Some scientists believe that human activity already has contributed significantly to global warming, which is increasing air and water temperatures worldwide and making it easier for hurricanes to form and gain destructive force. Other scientists believe that the increase in severe hurricanes over the past decade is due to natural salinity and temperature changes deep in the Atlantic part of a natural environmental cycle that shifts back and forth every 40-60 years.
While the scientific community debates the root cause of the temperature changes that are contributing to the current increase in destructive hurricanes, three things are apparent:
  • Air and water temperatures are rising worldwide. 
  • Human activities such as deforestation and greenhouse gas emissions from a wide range of industrial and agricultural processes are contributing to those temperature changes at a greater rate today than in the past. 
  • Failure to take action now to lower atmospheric levels of greenhouse gases is likely to lead to more frequent and severe hurricanes in the future.
Back in the 1960's Project Stormfury was an attempt to weaken tropical cyclones by flying aircraft into storms and seeding the eyewall with silver iodide. The project was run by the United States Government from 1962 to 1983. A similar project using soot was run in 1958, with inconclusive results.
The last experimental flight was flown in 1971, due to a lack of candidate storms and a changeover in NOAA's fleet. More than a decade after the last modification experiment, Project Stormfury was officially canceled. Although a failure in its goal of reducing the destructiveness of hurricanes, Project Stormfury was not without merit. The observational data and storm lifecycle research generated by Stormfury helped improve meteorologists' ability to forecast the movement and intensity of future hurricanes. Perhaps in recent years the increasing severity of hurricanes would require a man-made solution for weather modification. Considering the cost of prevention would prove to be less costly. The future suggests an increase in hurricanes with no end in sight of any other changes. The logical thing would be to open up old files of project storm-fury and look into ways of weather modification and prevention. By then we might have a chance of stopping a drought or reduce the destructive forces of a hurricane...

Sunday, 28 October 2012

The Factors of Divorce, what science tells us

Relationships in my opinion these days is getting harder to maintain considering that the divorce rate in first marriages probably peaked at about 40 percent for first marriages around 1980 and has been declining since to about 30 percent in the early 2000s. This is a dramatic difference. Rather than viewing marriage as a 50-50 shot in the dark it can be viewed as having a 70 percent likelihood of succeeding. But even to use that kind of generalization, i.e., one simple statistic for all marriages, grossly distorts what is actually going on.
The key is that the research shows that starting in the 1980s education, specifically a college degree for women, began to create a substantial divergence in marital outcomes, with the divorce rate for college-educated women dropping to about 20 percent, half the rate for non-college educated women. Even this is more complex, since the non-college educated women marry younger and are poorer than their college grad peers. These two factors, age at marriage and income level, have strong relationships to divorce rates; the older the partners and the higher the income, the more likely the couple stays married. Obviously, getting a college degree is reflected in both these factors. Thus, we reach an even more dramatic conclusion: That for college educated women who marry after the age of 25 and have established an independent source of income, the divorce rate is only 20 percent!.
In addition, the general data suggests that cohabiting couples break up at twice the rate of married couples. Of course, this kind of simple statistic hides many complex factors with regard to who actually constitutes the population of cohabiting couples and the likelihood that many choose to live together with no real intention of permanence. However, many couples may be choosing cohabition over marriage because they actually believe that the institution of marriage is unhealthy and too risky, a conclusion that my review of divorce rates strongly disputes.
When partners in a marriage disregard the sanctity of their relationship, the inevitable depletion and withering of the marriage system begins. Joy turns into boredom, passion slides into ambivalence or perfunctory sex, and respect declines toward disregard. Nature also might have a stake in the reasons of divorce.
Researchers led by Justin Garcia, an investigator and SUNY Doctoral Diversity Fellow at the State University of New York in Binghamton, looked at possible biological mechanisms behind the compulsion to be unfaithful to one’s partner or to be sexually promiscuous. They interviewed 181 young adults, asked them about their sexual behavior and relationships, and took samples of their DNA. Seventy-seven percent of the group reported a history of sexual intercourse.
Garcia and his team focused specifically on the DRD4 gene, which is associated with other behaviors linked with reward and feeling good. People with a genetic variation of DRD4 called 7R+ were more likely to commit infidelity or be promiscuous; 50% of people with 7R+ reported being unfaithful, compared with 22% of people who did not have this genetic variation. Gender did not play a role in genetic variation; 23% of women and 26% of men in the group were found to have the 7R+ genetic variation. The results are published in the Public Library of Science's PLoS ONE journal.
“What we found was that individuals with a certain variant of the DRD4 gene were more likely to have a history of uncommitted sex, including one-night stands and acts of infidelity,” Garcia says in a news release. “The motivation seems to stem from a system of pleasure and reward, which is where the release of dopamine comes in. In cases of uncommitted sex, the risks are high, the rewards substantial, and the motivation variable all elements that ensure a dopamine ‘rush.’”
Garcia notes that his findings do not indicate a cause-and-effect association between genetics and sexual behavior, but the study does provide evidence that biology affects human behavior and the decisions people make in their personal lives.
For years, researchers have wondered why females would cheat on their mates, given that there appears to be no direct benefit, but it could be that they retain the genes in order to pass them down to their sons, or just harbor them because the trait is positively selected for in males. DNA associated with large body size and risk-taking may persist in genomes for similar reasons.
A new study by UCLA researchers who look at subtle changes in behavior during ovulation. At their most fertile period, these women are less likely to feel close to their mates and more likely to find fault with them than women mated to more sexually desirable men, the research shows. "A woman evaluates her relationship differently at different times in her cycle, and her evaluation seems to be colored by how sexually attractive she perceives her partner to be," said Martie Haselton, a professor of psychology and communication studies at UCLA and senior author of the study.
Nevertheless, the negative feelings appear fleeting, and they don't seem to affect a woman's long-term commitment to her romantic relationship, the study found. "Even when these women are feeling less positive about their relationship, they don't want to end it," said Christina Larson, the study's lead author and a doctoral candidate in social psychology at UCLA.
There are telling changes that take place in women's behavior during ovulation. Possibly to increase the odds of attracting suitable mating partners, these behaviors include a tendency to dress up and to speak in a higher-pitched, more feminine voice and — in a potential inbreeding-avoidance mechanism — to refrain from contact with male kin. In addition, the lab has found that women whose mates are less sexy and masculine tend to be more attracted to other men during the few fertile days leading up to ovulation.
A lot of research has shown that women's preferences change over the course of the cycle, but this is the first time that these changes have been shown to have implications for relationship functioning.
By pinpointing the ovulation cycles of 41 undergraduate women involved in long-term heterosexual relationships. They asked the women to rate the sexual attractiveness of their mates by answering such questions as "How desirable do you think women find your partner as a short-term mate or casual sex partner, compared to most men.
They also asked the women a series of questions designed to measure their partner's stability or suitability as a long-term mate, including questions about how his present and future financial status compares with that of most men. Then at two different points in her monthly cycle — at high fertility (just before ovulation) and at low fertility — each woman was asked about the quality of her romantic relationship. The researchers, who used a questionnaire designed exclusively for the study, found no significant change across the cycle in how the women perceived their level of commitment to the relationship or, at least initially, in their satisfaction with it.
But an exercise that required the women to rate how close they felt to their men yielded dramatic results. As women mated to less sexually attractive men moved from their least fertile to most fertile period, their closeness scores dropped one point on a seven-point scale. Women mated to the most sexually attractive men, meanwhile, experienced the opposite effect. As these women moved from their least to most fertile period, their closeness scores rose by a point.
Women with the really good, stable guy felt more distant at high-fertility periods than low-fertility periods," Haselton said. "That isn't the case with women who were mated to particularly sexually attractive men. The closeness of their relationships got a boost just prior to ovulation.
The researchers found that women mated to the less sexually attractive men were significantly more likely to find fault with their partners and, again, feel less close to their partners during the high-fertility period than the low-fertility period. Women who rated their mates as more sexually attractive, meanwhile, did not exhibit these changes and instead reported being more satisfied with their relationship at high fertility than at low fertility.
It is possible that we evolved to feel drawn to these visible markers because, at least in the past, they proved to be indicators of good genes," she said. "Ancestral women who were attracted to these features could have produced offspring who were more successful in attracting mates and producing progeny.
The problem is that there is a limited number of potential mates who are high in both. So many women are forced to make trade-offs.
The urge for a stable long-term partner along with the increased desire for a more sexually attractive mate during periods of high fertility the "dual mating hypothesis."
Haselton and Larson next plan to look at whether fault-finding and the feelings of distance and dissatisfaction have any long-term destabilizing effects on the relationships of women with less sexually attractive men.
looking at the factors why people get divorce, it seems there are natural causes like infidelity genes and possibly a woman's menstrual cycle need to be included. Finding someone and saying with them may be hormonally programmed with oxytocine and vasopressin, which is present during sex and stays on long after child birth. The best thing to do is identify the factors of divorce and scientific research and navigate through the bad times. Considering divorce rates for women below the age of 25 are fairly high at around 30%. The negative aspects of natures programming seems to be more prominent. At this point its hard to quantify the real factors of separation as each relationship is different. The only alternative is to not try at all, but considering most married couples are on average happier then singletons. A new review by the University of Arizona of more than 30 published studies found divorced adults have a significantly higher risk of early death compared with married adults. The risk of dying early was 23 percent greater among divorced adults than married couples tracked by researchers for an average of 11 years. Researchers found the risks associated with divorce are similar to other well-established public-health risks, such as smoking up to 15 cigarettes a day, getting limited exercise, being overweight and drinking heavily, said the study’s lead author, UA psychology professor David Sbarra.
 In the end, tts better to try and fail then never try at all...

Saturday, 27 October 2012

The science of zombies and frankensteins monster

Apparently All hallows eve is on in a few days, which means people are getting in the mood for horror. But for me it seems the horror this year comes in the form of my gas and electricity bill, but I digress. Mad scientists through out the ages seem to been sadly ignored or used for inspiration for horror novels. Mary shelly heard of the experiments by Erasmus Darwin (Charles Darwin's grandfather) with galvanism, the contraction of muscles stimulated by electricity. This probably sparked off the idea that reanimating the dead by electricity which is the basis of the monsters creation.
The effect galvanism was named after the scientist Luigi Galvani, who investigated the effect of electricity on dissected animals in the 1780s and 1790s. When Galvani was doing some dissection work in his lab, his scalpel touched the body of a frog, and he saw the muscles in the frog's leg twitch. Galvani referred to the phenomenon as animal electricity, believing that he had discovered a distinct form of electricity.
Galvani did not perceive electricity as separable from biology. Galvani did not see electricity as the essence of life, which he regarded vitalistically. Galvani believed that the animal electricity came from the muscle. Galvani's associate Alessandro Volta, in opposition, reasoned that the animal electricity was a physical phenomenon caused by rubbing frog skin and not a metallic electricity. Every cell has a cell potential; biological electricity has the same chemical underpinnings as the current between electrochemical cells, and thus can be duplicated outside the body. Volta's intuition was correct. Volta, essentially, objected to Galvani’s conclusions about "animal electric fluid", but the two scientists disagreed respectfully and Volta coined the term "galvanism" for a direct current of electricity produced by chemical action. Thus, owing to an argument between the two in regard to the source or cause of the electricity,
A zombie  is an animated corpse resurrected back to life by mystical means, such as witchcraft. The term is often figuratively applied to describe a hypnotized person bereft of consciousness and self-awareness, yet ambulant and able to respond to surrounding stimuli. Since the late 19th century, zombies have acquired notable popularity, especially in North American and European folklore. In modern times, the term "zombie" has been applied to an undead being in horror fiction, largely drawn from George A. Romero's 1968 film Night of the Living Dead. They have appeared as plot devices in various books, films, television shows. Only recently have people try to explained a possible science to reanimate dead tissue, as the popularity grew from Romero's vision.
Parasites that turn victims into mindless, zombie-like slaves are fairly common in nature. There's one called toxoplasmosa gondii that seems to live in the guts of cats, sheddding eggs that can be picked up by rats and other animals that can just so happen be eaten by cats. Toxoplasma forms cysts throughout its intermediate host's body, including the brain. And yet a Toxoplasma-ridden rat is perfectly healthy. That makes good sense for the parasite, since a cat would not be particularly interested in eating a dead rat. But scientists at Oxford discovered that the parasite changes the rats in one subtle but vital way.
Then the researchers put Toxoplasma-carrying rats in the enclosure. Rats carrying the parasite are for the most part indistinguishable from healthy ones. They can compete for mates just as well and have no trouble feeding themselves. The only difference, the researchers found, is that they are more likely to get themselves killed. The scent of a cat in the enclosure didn't make them anxious, and they went about their business as if nothing was bothering them. They would explore around the odor at least as often as they did anywhere else in the enclosure. In some cases, they even took a special interest in the spot and came back to it over and over again. The scientists speculated that Toxoplasma was secreted some substance that was altering the patterns of brain activity in the rats. This manipulation likely evolved through natural selection, since parasites that were more likely to end up in cats would leave more offpsring.
The Oxford scientists knew that humans can be hosts to Toxoplasma, too. People can become infected by its eggs by handling soil or kitty litter. For most people, the infection causes no harm. Only if a person's immune system is weak does Toxoplasma grow uncontrollably. That's why pregnant women are advised not to handle kitty litter, and why toxoplasmosis is a serious risk for people with AIDS. Otherwise, the parasite lives quietly in people's bodies (and brains). It's estimated that about half of all people on Earth are infected with Toxoplasma. Pregnant women with high levels of Toxoplasma antibodies in their blood were more likely to give birth to children who would later develop schizophrenia. While none is a smoking gun, they are certainly food for thought. It's conceivable that exposure to Toxoplasma causes subtle changes in most people's personality, but in a small minority, it has more devastating effects.
The victims can then be brought back under the effects of a drug like datura stramonium (or other chemicals called alkaloids) that leave them in a trance-like state with no memory, but still able to perform simple tasks like eating, sleeping, moaning and shambling around with their arms outstretched.
What is definitely true is the story of Clairvius Narcisse. He was a Haitian guy who was declared dead by two doctors and buried in 1962. They found him wandering around the village 18 years later. It turned out the local voodoo priests had been using naturally occurring chemicals to basically zombify people and putting them to work on the sugar plantations.
Mad Cow gets in humans, they call it Creutzfeldt-Jakob disease. the symptoms: Changes in gait (walking) Hallucinations Lack of coordination (for example, stumbling and falling) Muscle twitching Myoclonic jerks or seizures Rapidly developing delirium or dementia. This gives plausibility in the idea of bio zombie.

According to studies, within a decade they'll have nanobots that can crawl inside your brain and set up neural connections to replace damaged ones. The nanobots will be able to rewire your thoughts, in the unlikely event of hacking zombie like behavior can be forced upon you.
The nanobots will be programmed to self-replicate, and the death of the host will mean the end of the nanobots. To preserve themselves, they'd need to transfer to a new host. Therefore, the last act of the nanobot zombie would be to bite a hole in a healthy victim, letting the nanobots steam in and set up camp in the new host. Once in, they can shut down the part of the brain that resists (the cortex) and leave the brain stem intact. They will have added a new member to the unholy army of the undead.
Scarily,In the 40′s, the Soviets were working on experiments involving reanimating mammals, specifically canines.
In this film, witness the shock and horror as organs are reanimated though electricity and with mechanical hearts and lungs! Now, it’s noted that this is no outstanding feat, a human heart can operate with nutrient rich blood and plasma alone. What’s fascinating in this film, is the apparently conscious and reactive head of a dog. Is it merely muscle synapses and reflexes? Perhaps, but the dog shows a keen awareness to its surroundings, suggesting activated sight, sound and other senses.
The dog is brought to clinical death (depicted mostly via a graphical plot of lung and heart activity) by draining all blood from it, left for ten minutes, then connected to the heart-lung machine described earlier.
After several minutes, the heart fibrillates, then restarts a normal rhythm. Respiration likewise resumes, the machine is removed and the dog is shown to continue living a healthy life. Recent advances of oxygenating blood using allows for a continued success in this field of  medical science. The simple matter of reconnecting nerves and avoiding tissue rejection may perhaps be overcome one-day, as people point out the singularity of immortality through machines. The alternative, could be a body swopping old worn out parts with new flesh. The whole macabre subject of raising the dead and possible threats from such manifestations could be a paranoid fantasy. But the recent emerging technological advances particularly on the nanoscale, could effectively bring back or extend life. Hacking of any kind today is done by the enthusiastic hobbyist. It could very well be the next step for some future hacker to try new tech to make the mistake of creating the undead. I hope by then there will be rights for the people to have a tamper free funeral or laws on Biohacking. Until then don't have night mares and enjoy your Halloween....

Friday, 26 October 2012

The probability of Parkinson's Disease, potential cures and surgery

The Scary thing of Parkinson's disease there is a chance it can be inherited, if the genes in a childs DNA is half of each parent then the odds are logically 50% of risk. Whether we pass on the gene we got from our father or the one from our mother is purely by chance, like flipping a coin heads or tails.
We all have genes that don't work properly. In most cases the other copy of the gene makes up for the one that does not work properly and we are healthy. A problem only arises if we meet someone else who has a non-working copy of the same gene and we have a child who inherits two non-working copies of that gene. This is called recessive inheritance.
Sometimes if one of our genes is not working properly the other copy of the gene cannot make up for it and that causes a condition or an increased risk of developing a condition. Each time we have a child we randomly pass on one copy of each gene. If the child inherits the copy that doesn't work properly, they too may develop the condition. This is called dominant inheritance.
In 1997, we studied a large family that came from a small town in Southern Italy in which PD was inherited from parent to child (dominant inheritance). Researchers found the gene that caused their inherited Parkinson's Disease and it coded for a protein called alpha-synuclein.
A research team from the Taub Institute at CUMC (Columbia University Medical Center) managed to identify the main mechanism that causes the progressive movement disorder in sporadic Parkinson’s disease patients. heritable forms of Parkinson’s disease have shown that a very important role in the onset and development of the disease is played by a protein called alpha-synuclein. Patients that have a higher number of alpha-synuclein gene copies will produce a higher quantity of this protein, thus damaging their neurons. Parkinson’s patients also show an excess of alpha-synuclein aggregates in the brain.
If one studies the brains of people with PD after they die, one can see tiny little accumulations of protein called Lewy Bodies (named after the doctor who first found them). Research has shown that there is a large amount of alpha-synuclein protein in the Lewy Bodies of people who have non-inherited PD as well as in the brains of people who have inherited PD. This immediately told us that alpha-synuclein played an important role in all forms of PD and we are still doing a lot of research to better understand this role.
. The longer forms of the alpha-synuclein gene were found to be specific to human patients, as well as some of the genetic variants that are in close connection to the onset of the disease. The research team also showed that if patients are exposed to environmental toxins that are related to Parkinson’s disease, there is an increase in alpha-synuclein. Currently, seven genes that cause some form of Parkinson's disease have been identified. Mutations (changes) in three known genes called SNCA (PARK1), UCHL1 (PARK 5), and LRRK2 (PARK8) and another mapped gene (PARK3) have been reported in families with dominant inheritance. Mutations in three known genes, PARK2 (PARK2), PARK7 (PARK7), and PINK1 (PARK6) have been found in affected individuals who had siblings with the condition but whose parents did not have Parkinson's disease (recessive inheritance). There is some research to suggest that these genes are also involved in early-onset Parkinson's disease (diagnosed before the age of 30) or in dominantly inherited Parkinson's disease but it is too early yet to be certain.
In most cases inheriting a non-working copy of a single gene will not cause someone to develop Parkinson's disease. many other complicating factors such as additional genes and environmental factors determine who will get the condition, when they get it and how it affects them.
By reprogramming skin cells from Parkinson's disease patients with a known genetic mutation, researchers at the Salk Institute for Biological Studies have identified damage to neural stem cells as a powerful player in the disease. The findings, reported online October 17, 2012 in Nature, may lead to new ways to diagnose and treat the disease. The scientists found that a common mutation to a gene that produce the enzyme LRRK2, which is responsible for both familial and sporadic cases of Parkinson's disease, deforms the membrane surrounding the nucleus of a neural stem cell. Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, such as the ones that respond to dopamine.
This discovery helps explain how Parkinson's disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations,such as depression and anxiety.

Its possible to use targeted gene-editing technologies to correct the mutation in patient's nuclear stem cells. This genetic correction repaired the disorganization of the nuclear envelope, and improved overall survival and functioning of the neural stem cells. To be able to chemically inhibit damage to the nucleus, producing the same results seen with genetic correction. This opens the door for drug treatment of Parkinson's disease patients who have this genetic mutation, The new finding may also help clinicians better diagnose this form of Parkinson's disease. Due to the striking appearance in patient samples, nuclear deformation parameters could add to the pool of diagnostic features for Parkinson's disease. The new finding may also help clinicians better diagnose this form of Parkinson's disease. Its the first time to our knowledge that human neural stem cells have been shown to be affected during Parkinson's pathology due to aberrant LRRK2.
The study shows that these reprogramming technologies are very useful for modeling disease as well as dysfunction caused by aging.
Alternatively new compounds target and shut a relatively rare membrane protein that allows the destructive calcium to flood into dopamine neurons. Previously published research showed that calcium entry through this protein stresses dopamine neurons, potentially leading to premature aging and death. The earlier research identified the precise protein involved—the Cav1.3 channel.
"These are the first compounds to selectively target this channel,” says D. James Surmeier, chair of physiology at Northwestern University Feinberg School of Medicine. “By shutting down the channel, we should be able to slow the progression of the disease or significantly reduce the risk that anyone would get Parkinson’s disease if they take this drugearly enough.”
As reported in the October 23 Nature Communications, the compounds work in a similar way to the drug isradipine, for which a Phase 2 national clinical trial with Parkinson’s patients—led by Northwestern Medicine neurologist Tanya Simuni—was recently completed. But because isradipine interacts with other channels found in the walls of blood vessels, it can’t be used in a high enough concentration to be highly effective for Parkinson’s disease.
For the next step, the Northwestern team has to improve the pharmacology of the compounds to make them suitable for human use, test them on animals, and move to a Phase 1 clinical trial.
The final technique if drugs don't work, is extradural motor cortex stimulation (EMCS), may provide a less-invasive alternative to electrical deep brain stimulation (DBS) for some patients with the movement disorder Parkinson's disease. The study was led by Dr. Beatrice Cioni of Catholic University, Rome. The researchers evaluated EMCS in nine patients with Parkinson's disease. Over the past decade, DBS using electrodes implanted in specific areas within the brain has become an accepted treatment for Parkinson's disease. In the EMCS technique, a relatively simple surgical procedure is performed to place a strip of four electrodes in an "extradural" location—on top of the tough membrane (dura) lining the brain. The electrodes were placed over a brain area called the motor cortex, which governs voluntary muscle movements. The study was designed to demonstrate the safety of the EMCS approach, and to provide preliminary information on its effectiveness in relieving the various types of movement abnormalities in Parkinson's disease. The electrode placement procedure and subsequent electrical stimulation were safe, with no surgical complications or other adverse events.
In particular, the patients had no changes in intellectual function or behavior and no seizures or other signs of epilepsy. Extradural stimulation led to small but significant and lasting improvements in control of voluntary movement. After one year, motor symptoms improved by an average of 13 percent on a standard Parkinson's disease rating scale, while the patient was off medications. Although DBS is an effective treatment for Parkinson's disease, it's not appropriate for all patients. Some patients have health conditions or old age that would make surgery for electrode placement too risky. Other patients—including four of the nine patients in the new study—are eligible for DBS but don't want to undergo electrode placement surgery.
According to certain web sites, family history of PD in a first degree relative is seen in about 15% of people with PD. There is a 2x risk of developing PD if you have a family history of PD in a first degree relative. Although increased, this risk is still relatively low. The  study also found elevated levels of the alpha-synuclein elongated transcripts in the blood of a group of patients with sporadic Parkinson's, compared with unaffected controls. This would suggest that a test for alpha-synuclein may serve as a biomarker for the disease.
Possible early detection for Parkinson's Disease, would lead to preventative actions. The possible gene reprograming offers a non invasive opportunity of a possible cure. Although another technique is calcium entry of a protein might Cav1.3 channel. Shutting it down might prove a slow progression or a cure. Its is still too early for research to come up with a cure and that avenues of gene manipulation or compound cures can resolve the almost hidden causes to Parkinson's. The last resort would be a surgical approach as deep brail stimulation offers a comfort to those who would risk the dangers for the sake of mobility. Having  pace maker for the brain in my view seems a bit cumbersome as the technology hasn't shrunk the equipment. Instead the current research in a non invasive cure, continues to offer hope. Perhaps in the future it may be a matter of popping a pill to prevent a neurodegenerative disease...