The Flu Vaccine Is Little Effect On Men.
The flu vaccine is less in operation for men than women, and researchers at Stanford University hold they've figured out why. The man's hormone testosterone causes genes in the immune way to produce fewer antibodies, or defense mechanisms, in response to the vaccine, they found extenderdlx.com. "Men, typically, do worse than women in protected response to infection and vaccination," said Stanford research mate David Furman, the lead study investigator.
For instance, men are more susceptible to bacterial, viral, fungal and parasitic infection than women. And men's untouched systems don't come back as robustly as women's to vaccinations against flu, yellow fever, measles, hepatitis and many other diseases source. 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 answer to the flu vaccine across the board. Testosterone is tied to standard manful reproductive characteristics, such as muscle strength, beard growth and risk-taking. "We found a set of genes in men that when activated caused a lousy response to the vaccine, but were not involved in female response. Some of these genes are regulated by testosterone".
It's testosterone's obtain on these genes that causes the poor vaccine response. "This has a lot of implications for vaccine development". Vaccine reaction might be better if men were given twice the dose, he suggested, or possibly if testosterone levels were reduced. The whole picture isn't quite 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
Wednesday 30 January 2019
Monday 24 December 2018
The New Role Of Stem Cells For Treatment Of Neoplastic Diseases
The New Role Of Stem Cells For Treatment Of Neoplastic Diseases.
For wise myeloid leukemia patients, overactive genes in their leukemic staunch cells (LSC) can forward into a more difficult struggle to overcome their disease and achieve prolonged remission, unknown research reveals. "In many cancers, specific subpopulations of cells appear to be uniquely efficient of initiating and maintaining tumors," the study authors explained in their report barbati. The researchers identified 52 LSC genes that, when strongly active, appear to prompt worse outcomes to each acute myeloid leukemia (AML) patients.
The finding is reported in the Dec 22/29 2010 discharge of the Journal of the American Medical Association. Between 2005 and 2007, con author Andrew J Gentles, of Stanford University in Palo Alto, California, and colleagues examined gene motion in a group of AML patients as well as healthy individuals visit your url. Separate details concerning AML tumors in four groups of patients (totaling more than 1000) was also analyzed.
In one of the tireless groups, the investigators found that higher activity levels among 52 LSC genes meant a 78 percent peril of death within a three-year period. This compared with a 57 percent imperil of death in the same time frame for AML patients with lower gene activity amongst these specific "signature" genes. In another AML patient group, the research team observed that higher gene work prompted an 81 percent risk for experiencing a disease impediment over three years, compared with just a 48 percent risk among patients with low gene activity.
What's more, Gentles and his colleagues found that higher undertaking among these 52 LSC genes in a general way meant a poorer response to chemotherapy treatment and lower remission rates. The authors suggested that by "scoring" the vigour levels of these 52 genes from low to high, clinicians might be able to better forecast how well AML patients will respond to therapy.
For wise myeloid leukemia patients, overactive genes in their leukemic staunch cells (LSC) can forward into a more difficult struggle to overcome their disease and achieve prolonged remission, unknown research reveals. "In many cancers, specific subpopulations of cells appear to be uniquely efficient of initiating and maintaining tumors," the study authors explained in their report barbati. The researchers identified 52 LSC genes that, when strongly active, appear to prompt worse outcomes to each acute myeloid leukemia (AML) patients.
The finding is reported in the Dec 22/29 2010 discharge of the Journal of the American Medical Association. Between 2005 and 2007, con author Andrew J Gentles, of Stanford University in Palo Alto, California, and colleagues examined gene motion in a group of AML patients as well as healthy individuals visit your url. Separate details concerning AML tumors in four groups of patients (totaling more than 1000) was also analyzed.
In one of the tireless groups, the investigators found that higher activity levels among 52 LSC genes meant a 78 percent peril of death within a three-year period. This compared with a 57 percent imperil of death in the same time frame for AML patients with lower gene activity amongst these specific "signature" genes. In another AML patient group, the research team observed that higher gene work prompted an 81 percent risk for experiencing a disease impediment over three years, compared with just a 48 percent risk among patients with low gene activity.
What's more, Gentles and his colleagues found that higher undertaking among these 52 LSC genes in a general way meant a poorer response to chemotherapy treatment and lower remission rates. The authors suggested that by "scoring" the vigour levels of these 52 genes from low to high, clinicians might be able to better forecast how well AML patients will respond to therapy.
Monday 18 December 2017
The Rate Of Blood Coagulation Is Determined Genetically
The Rate Of Blood Coagulation Is Determined Genetically.
In an essay to uncover why some people's blood platelets lump faster than others, a genetic opinion has turned up a specific grouping of overactive genes that seems to control the process. On the with side, platelets are critical for fending off infections and healing wounds cheapest. On the down side, they can impel heart disease, heart attacks and stroke, the study authors noted.
The current declaration regarding the genetic roots driving platelet behavior comes from what is believed to be the largest parade 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 enlargement. "Our results give us a unquestioned set of brand-new molecular targets, the proteins produced from these genes, to develop tests that could help us identify family more at risk for blood clots and for whom certain blood-thinning drugs may work best or not," Becker said in a Johns Hopkins advice release.
So "We can even look toward testing new treatments that may celerity up how the body fights infection or recovers from wounds". The study findings were published online June 7 in Nature Genetics.
In an essay to uncover why some people's blood platelets lump faster than others, a genetic opinion has turned up a specific grouping of overactive genes that seems to control the process. On the with side, platelets are critical for fending off infections and healing wounds cheapest. On the down side, they can impel heart disease, heart attacks and stroke, the study authors noted.
The current declaration regarding the genetic roots driving platelet behavior comes from what is believed to be the largest parade 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 enlargement. "Our results give us a unquestioned set of brand-new molecular targets, the proteins produced from these genes, to develop tests that could help us identify family more at risk for blood clots and for whom certain blood-thinning drugs may work best or not," Becker said in a Johns Hopkins advice release.
So "We can even look toward testing new treatments that may celerity up how the body fights infection or recovers from wounds". The study findings were published online June 7 in Nature Genetics.
Friday 2 September 2016
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 seal the abrade condition is, indeed, an autoimmune disorder. Vitiligo is a pigmentation free-for-all that causes white splotches to appear on the skin; the preceding 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 conscious of the pathway that leads to the holocaust 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 trivial determining related to the deadly skin cancer melanoma: People with vitiligo are less likely to blossom melanoma and vice-versa.
But "That was absolutely unexpected," said Dr Richard A Spritz, cable author of a paper appearing in the April 21 online issue of the New England Journal of Medicine. This finding, too, could tether to better treatments for this insidious skin cancer. Vitiligo, identical to a collection of about 80 other diseases including rheumatoid arthritis, type 1 diabetes and lupus, was strongly suspected to be an autoimmune sickness in which the body's own immune routine attacks itself, in this case, the skin's melanocytes, or pigment-producing cells.
People with the disorder, which typically appears around the epoch 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 query of whether or not vitiligo really is an autoimmune infection has been a controversial one a professor in the Human Medical Genetics Program at the University of Colorado School of Medicine in Aurora.
At the urging of various self-possessed groups, these authors conducted a genome-wide association 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 sort 1 diabetes and rheumatoid arthritis.
Scientists have discovered several genes linked to acquired leukoderma (vitiligo) that seal the abrade condition is, indeed, an autoimmune disorder. Vitiligo is a pigmentation free-for-all that causes white splotches to appear on the skin; the preceding 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 conscious of the pathway that leads to the holocaust 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 trivial determining related to the deadly skin cancer melanoma: People with vitiligo are less likely to blossom melanoma and vice-versa.
But "That was absolutely unexpected," said Dr Richard A Spritz, cable author of a paper appearing in the April 21 online issue of the New England Journal of Medicine. This finding, too, could tether to better treatments for this insidious skin cancer. Vitiligo, identical to a collection of about 80 other diseases including rheumatoid arthritis, type 1 diabetes and lupus, was strongly suspected to be an autoimmune sickness in which the body's own immune routine attacks itself, in this case, the skin's melanocytes, or pigment-producing cells.
People with the disorder, which typically appears around the epoch 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 query of whether or not vitiligo really is an autoimmune infection has been a controversial one a professor in the Human Medical Genetics Program at the University of Colorado School of Medicine in Aurora.
At the urging of various self-possessed groups, these authors conducted a genome-wide association 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 sort 1 diabetes and rheumatoid arthritis.
Friday 25 December 2015
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 bug and could become targets for rejuvenated treatments for the neurodegenerative condition. Genetic variants appear to entertainment an important take 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 venerable 65 will develop Alzheimer's disease in their lifetime, the researchers added.
Genome-wide camaraderie studies are increasing scientists' understanding of the biological pathways underlying Alzheimer's disease, which may bring to new therapies, said study author Dr Sudha Seshadri, an fellow-worker professor of neurology at Boston University School of Medicine. For now, society should realize that genes likely interact with other genes and with environmental factors.
Maria Carrillo, senior commander of medical and scientific relations at the Alzheimer's Association, said that "these are the types of studies we paucity in terms of future genetic analysis and things must be confirmed in much larger samples, as was done in this study". The turn up is published in the May 12 issue of the Journal of the American Medical Association.
Although it was known that three genes are chargeable for rare cases of Alzheimer's disease that run in families, researchers had been trusty of only one gene, apolipoprotein E (APOE), that increased the risk of the common type of Alzheimer's disease. Using a genome-wide cooperative analysis study of 3006 people with Alzheimer's and 14642 folk 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 bug and could become targets for rejuvenated treatments for the neurodegenerative condition. Genetic variants appear to entertainment an important take 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 venerable 65 will develop Alzheimer's disease in their lifetime, the researchers added.
Genome-wide camaraderie studies are increasing scientists' understanding of the biological pathways underlying Alzheimer's disease, which may bring to new therapies, said study author Dr Sudha Seshadri, an fellow-worker professor of neurology at Boston University School of Medicine. For now, society should realize that genes likely interact with other genes and with environmental factors.
Maria Carrillo, senior commander of medical and scientific relations at the Alzheimer's Association, said that "these are the types of studies we paucity in terms of future genetic analysis and things must be confirmed in much larger samples, as was done in this study". The turn up is published in the May 12 issue of the Journal of the American Medical Association.
Although it was known that three genes are chargeable for rare cases of Alzheimer's disease that run in families, researchers had been trusty of only one gene, apolipoprotein E (APOE), that increased the risk of the common type of Alzheimer's disease. Using a genome-wide cooperative analysis study of 3006 people with Alzheimer's and 14642 folk without the disease, Seshadri's group identified two other genes associated with Alzheimer's disease, located on chromosomes 2 and 19.
Wednesday 19 August 2015
The Genes Of Autism Spectrum Disorder
The Genes Of Autism Spectrum Disorder.
Siblings who quota a diagnosis of autism often don't divide up the same autism-linked genes, according to a new study. Researchers previously have identified more than 100 genetic mutations that can designate a person more susceptible to an autism spectrum disorder, said ranking author Dr Stephen Scherer, director of the Center for Applied Genomics at the Hospital for Sick Children in Toronto. But this think over revealed that genes linked to autism can diverge among family members who would be expected to be genetically similar.
And "We found when we could identify the genes convoluted in autism, for two-thirds of those families, the children carry different genetic changes. In one-third, the children had the same genetic vary and it was inherited from one of the parents". The study was published online Jan 26, 2015 in Nature Medicine. Autism is a developmental disarrange in which children have trouble communicating with others and expose repetitive or obsessive behaviors.
About one in 68 children in the United States has been diagnosed with autism spectrum disorder, according to the US Centers for Disease Control and Prevention. The study's findings could cover the procedure toward more accurate diagnosis and earlier treatment for children with a genetic predisposition toward autism. Previously, if a folks had a child with autism, doctors would focus only on the gene related to that child's autism in structure to predict whether another sibling also could be at risk.
So "We're saying that's the wrong whatsis to do. You need to sequence the whole genome, because more likely than not, it's universal to be something different". Through such a comprehensive scan, doctors can get children with autism very early treatment, which has been shown to rectify their development. This research relies on "whole-genome sequencing," a more technologically advanced compose of testing that doubles the amount of genetic information produced by each scan.
Siblings who quota a diagnosis of autism often don't divide up the same autism-linked genes, according to a new study. Researchers previously have identified more than 100 genetic mutations that can designate a person more susceptible to an autism spectrum disorder, said ranking author Dr Stephen Scherer, director of the Center for Applied Genomics at the Hospital for Sick Children in Toronto. But this think over revealed that genes linked to autism can diverge among family members who would be expected to be genetically similar.
And "We found when we could identify the genes convoluted in autism, for two-thirds of those families, the children carry different genetic changes. In one-third, the children had the same genetic vary and it was inherited from one of the parents". The study was published online Jan 26, 2015 in Nature Medicine. Autism is a developmental disarrange in which children have trouble communicating with others and expose repetitive or obsessive behaviors.
About one in 68 children in the United States has been diagnosed with autism spectrum disorder, according to the US Centers for Disease Control and Prevention. The study's findings could cover the procedure toward more accurate diagnosis and earlier treatment for children with a genetic predisposition toward autism. Previously, if a folks had a child with autism, doctors would focus only on the gene related to that child's autism in structure to predict whether another sibling also could be at risk.
So "We're saying that's the wrong whatsis to do. You need to sequence the whole genome, because more likely than not, it's universal to be something different". Through such a comprehensive scan, doctors can get children with autism very early treatment, which has been shown to rectify their development. This research relies on "whole-genome sequencing," a more technologically advanced compose of testing that doubles the amount of genetic information produced by each scan.
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