The Flu Vaccine Is Little Effect On Men.
The flu vaccine is less impressive for men than women, and researchers at Stanford University suppose they've figured out why. The manly hormone testosterone causes genes in the immune arrangement to produce fewer antibodies, or defense mechanisms, in response to the vaccine, they found. "Men, typically, do worse than women in vaccinated response to infection and vaccination," said Stanford research affiliate David Furman, the lead study investigator.
For instance, men are more susceptible to bacterial, viral, fungal and parasitic infection than women. And men's safe systems don't come back as robustly as women's to vaccinations against flu, yellow fever, measles, hepatitis and many other diseases. For the study, published online Dec 23, 2013 in the Proceedings of the National Academy of Sciences, the researchers analyzed the blood of nearly 90 adults after they received a seasonal flu shot.
Men with the highest testosterone levels had the worst effect to the flu vaccine across the board. Testosterone is tied to immortal man's sensual characteristics, such as muscle strength, beard growth and risk-taking. "We found a set of genes in men that when activated caused a jinxed response to the vaccine, but were not involved in female response. Some of these genes are regulated by testosterone".
It's testosterone's accomplish on these genes that causes the poor vaccine response. "This has a lot of implications for vaccine development". Vaccine comeback might be better if men were given twice the dose, he suggested, or peradventure if testosterone levels were reduced. The whole picture isn't in effect clear or simple. Men's weaker response to the flu vaccine is only seen for some strains of flu.
Showing posts with label genes. Show all posts
Showing posts with label genes. Show all posts
Tuesday, 21 January 2020
Sunday, 19 January 2020
Scientists Have Identified New Genes That Increase The Risk Of Alzheimer's Disease
Scientists Have Identified New Genes That Increase The Risk Of Alzheimer's Disease.
Scientists have pinpointed two genes that are linked to Alzheimer's c murrain and could become targets for supplementary treatments for the neurodegenerative condition. Genetic variants appear to treatment an important fragment in the development of Alzheimer's since having parents or siblings with the disease increases a person's risk. It is estimated that one of every five persons elderly 65 will develop Alzheimer's disease in their lifetime, the researchers added.
Genome-wide federation studies are increasing scientists' understanding of the biological pathways underlying Alzheimer's disease, which may hero to new therapies, said study author Dr Sudha Seshadri, an confederate professor of neurology at Boston University School of Medicine. For now, bourgeoisie should realize that genes likely interact with other genes and with environmental factors.
Maria Carrillo, senior pilot of medical and scientific relations at the Alzheimer's Association, said that "these are the types of studies we essential in terms of future genetic analysis and things must be confirmed in much larger samples, as was done in this study". The statement is published in the May 12 issue of the Journal of the American Medical Association.
Although it was known that three genes are culpable for rare cases of Alzheimer's disease that run in families, researchers had been steady of only one gene, apolipoprotein E (APOE), that increased the risk of the common type of Alzheimer's disease. Using a genome-wide relationship analysis study of 3006 people with Alzheimer's and 14642 commoners without the disease, Seshadri's group identified two other genes associated with Alzheimer's disease, located on chromosomes 2 and 19.
Scientists have pinpointed two genes that are linked to Alzheimer's c murrain and could become targets for supplementary treatments for the neurodegenerative condition. Genetic variants appear to treatment an important fragment in the development of Alzheimer's since having parents or siblings with the disease increases a person's risk. It is estimated that one of every five persons elderly 65 will develop Alzheimer's disease in their lifetime, the researchers added.
Genome-wide federation studies are increasing scientists' understanding of the biological pathways underlying Alzheimer's disease, which may hero to new therapies, said study author Dr Sudha Seshadri, an confederate professor of neurology at Boston University School of Medicine. For now, bourgeoisie should realize that genes likely interact with other genes and with environmental factors.
Maria Carrillo, senior pilot of medical and scientific relations at the Alzheimer's Association, said that "these are the types of studies we essential in terms of future genetic analysis and things must be confirmed in much larger samples, as was done in this study". The statement is published in the May 12 issue of the Journal of the American Medical Association.
Although it was known that three genes are culpable for rare cases of Alzheimer's disease that run in families, researchers had been steady of only one gene, apolipoprotein E (APOE), that increased the risk of the common type of Alzheimer's disease. Using a genome-wide relationship analysis study of 3006 people with Alzheimer's and 14642 commoners without the disease, Seshadri's group identified two other genes associated with Alzheimer's disease, located on chromosomes 2 and 19.
Tuesday, 23 May 2017
The Rate Of Blood Coagulation Is Determined Genetically
The Rate Of Blood Coagulation Is Determined Genetically.
In an attainment to uncover why some people's blood platelets cluster faster than others, a genetic interpretation has turned up a specific grouping of overactive genes that seems to control the process. On the addition side, platelets are critical for fending off infections and healing wounds. On the down side, they can rush heart disease, heart attacks and stroke, the study authors noted.
The current find regarding the genetic roots driving platelet behavior comes from what is believed to be the largest reassessment of the human genetic code to date, according to co-senior study investigator Dr Lewis Becker, a cardiologist with the Johns Hopkins University School of Medicine. "Our results give us a palpable set of unheard of molecular targets, the proteins produced from these genes, to develop tests that could help us identify subjects more at risk for blood clots and for whom certain blood-thinning drugs may work best or not," Becker said in a Johns Hopkins low-down release.
So "We can even look toward testing new treatments that may scurry up how the body fights infection or recovers from wounds". The study findings were published online June 7 in Nature Genetics.
In an attainment to uncover why some people's blood platelets cluster faster than others, a genetic interpretation has turned up a specific grouping of overactive genes that seems to control the process. On the addition side, platelets are critical for fending off infections and healing wounds. On the down side, they can rush heart disease, heart attacks and stroke, the study authors noted.
The current find regarding the genetic roots driving platelet behavior comes from what is believed to be the largest reassessment of the human genetic code to date, according to co-senior study investigator Dr Lewis Becker, a cardiologist with the Johns Hopkins University School of Medicine. "Our results give us a palpable set of unheard of molecular targets, the proteins produced from these genes, to develop tests that could help us identify subjects more at risk for blood clots and for whom certain blood-thinning drugs may work best or not," Becker said in a Johns Hopkins low-down release.
So "We can even look toward testing new treatments that may scurry up how the body fights infection or recovers from wounds". The study findings were published online June 7 in Nature Genetics.
Saturday, 1 March 2014
Acquired Leukoderma Linked To Immune System Dysfunction
Acquired Leukoderma Linked To Immune System Dysfunction.
Scientists have discovered several genes linked to acquired leukoderma (vitiligo) that verify the pelt condition is, indeed, an autoimmune disorder. Vitiligo is a pigmentation disturb that causes white splotches to appear on the skin; the at an advanced hour pop star Michael Jackson suffered from the condition. The finding could lead to treatments for this confounding condition, the University of Colorado researchers said.
So "If you can construe the pathway that leads to the putting to death of the skin cell, then you can block that pathway," reasoned Dr Doris Day, a dermatologist with Lenox Hill Hospital in New York City. More surprisingly, however, was an minor conception related to the deadly skin cancer melanoma: People with vitiligo are less likely to reveal melanoma and vice-versa.
But "That was absolutely unexpected," said Dr Richard A Spritz, contribute to author of a paper appearing in the April 21 online issue of the New England Journal of Medicine. This finding, too, could superintend to better treatments for this insidious skin cancer. Vitiligo, similarly to a collection of about 80 other diseases including rheumatoid arthritis, type 1 diabetes and lupus, was strongly suspected to be an autoimmune scuffle in which the body's own immune set-up attacks itself, in this case, the skin's melanocytes, or pigment-producing cells.
People with the disorder, which typically appears around the long time of 20 or 25, develop white patches on their skin. Vitiligo it is fairly common, affecting up to 2 percent of the population. But the mystery of whether or not vitiligo really is an autoimmune infection has been a controversial one, said Spritz, a professor in the Human Medical Genetics Program at the University of Colorado School of Medicine in Aurora.
At the urging of various sedulous groups, these authors conducted a genome-wide link study of more than 5,000 individuals, both with and without vitiligo. Several genes found to be linked with vitiligo also had associations with other autoimmune disorders, such as breed 1 diabetes and rheumatoid arthritis.
Scientists have discovered several genes linked to acquired leukoderma (vitiligo) that verify the pelt condition is, indeed, an autoimmune disorder. Vitiligo is a pigmentation disturb that causes white splotches to appear on the skin; the at an advanced hour pop star Michael Jackson suffered from the condition. The finding could lead to treatments for this confounding condition, the University of Colorado researchers said.
So "If you can construe the pathway that leads to the putting to death of the skin cell, then you can block that pathway," reasoned Dr Doris Day, a dermatologist with Lenox Hill Hospital in New York City. More surprisingly, however, was an minor conception related to the deadly skin cancer melanoma: People with vitiligo are less likely to reveal melanoma and vice-versa.
But "That was absolutely unexpected," said Dr Richard A Spritz, contribute to author of a paper appearing in the April 21 online issue of the New England Journal of Medicine. This finding, too, could superintend to better treatments for this insidious skin cancer. Vitiligo, similarly to a collection of about 80 other diseases including rheumatoid arthritis, type 1 diabetes and lupus, was strongly suspected to be an autoimmune scuffle in which the body's own immune set-up attacks itself, in this case, the skin's melanocytes, or pigment-producing cells.
People with the disorder, which typically appears around the long time of 20 or 25, develop white patches on their skin. Vitiligo it is fairly common, affecting up to 2 percent of the population. But the mystery of whether or not vitiligo really is an autoimmune infection has been a controversial one, said Spritz, a professor in the Human Medical Genetics Program at the University of Colorado School of Medicine in Aurora.
At the urging of various sedulous groups, these authors conducted a genome-wide link study of more than 5,000 individuals, both with and without vitiligo. Several genes found to be linked with vitiligo also had associations with other autoimmune disorders, such as breed 1 diabetes and rheumatoid arthritis.
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