Think about this the next time you fill your plate with kale or spinach: a study published recently in JAMA Ophthalmology, found that boosting leafy green vegetable intake is associated with a reduced risk of developing glaucoma, a leading cause of blindness.
Harvard researchers analyzed the dietary information reported by more than 100,000 men and women in two long-term studies, each lasting more than 25 years. Those who ate the most leafy greens had a risk of developing glaucoma that was 20% to 30% lower than that of those who ate the least. What’s the link? Glaucoma causes damage to the optic nerve, through increased pressure from fluid in the eye or impaired blood flow to the optic nerve. Leafy greens are loaded with nitrate, which the body converts to nitric oxide. “Nitric oxide is important for maintaining optimal blood flow, and possibly for keeping eye pressure low” speculates Dr. Jae Hee Kang, the lead author of the study and a Harvard Medical School assistant professor. The study doesn’t prove that leafy greens reduce glaucoma risk; it only shows an association between the two. Eating leafy greens is also linked to lower rates of inflammation, cancer, heart disease, and even macular degeneration.
Klinefelter’s syndrome is a chromosomal abnormality that affects males who carry an extra one or more X chromosomes. Females have XX chromosomes and males have XY chromosomes. A male with Klinefelter’s would have XXY or XXXY. Because of the extra chromosome, individuals with the condition are usually referred to as “XXY Males”, or “47, XXY Males. It can lead to a variety of physical and physiological characteristics……CLICK & SEE THE PICTURES
Klinefelter syndrome is the most common sex chromosome disorder in males and the second most common condition caused by the presence of extra chromosomes. The condition exists in roughly 1 out of every 650 males. One in every 500 males has an extra X chromosome but does not have the syndrome. Other mammals also have the XXY syndrome, including mice.
The syndrome can affect different stages of physical, language and social development .Principal effects sometimes include development of small testicles and reduced fertility. Because they often don’t make as much of the male hormone testosterone as other boys, teenagers with Klinefelter’s syndrome may have less facial and body hair and may be less muscular than other boys. They may have trouble using language to express themselves. They may be shy and have trouble fitting in.
XXY occurs in approximately 1 out of 1,000 live male births, but many men with it do not develop KS. When KS does develop, it usually goes undetected until puberty or sometimes much later.
Characteristics may include:
*Smaller birth weight and slower muscle and motor development •For children and adults:
*Tallness with extra long arms and legs
*Abnormal body proportions (long legs, short trunk)
*Enlarged breasts (common)
*Lack of facial and body hair
*Small firm testes, small penis
*Lack of ability to produce sperm (common)
*Diminished sex drive, sexual dysfunction
*Social and learning disabilities (common)
*Attention deficit hyperactivity disorder (ADHD)
*Normal to borderline IQ
*Speech and language problems—Children with KS often learn to speak later than other children. They may have a difficult time reading and writing.
Men with KS have an increased risk of:
•Type 2 diabetes
In contrast to these potentially increased risks, it is currently thought that rare X-linked recessive conditions occur less frequently in XXY males than in normal XY males, since these conditions are transmitted by genes on the X chromosome, and people with two X chromosomes are typically only carriers rather than affected by these X-linked recessive conditions.
There are many variances within the XXY population, just as in the most common 46,XY population. While it is possible to characterise 47,XXY males with certain body types, that in itself should not be the method of identification as to whether or not someone has 47,XXY. The only reliable method of identification is karyotype
The extra X chromosome is retained because of a nondisjunction event during meiosis I (gametogenesis). Nondisjunction occurs with when homologous chromosomes, in the case the X and Y sex chromosomes, fail to separate, producing a sperm with an X and a Y chromosome. Fertilizing a normal (X) egg produces an XXY offspring.
The XXY chromosome arrangement is one of the most common genetic variations from the XY karyotype, occurring in about 1 in 500 live male births.
Another mechanism for retaining the extra X chromosome is through a nondisjunction event during meiosis II in the female. Nondisjunction will occur when sister chromatids on the sex chromosome, in this case an X and an X, fail to separate. An XX egg is produced which, when fertilized with a Y sperm, yields XXY offspring.
In mammals with more than one X chromosome, the genes on all but one X chromosome are not expressed; this is known as X inactivation. This happens in XXY males as well as normal XX females. However, in XXY males, a few genes located in the pseudoautosomal regions of their X chromosomes, have corresponding genes on their Y chromosome and are capable of being expressed. These triploid genes in XXY males may be responsible for symptoms associated with Klinefelter syndrome.
The first published report of a man with a 47,XXY karyotype was by Patricia A. Jacobs and Dr. J.A. Strong at Western General Hospital in Edinburgh, Scotland in 1959. This karyotype was found in a 24-year-old man who had signs of Klinefelter syndrome. Dr. Jacobs described her discovery of this first reported human or mammalian chromosome aneuploidy in her 1981 William Allan Memorial Award address
The 48, XXYY (male) syndrome occurs in 1 in 18,000–40,000 births and has traditionally been considered to be a variation of Klinefelter syndrome. XXYY tetrasomy is no longer generally considered a variation of KS, although it has not yet been assigned an ICD-10 code.
Males with Klinefelter syndrome may have a mosaic 47,XXY/46,XY constitutional karyotype and varying degrees of spermatogenic failure. Mosaicism 47,XXY/46,XX with clinical features suggestive of Klinefelter syndrome is very rare. Thus far, only about 10 cases have been described in literature
Cases are sporadic but there’s an increased risk in the children of older mothers. Older mothers at risk may be offered pre-natal tests.
A karyotype is used to confirm the diagnosis. In this procedure, a small blood sample is drawn. White blood cells are then separated from the sample, mixed with tissue culture medium, incubated, and checked for chromosomal abnormalities, such as an extra X chromosome.
Diagnosis can also be made prenatally via chorionic villus sampling or amniocentesis, tests in which fetal tissue is extracted and the fetal DNA is examined for genetic abnormalities. A 2002 literature review of elective abortion rates found that approximately 58% of pregnancies in the United States with a diagnosis of Klinefelter syndrome were terminated
The genetic variation is irreversible. Testosterone treatment is an option for some individuals who desire a more masculine appearance and identity.(but testosterone replacement therapy may induce a more male appearance and reduce the risk of osteoporosis in many cases. Fertility can often be accomplished with fertility treatment.)
Often individuals that have noticeable breast tissue or hypogonadism experience depression and/or social anxiety because they are outside of social norms. This is academically referred to as psychosocial morbidity. At least one study indicates that planned and timed support should be provided for young men with Klinefelter syndrome to ameliorate current poor psychosocial outcomes.
By 2010 over 100 successful pregnancies have been reported using IVF technology with surgically removed sperm material from men with Klinefelter syndrome
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose
Patients often fail to take their medication properly. Technology steps in with some ideas. Amber Dance reports .
Did you take your medicine today?” Soon, patients won’t have to rely on their memories for the answer. Scientists are developing tablets and capsules that track when they’ve been popped, turning the humble pill into a high-tech monitoring machine. The goal: new devices to help people take their medicines on time and improve the results of clinical trials for new drugs. CLICK & SEE THE PICTURES
Doctors can already prescribe pills that release drugs slowly or at a specific time. They even have camera pills that take snaps of their six to 12-metre journey through the gastrointestinal tract. The new pills tote microchips that make them even cleverer: they will report back to a recorder or smart phone exactly what kind and how much medicine has gone down the hatch and landed in the stomach. Someday they may also report on heart rate and other bodily data.
This next generation of pills is all about compliance, as it’s termed in doctor-speak — the tendency of patients to follow their doctors’ instructions (or not). According to the World Health Organisation (WHO), half of patients don’t take their pills properly. They skip doses, take the wrong amount at the wrong time or simply ignore prescriptions altogether.
The most common reason for medication mistakes is forgetfulness, particularly among the elderly. “The number of prescriptions they get is mind-boggling,” says Jill Winters, dean, Columbia College of Nursing in Milwaukee, Wisconsin. According to a 2004 report by the Centers for Disease Control and Prevention and the Merck Institute of Aging and Health, the average 75-year-old takes five different drugs.
Often, occasional lapses don’t matter. Smart pills like these are “not for your aspirin or even simple antibiotics,” says Maysam Ghovanloo, an electrical engineer at the Georgia Institute of Technology in Atlanta. The new technology is aimed at time-sensitive or costly medications.
For certain medications, not taking every pill can have serious consequences. For example, those mentally ill may require regular treatment to stay stable. Chemotherapy drugs and antibiotics for treating tuberculosis (TB) are also time-sensitive.
Blood pressure (BP) medication works only when taken on a regular basis; suddenly stopping it can cause the BP to skyrocket, says Daniel Touchette, a pharmacist and researcher at the University of Illinois, Chicago.
With drugs for transplant patients, a person who misses a dose risks rejection of the new organ. Novartis International AG, based in Basel, Switzerland, is developing pills for transplant recipients; the pills communicate with a patch on the skin when they reach the stomach.
And in the case of TB, treatment requires a six-month course of antibiotics that come with side effects such as nausea and heartburn. Many people don’t understand why they have to keep taking the unpleasant drugs once they feel better — but going off the medication may make patients contagious again and allow drug-resistant TB to develop.
Yet another arena where compliance is crucial is clinical drug trials. Drugmakers can only be sure their medicine works if they’re sure subjects are actually taking it as directed. For now, experimenters rely on diaries where participants record their medication use. But people may fudge the data, not wanting to admit they dropped a pill down the drain or forgot to take it for a few days. To account for those who miss their medicines, firms have to spend extra — trials cost hundreds of millions of dollars — for larger trials just so enough people will actually take the drug.
Technology already offers some solutions, with mobile phone reminders and pill bottles that record when they’re opened. But none of these actually confirms that the medicine has been swallowed.
Ghovanloo hopes to improve compliance with a necklace that records every time a special pill slides down the esophagus. He calls it MagneTrace. By sounding an alarm or sending a mobile phone message, the necklace also would inform the wearer when it’s time for another dose. Caretakers or doctors could monitor the signals too.
The system works by radio-frequency identification, or RFID. Three magnets on a choker-type necklace act like pillars, continually surveying the neck. The pill contains an RFID chip to communicate with the magnets. When Ghovanloo tested the system in an artificial neck made of PVC pipe, the necklace detected 94 per cent of pills passing through it. He hopes to get that number up to 99 per cent and is adding a microchip that will also transmit information about the specific drug taken and its dose.
Ghovanloo coats the chips with a non-reactive material so that after the medicine dissolves, the hardware simply passes through and out of the digestive tract. However, Ghovanloo says he needs make the design more fashionable. “Right now, it’s not something that a lady would be willing to wear,” he says. For men, he might embed the device in a shirt collar.
Rizwan Bashirullah, an electrical engineer at the University of Florida in Gainesville, is also working on pills that will confirm they’ve been taken. “They’re essentially little stickers,” he says of his technology, called the ID-Cap. Gainesville-based eTect is developing the product.
Each sticker contains three components: a microchip, an antenna and an acid sensor. Altogether it’s approximately half the size of a postage stamp, says eTect President Eric Buffkin. The sensor activates the device when it lands in the acid environment of the stomach, and the chip uses the antenna to send electronic signals directly through the body’s tissues to a receiver, worn on a wristband. The silver antenna and sensor dissolve into safe components; these and the microchip, about as big as a grain of sand, are flushed out of the gut. Over the next year, the company plans to test the capsule for safety in animals and people, Buffkin says.
Source : Los Angerles Times
Published byThe Telegraph ( Kolkata India)
In another study, a total of 1,000 post-menopausal women were asked to take natural supplements that contained vitamin D and calcium. The researchers found that the participants had a much lower risk of being diagnosed with breast cancer, the news source reports.
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A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
………………...CLICK & SEE THE PICTURES
For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.
The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.
But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.
Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.
The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.
To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.
That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”
He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.
In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.
The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”
Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.
Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.
And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?
That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.
Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.
As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.
But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.
“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.
But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.