"You are what you eat." Can these pithy words explain the evolution of the human species?
Yes, says Richard Wrangham of Harvard University, who argues in a new book that the invention of cooking -- even more than agriculture, the eating of meat, or the advent of tools -- is what led to the rise of humanity.
Wrangham's book, "Catching Fire: How Cooking Made Us Human," is published by Basic Books. In it, he makes the case that the ability to harness fire and cook food allowed the brain to grow and the digestive tract to shrink, giving rise to our ancestor Homo erectus some 1.8 million years ago.
"Cooking is the signature feature of the human diet, and indeed, of human life -- but we have no idea why," says Wrangham, the Ruth Moore Professor of Biological Anthropology in Harvard's Faculty of Arts and Sciences. "It's the development that underpins many other changes that have made humans so distinct from other species."
Drawing on a wide body of research, Wrangham makes the case that cooking makes eating faster and easier, and wrings more caloric benefit from food. Moreover, he writes, cooking is vitally important to supporting the outsize human brain, which consumes a quarter of the body's energy.
By freeing humans from having to spend half the day chewing tough raw food -- as most of our primate relatives do -- cooking allowed early humans to devote themselves to more productive activities, ultimately allowing the development of tools, agriculture, and social networks. Cooked food is also softer, meaning the body uses less energy merely digesting what it takes in.
Since physical remnants of fire tend to degrade rapidly, archaeological evidence of fire and cooking dates back only about 800,000 years. Wrangham looked to biological evidence, which shows that around 1.8 million years ago, Homo erectus arose with larger brains and bodies and smaller guts, jaws, and teeth -- changes consistent with the switch to a more tender and energetically rich diet of cooked food.
"Cooking is what makes the human diet 'human,' and the most logical explanation for the advances in brain and body size over our ape ancestors," Wrangham says. "It's hard to imagine the leap to Homo erectus without cooking's nutritional benefits."
While others have posited that meat-eating enabled the rise of Homo erectus some 1.8 million years ago, Wrangham says those theories don't mesh with that species' smaller jaws and teeth. Instead, he claims meat enabled the shift from Australopithecines to Homo habilis -- a species about the size of a chimp, but with a bigger brain -- more than half a million years earlier.
Wrangham says the adoption of cooking had profound impacts on human families and relationships, making hearth and home central to humanity and driving humans into paired mating and perhaps even traditional male-female household roles.
He writes that the advent of cooking permitted a new distribution of labor between men and women: Men entered into relationships to have someone to cook for them, freeing them up for socializing and other pursuits and bolstering their social standing. Women benefited from men's protection, safeguarding their food from thieves. Homo sapiens remains the only species in which theft of food is uncommon even when it would be easy.
"To this day, cooking continues in every known human society," Wrangham says. "We are biologically adapted to cook food. It's part of who we are and affects us in every way you can imagine: biologically, anatomically, socially."
Source:
Steve Bradt
Harvard University
четверг, 20 октября 2011 г.
понедельник, 17 октября 2011 г.
Double Trouble With Insecticide-Resistant Mosquitoes
Mosquitoes harbouring two insecticide-resistance genes have been found to survive unexpectedly well in an insecticide-free environment where carrying such genes would normally be expected to be a burden. As outlined in research published by the open access journal BMC Evolutionary Biology, this results from the genes interacting with one another to the advantage of the host Culex quinquefasciatus mosquitoes and to the detriment of pest management strategies affecting human health.
The research team, led by Dr Vincent Corbel and colleagues from the UniversitГ© Montpellier II, Genetics and Evolution of Infectious Diseases and The Research Institute for Development (IRD) in France compared the survival rates or evolutionary fitness of one strain of the mosquito that carried two resistance genes (ace-1R and KdrR) for two different insecticides to mosquitoes that only had one insecticide-resistance gene, a French research team discovered that the survival cost of having both genes was far lower than the cost of having just ace-1R.
"We know from evolutionary theory that mutations such as these are likely to be costly to their owners in environments where they have not been selected for" explained Dr Corbel. "We've found that in C. quinquefasciatus the cost of having the ace-1R mutation in the absence of insecticides is counterbalanced when the mosquito also has the KdrR mutation. Mosquitoes with both mutations will also be harder to control as they are resistant to two different types of insecticide."
The authors also found evidence that resistance alleles interact with one another in the presence of insecticides. For instance, synergism (that is, a more than an additive effect) in toxicity was observed when a pyrethroid insecticide and a carbamate insecticide were applied simultaneously to the strain sharing both mutations (the insecticide had a greater activity and more of the mosquitoes died), whereas antagonism (that is, a less than an additive effect) was noted with Culex mosquitoes carrying only ace-1R.
Resistance to so-called xenobiotics (antibiotics, insecticides and herbicides) is a problem affecting the control of organisms of medical or economic importance. In C. quinquefasciatus insecticide resistance mutations interacted to positively and negatively influence the mosquitoes' fitness. Costs were associated with both resistance genes in an insecticide-free environment. The KdrR form of the gene, or allele, however, compensated for the costs associated with the ace-1R allele, suggesting that mosquitoes with both genes in the wild could be more prevalent. Females with both alleles were more likely to mature than those with just the ace-1R mutation."
"It is important to identify genetic interactions such as this and how they influence the fitness of multiply resistant organisms in order to better structure management strategies" says Dr Corbel. "We have found in this case that resistance genes do interact and even compensate. We will have to be very careful in how we use insecticides in future as our results have major implications for pest and health management."
1. Costs and benefits of multiple resistance to insecticides for Culex quinquefasciatus mosquitoes
Claire Berticat, Julien Bonnet, Stephane Duchon, Philip Agnew, Mylene Weill and Vincent Corbel
BMC Evolutionary Biology (in press)
Article available at journal website: biomedcentral/bmcevolbiol/
All articles are available free of charge, according to BioMed Central's open access policy.
2. Culex quinquefasciatus is an important carrier of West Nile virus in North America and bancraftian filariasis in Africa. 4 strains of C. quinquefasciatus were used in this study: SLAB, SR, BC, BCSR. All share the same genetic background and cytoplasm and only differ in their genotype at ace-1R and KdrR ace-1R and KdrR confer resistance to carbamate and pyrethroid insecticides respectively
3. BMC Evolutionary Biology is an open access journal publishing original peer-reviewed research articles in all aspects of molecular and non-molecular evolution of all organisms, as well as phylogenetics and palaeontology. BMC Evolutionary Biology (ISSN 1471-2148) is indexed/tracked/covered by PubMed, MEDLINE, BIOSIS, CAS, Zoological Record, Thomson Scientific (ISI) and Google Scholar.
4. BioMed Central (biomedcentral/) is an independent online publishing house committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open access to research is essential to the rapid and efficient communication of science.
Source: Charlotte Webber
BioMed Central
The research team, led by Dr Vincent Corbel and colleagues from the UniversitГ© Montpellier II, Genetics and Evolution of Infectious Diseases and The Research Institute for Development (IRD) in France compared the survival rates or evolutionary fitness of one strain of the mosquito that carried two resistance genes (ace-1R and KdrR) for two different insecticides to mosquitoes that only had one insecticide-resistance gene, a French research team discovered that the survival cost of having both genes was far lower than the cost of having just ace-1R.
"We know from evolutionary theory that mutations such as these are likely to be costly to their owners in environments where they have not been selected for" explained Dr Corbel. "We've found that in C. quinquefasciatus the cost of having the ace-1R mutation in the absence of insecticides is counterbalanced when the mosquito also has the KdrR mutation. Mosquitoes with both mutations will also be harder to control as they are resistant to two different types of insecticide."
The authors also found evidence that resistance alleles interact with one another in the presence of insecticides. For instance, synergism (that is, a more than an additive effect) in toxicity was observed when a pyrethroid insecticide and a carbamate insecticide were applied simultaneously to the strain sharing both mutations (the insecticide had a greater activity and more of the mosquitoes died), whereas antagonism (that is, a less than an additive effect) was noted with Culex mosquitoes carrying only ace-1R.
Resistance to so-called xenobiotics (antibiotics, insecticides and herbicides) is a problem affecting the control of organisms of medical or economic importance. In C. quinquefasciatus insecticide resistance mutations interacted to positively and negatively influence the mosquitoes' fitness. Costs were associated with both resistance genes in an insecticide-free environment. The KdrR form of the gene, or allele, however, compensated for the costs associated with the ace-1R allele, suggesting that mosquitoes with both genes in the wild could be more prevalent. Females with both alleles were more likely to mature than those with just the ace-1R mutation."
"It is important to identify genetic interactions such as this and how they influence the fitness of multiply resistant organisms in order to better structure management strategies" says Dr Corbel. "We have found in this case that resistance genes do interact and even compensate. We will have to be very careful in how we use insecticides in future as our results have major implications for pest and health management."
1. Costs and benefits of multiple resistance to insecticides for Culex quinquefasciatus mosquitoes
Claire Berticat, Julien Bonnet, Stephane Duchon, Philip Agnew, Mylene Weill and Vincent Corbel
BMC Evolutionary Biology (in press)
Article available at journal website: biomedcentral/bmcevolbiol/
All articles are available free of charge, according to BioMed Central's open access policy.
2. Culex quinquefasciatus is an important carrier of West Nile virus in North America and bancraftian filariasis in Africa. 4 strains of C. quinquefasciatus were used in this study: SLAB, SR, BC, BCSR. All share the same genetic background and cytoplasm and only differ in their genotype at ace-1R and KdrR ace-1R and KdrR confer resistance to carbamate and pyrethroid insecticides respectively
3. BMC Evolutionary Biology is an open access journal publishing original peer-reviewed research articles in all aspects of molecular and non-molecular evolution of all organisms, as well as phylogenetics and palaeontology. BMC Evolutionary Biology (ISSN 1471-2148) is indexed/tracked/covered by PubMed, MEDLINE, BIOSIS, CAS, Zoological Record, Thomson Scientific (ISI) and Google Scholar.
4. BioMed Central (biomedcentral/) is an independent online publishing house committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open access to research is essential to the rapid and efficient communication of science.
Source: Charlotte Webber
BioMed Central
пятница, 14 октября 2011 г.
Merkel Cell Originates From Skin, Not The Neural Crest, Case Western Reserve University Discovers
Case Western Reserve University School of Medicine assistant professor of pediatrics, neurosciences and otolaryngology, Stephen M. Maricich, M.D., Ph.D., and his team found that Merkel cells originate in the skin, not the neural crest lineage, as previously speculated.
The study, "Mammalian Merkel Cells are Descended from the Epidermal Lineage", was recently published in the online version of Developmental Biology and is slated its future print edition.
"Merkel cells," discovered by Friedrich Sigmund Merkel in 1875, are found in multiple regions of the skin and make contact with specialized never fibers, participating in the perception of touch.
"A real mystery surrounding Merkel cells was their developmental site of origin. Conflicting evidence suggested that these cells arose from either the skin or neural crest lineages, but there was no definitive proof of either origin," said lead author, Dr. Maricich.
Using genetically engineered mouse lines, the researchers were able to delete Atoh1, a gene essential to the formation of Merkel cells, from different areas of developing embryos. This "conditional deletion" of Atoh1 in the neural crest did not affect the Merkel cell population, however using this same technique in the skin lineage resulted in the loss of all Merkel cells.
"Knocking out Atoh1 in the neural crest line caused other problems for developing embryos, but Merkel cells were completely unaffected. However, loss of Atoh1 expression in the skin deleted all the Merkel cells," said Dr. Maricich. "This showed us that we had specifically targeted the Merkel cells and that Atoh1 expression by skin cells is necessary to their development."
The researchers also fate mapped the cells, a technique used to trace developmental fates of embryonic tissues. This analysis further supported their conditional knockout findings.
"The techniques used in this study will help neuroscientists to further explore the function of Merkel cells, including the behavioral consequences when only Merkel cells have been deleted," said Ellen Lumpkin, Ph.D., a study co-author and assistant professor of neuroscience, molecular physiology and biophysics and molecular and human genetics at the Baylor College of Medicine.
"It is thought that Merkel cells give rise to Merkel cell carcinoma, a rare but aggressive form of skin cancer that responds poorly to current treatments," said Dr. Maricich. "In addition to solving a 130 year-old mystery, our data may be relevant to the understanding of Merkel cell carcinoma, and may provide important clues in the search for novel therapeutic targets."
Funding for this study came from the National Institute of Neurological Disorders and Stroke and the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Both are of the National Institutes of Health.
Source:
Christina DeAngelis
Case Western Reserve University
The study, "Mammalian Merkel Cells are Descended from the Epidermal Lineage", was recently published in the online version of Developmental Biology and is slated its future print edition.
"Merkel cells," discovered by Friedrich Sigmund Merkel in 1875, are found in multiple regions of the skin and make contact with specialized never fibers, participating in the perception of touch.
"A real mystery surrounding Merkel cells was their developmental site of origin. Conflicting evidence suggested that these cells arose from either the skin or neural crest lineages, but there was no definitive proof of either origin," said lead author, Dr. Maricich.
Using genetically engineered mouse lines, the researchers were able to delete Atoh1, a gene essential to the formation of Merkel cells, from different areas of developing embryos. This "conditional deletion" of Atoh1 in the neural crest did not affect the Merkel cell population, however using this same technique in the skin lineage resulted in the loss of all Merkel cells.
"Knocking out Atoh1 in the neural crest line caused other problems for developing embryos, but Merkel cells were completely unaffected. However, loss of Atoh1 expression in the skin deleted all the Merkel cells," said Dr. Maricich. "This showed us that we had specifically targeted the Merkel cells and that Atoh1 expression by skin cells is necessary to their development."
The researchers also fate mapped the cells, a technique used to trace developmental fates of embryonic tissues. This analysis further supported their conditional knockout findings.
"The techniques used in this study will help neuroscientists to further explore the function of Merkel cells, including the behavioral consequences when only Merkel cells have been deleted," said Ellen Lumpkin, Ph.D., a study co-author and assistant professor of neuroscience, molecular physiology and biophysics and molecular and human genetics at the Baylor College of Medicine.
"It is thought that Merkel cells give rise to Merkel cell carcinoma, a rare but aggressive form of skin cancer that responds poorly to current treatments," said Dr. Maricich. "In addition to solving a 130 year-old mystery, our data may be relevant to the understanding of Merkel cell carcinoma, and may provide important clues in the search for novel therapeutic targets."
Funding for this study came from the National Institute of Neurological Disorders and Stroke and the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Both are of the National Institutes of Health.
Source:
Christina DeAngelis
Case Western Reserve University
вторник, 11 октября 2011 г.
Cancer Surgery Revolutionized By Tumor Painting
A tumor paint developed by researchers at Seattle Children's Hospital Research Institute and Fred Hutchinson Cancer Research Center will help surgeons see where a tumor begins and ends more precisely by illuminating the cancerous cells. The study, published in Cancer Research, shows that the tumor paint can help surgeons distinguish between cancer cells and normal brain tissue in the operating room. The paint is a scorpion-derived peptide called chlorotoxin that is linked to the molecular beacon Cy5.5.Until now there has been no way to allow surgeons to see tumors 'live' during surgery.
Chlorotoxin:Cy5.5 is a fluorescent molecular beacon that emits photons in the near infrared spectrum. This illumination gives surgeons a better chance of removing all of the cancerous cells during surgery without injuring surrounding healthy tissue. This is particularly significant in the brain, where approximately 80% of malignant cancers recur at the edges of the surgical site. Current technology, such as magnetic resonance imaging (MRI) can distinguish tumors from healthy tissue only if more than 1 million cancer cells are present. But Cy5.5 can identify tumors with as few as 2000 cancer cells, making it 500 times more sensitive than MRI.
"My greatest hope is that tumor paint will fundamentally improve cancer therapy," said James M. Olson, MD, PhD, of Seattle Children's Hospital and The Hutchison Center who is the senior author of the study. "By allowing surgeons to see cancer that would be undetectable by other means, we can give our patients better outcomes."
Olson led the team that included neurosurgeons, engineers and biologists. The bioconjugate, Chlorotoxin:Cy5.5 which, when injected, emits a near-infrared light, was created in his laboratory at the Hutchinson Center. In mouse models, the team demonstrated that they could light up brain tumors as small as 1 millimeter in diameter without lighting up the surrounding normal brain tissue. In a prostate cancer model, as few as 200 cancer cells traveling in a mouse lymph channel could be detected.
Chlorotoxin:Cy5.5 is applicable to many cancers, but is especially helpful to surgeons operating on brain tumors. Not only would it reveal whether they'd left behind any bits of tumor, it would also help them avoid removing normal tissue. Chlorotoxin:Cy5.5 activates within hours and it begins binding to cancer cells within minutes. The Chlorotoxin:Cy5.5 signal lasts for 14 days, illuminating cancer cells. Contrast agents currently in use only last for a few minutes.
"I feel fortunate to be working with gifted scientists to bring this revolutionary imaging technique from the laboratory to the bedside," said Richard Ellenbogen, MD, Pediatric Neurosurgeon, Seattle Children's Hospital and co-investigator on the study. "This development has the potential to save lives and make brain tumor resection safer."
Surgery remains a primary form of cancer therapy. Despite advances in surgical tools, surgeons currently rely on color, texture or blood supply to differentiate tumor from normal tissue, a distinction that is often subtle and imperfect. The limitations of this method contribute to cancer growth or patient mortality that is potentially preventable. The tumor painting technique combines a visual guide for the surgeon with the potential for significant improvement in accuracy and safety.
Tumor painting has been successfully tested in mice and the pilot safety trials are complete. Olson and his team are preparing the necessary toxicity studies before seeking approval from the Food and Drug Administration to begin clinical trials. Chlorotoxin:Cy5.5 could be used in operating rooms in as little as 18 months. All clinical studies will have consenting adult participants.
Olson and his team believe that Chlorotoxin:Cy5.5 has the potential to be used in the future as a non-invasive screening tool for early detection of skin, cervical, esophageal, colon and lung cancers. It is also useful in identifying positive lymph nodes which could mean a significant advancement for breast, prostate and testicular cancers.
Children's and the Hutchison Center's role as leading research institutions is underscored by their membership in the Pediatric Brain Tumor Consortium (PBTC), a group of 10 medical centers selected by the National Cancer Institute (NCI). The consortium's members were chosen by the NCI based on their experience, dedication to research and quality of patient care.
Other Children's and Hutchison Center researchers on the team include Mandana Veiseh, PhD; Patrik Gabikian, S-Bahram Bahrami, PhD; Omid Veiseh, Miqin Zhang, Robert C. Hackman, MD; Ali C. Ravanpay, Mark R. Stroud, PhD; Yumiko Kusuma, Stacey J. Hansen, Deborah Kwok, Nina M. Munoz, PhD; Raymond W. Sze, MD; William M. Grady, MD; and Norman M. Greenberg, PhD.
About Seattle Children's Hospital Research Institute, Seattle, Wash.
At the forefront of pediatric research, the Seattle Children's Hospital Research Institute at Children's Hospital and Regional Medical Center in Seattle conducts research under nine major centers and is internationally recognized for its discoveries in cancer, genetics, health services, immunology, pathology, infectious disease and vaccines. Consistently ranked as one of the best children's hospitals in the country by U.S. News & World Report, Children's serves as the pediatric referral center for Washington, Alaska, Montana and Idaho. Children's has been delivering superior patient care for 100 years, including advancing new discoveries and treatments in pediatric research, and serving as a primary teaching, clinical and research site for the Department of Pediatrics at the University of Washington School of Medicine. For more information about the Institute visit research.seattlechildrens/.
At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit fhcrc/.
Source: Jennifer Seymour
Children's Hospital and Regional Medical Center of Seattle
Chlorotoxin:Cy5.5 is a fluorescent molecular beacon that emits photons in the near infrared spectrum. This illumination gives surgeons a better chance of removing all of the cancerous cells during surgery without injuring surrounding healthy tissue. This is particularly significant in the brain, where approximately 80% of malignant cancers recur at the edges of the surgical site. Current technology, such as magnetic resonance imaging (MRI) can distinguish tumors from healthy tissue only if more than 1 million cancer cells are present. But Cy5.5 can identify tumors with as few as 2000 cancer cells, making it 500 times more sensitive than MRI.
"My greatest hope is that tumor paint will fundamentally improve cancer therapy," said James M. Olson, MD, PhD, of Seattle Children's Hospital and The Hutchison Center who is the senior author of the study. "By allowing surgeons to see cancer that would be undetectable by other means, we can give our patients better outcomes."
Olson led the team that included neurosurgeons, engineers and biologists. The bioconjugate, Chlorotoxin:Cy5.5 which, when injected, emits a near-infrared light, was created in his laboratory at the Hutchinson Center. In mouse models, the team demonstrated that they could light up brain tumors as small as 1 millimeter in diameter without lighting up the surrounding normal brain tissue. In a prostate cancer model, as few as 200 cancer cells traveling in a mouse lymph channel could be detected.
Chlorotoxin:Cy5.5 is applicable to many cancers, but is especially helpful to surgeons operating on brain tumors. Not only would it reveal whether they'd left behind any bits of tumor, it would also help them avoid removing normal tissue. Chlorotoxin:Cy5.5 activates within hours and it begins binding to cancer cells within minutes. The Chlorotoxin:Cy5.5 signal lasts for 14 days, illuminating cancer cells. Contrast agents currently in use only last for a few minutes.
"I feel fortunate to be working with gifted scientists to bring this revolutionary imaging technique from the laboratory to the bedside," said Richard Ellenbogen, MD, Pediatric Neurosurgeon, Seattle Children's Hospital and co-investigator on the study. "This development has the potential to save lives and make brain tumor resection safer."
Surgery remains a primary form of cancer therapy. Despite advances in surgical tools, surgeons currently rely on color, texture or blood supply to differentiate tumor from normal tissue, a distinction that is often subtle and imperfect. The limitations of this method contribute to cancer growth or patient mortality that is potentially preventable. The tumor painting technique combines a visual guide for the surgeon with the potential for significant improvement in accuracy and safety.
Tumor painting has been successfully tested in mice and the pilot safety trials are complete. Olson and his team are preparing the necessary toxicity studies before seeking approval from the Food and Drug Administration to begin clinical trials. Chlorotoxin:Cy5.5 could be used in operating rooms in as little as 18 months. All clinical studies will have consenting adult participants.
Olson and his team believe that Chlorotoxin:Cy5.5 has the potential to be used in the future as a non-invasive screening tool for early detection of skin, cervical, esophageal, colon and lung cancers. It is also useful in identifying positive lymph nodes which could mean a significant advancement for breast, prostate and testicular cancers.
Children's and the Hutchison Center's role as leading research institutions is underscored by their membership in the Pediatric Brain Tumor Consortium (PBTC), a group of 10 medical centers selected by the National Cancer Institute (NCI). The consortium's members were chosen by the NCI based on their experience, dedication to research and quality of patient care.
Other Children's and Hutchison Center researchers on the team include Mandana Veiseh, PhD; Patrik Gabikian, S-Bahram Bahrami, PhD; Omid Veiseh, Miqin Zhang, Robert C. Hackman, MD; Ali C. Ravanpay, Mark R. Stroud, PhD; Yumiko Kusuma, Stacey J. Hansen, Deborah Kwok, Nina M. Munoz, PhD; Raymond W. Sze, MD; William M. Grady, MD; and Norman M. Greenberg, PhD.
About Seattle Children's Hospital Research Institute, Seattle, Wash.
At the forefront of pediatric research, the Seattle Children's Hospital Research Institute at Children's Hospital and Regional Medical Center in Seattle conducts research under nine major centers and is internationally recognized for its discoveries in cancer, genetics, health services, immunology, pathology, infectious disease and vaccines. Consistently ranked as one of the best children's hospitals in the country by U.S. News & World Report, Children's serves as the pediatric referral center for Washington, Alaska, Montana and Idaho. Children's has been delivering superior patient care for 100 years, including advancing new discoveries and treatments in pediatric research, and serving as a primary teaching, clinical and research site for the Department of Pediatrics at the University of Washington School of Medicine. For more information about the Institute visit research.seattlechildrens/.
At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit fhcrc/.
Source: Jennifer Seymour
Children's Hospital and Regional Medical Center of Seattle
суббота, 8 октября 2011 г.
54 Million Americans Have Pre-Diabetes
Periodontal diseases may contribute to the progression to pre-diabetes, according to a new study that appears in the March issue of the Journal of Periodontology.
Pre-diabetes is a condition in which blood glucose levels are higher than normal, but not high enough to be diagnosed as diabetes. The American Diabetes Association estimates 54 million people in the United States have pre-diabetes, and a significant portion of those people will develop Type 2 diabetes within 10 years.
Researchers from Denmark investigated if having periodontal diseases can influence pre-diabetes and contribute to the progression of diabetes. They found that having periodontal disease can cause someone to develop pre-diabetic characteristics, and probably disturb the glucose regulation of a non-diabetic who has pre-diabetic characteristics, contributing to the progression of Type 2 diabetes. The study, conducted with rat models known to exhibit pre-diabetes characteristics, is believed to be the first to evaluate the relationship between periodontitis and pre-diabetes.
"This study found that having periodontal diseases can alter the metabolic conditions which would probably lead to the progression to pre-diabetic characteristics and Type 2 diabetes," said Dr. Carla Pontes Andersen, Department of Periodontology at the University of Copenhagen.
"We have known that people with diabetes are more susceptible to periodontal diseases and have more severe disease," said Dr. Preston D. Miller, Jr., President of the American Academy of Periodontology. "This breakthrough research shows having periodontal disease may aggravate pre-diabetes which is a precursor for diabetes. These findings underscore the importance of taking good care of your teeth and gums: it may be a simple way to prevent diabetes, or to prevent the progression of diabetes."
To asses your periodontal health visit perio/ and click on "Assess your gum disease risk". To check if you may be at risk of developing diabetes, visit diabetes/risk-test.jsp.
Visit the AAP website, perio/ for a referral to a periodontist and free brochure titled Diabetes & Periodontal Diseases.
The American Academy of Periodontology is an 8,000-member association of dental professionals specializing in the prevention, diagnosis and treatment of diseases affecting the gums and supporting structures of the teeth and in the placement and maintenance of dental implants. Periodontics is one of nine dental specialties recognized by the American Dental Association.
Contact: Kerry Gutshall
American Academy of Periodontology
Pre-diabetes is a condition in which blood glucose levels are higher than normal, but not high enough to be diagnosed as diabetes. The American Diabetes Association estimates 54 million people in the United States have pre-diabetes, and a significant portion of those people will develop Type 2 diabetes within 10 years.
Researchers from Denmark investigated if having periodontal diseases can influence pre-diabetes and contribute to the progression of diabetes. They found that having periodontal disease can cause someone to develop pre-diabetic characteristics, and probably disturb the glucose regulation of a non-diabetic who has pre-diabetic characteristics, contributing to the progression of Type 2 diabetes. The study, conducted with rat models known to exhibit pre-diabetes characteristics, is believed to be the first to evaluate the relationship between periodontitis and pre-diabetes.
"This study found that having periodontal diseases can alter the metabolic conditions which would probably lead to the progression to pre-diabetic characteristics and Type 2 diabetes," said Dr. Carla Pontes Andersen, Department of Periodontology at the University of Copenhagen.
"We have known that people with diabetes are more susceptible to periodontal diseases and have more severe disease," said Dr. Preston D. Miller, Jr., President of the American Academy of Periodontology. "This breakthrough research shows having periodontal disease may aggravate pre-diabetes which is a precursor for diabetes. These findings underscore the importance of taking good care of your teeth and gums: it may be a simple way to prevent diabetes, or to prevent the progression of diabetes."
To asses your periodontal health visit perio/ and click on "Assess your gum disease risk". To check if you may be at risk of developing diabetes, visit diabetes/risk-test.jsp.
Visit the AAP website, perio/ for a referral to a periodontist and free brochure titled Diabetes & Periodontal Diseases.
The American Academy of Periodontology is an 8,000-member association of dental professionals specializing in the prevention, diagnosis and treatment of diseases affecting the gums and supporting structures of the teeth and in the placement and maintenance of dental implants. Periodontics is one of nine dental specialties recognized by the American Dental Association.
Contact: Kerry Gutshall
American Academy of Periodontology
среда, 5 октября 2011 г.
Cell Death In The Colon Influenced By Vitamin D And Calcium
Researchers at Emory University are learning how vitamins and minerals in the diet can stimulate or prevent the appearance of colon cancer.
Emory investigators will present their findings on biological markers that could influence colon cancer risk in three abstracts at the American Association for Cancer Research meeting in San Diego, April 12-16, 2008.
In a clinical study of 92 patients, supplementing diet with calcium and vitamin D appeared to increase the levels of a protein called Bax that controls programmed cell death in the colon. More Bax might be pushing pre-cancerous cells into programmed cell death, says Emory researcher Veronika Fedirko, who will present her team's results (abstract 464).
Previous studies have shown that calcium and vitamin D tend to reduce colon cancer risk.
"We were pleased that the effects of calcium and vitamin D were visible enough in this small study to be significant and reportable," Fedirko says. "We will have to fully evaluate each marker's strength as we accumulate more data."
The studies of colorectal biopsy samples are part of a larger effort to identify a portfolio of measurements that together can gauge someone's risk of getting colon cancer, says Roberd Bostick, MD, MPH, professor of epidemiology at Emory's Rollins School of Public Health.
"We want to have the equivalent of measuring cholesterol or high blood pressure, but for colon cancer instead of heart disease," Bostick says. "These measurements will describe the climate of risk in the colon rather than spotting individual tumors or cells that may become tumors."
More about Bostick's plans for developing non-invasive blood or urine tests for colon cancer risk is available in an Emory Health Sciences Magazine article.
Another abstract from Bostick and his colleagues (565) demonstrates in a 200-patient case-control study that high levels of calcium and vitamin D together are associated with increased levels of E-cadherin, which moderates colon cells' movement and proliferation.
A third abstract on the same case-control study (5504) shows that high levels of iron in the diet are linked to low levels of APC, a protein whose absence in colon cancer cells leads to their runaway growth.
Bostick and his colleagues are participating in a ten-year multi-center study of the effects of increased vitamin D and calcium and biomarker-guided treatment of colon cancer recurrence. The study involves almost 2,500 people nationwide who have regular colonoscopies.
The Bostick team's research is funded by the National Cancer Institute and the Wilson and Anne Franklin Foundation.
Source: Ashante Dobbs
Emory University
Emory investigators will present their findings on biological markers that could influence colon cancer risk in three abstracts at the American Association for Cancer Research meeting in San Diego, April 12-16, 2008.
In a clinical study of 92 patients, supplementing diet with calcium and vitamin D appeared to increase the levels of a protein called Bax that controls programmed cell death in the colon. More Bax might be pushing pre-cancerous cells into programmed cell death, says Emory researcher Veronika Fedirko, who will present her team's results (abstract 464).
Previous studies have shown that calcium and vitamin D tend to reduce colon cancer risk.
"We were pleased that the effects of calcium and vitamin D were visible enough in this small study to be significant and reportable," Fedirko says. "We will have to fully evaluate each marker's strength as we accumulate more data."
The studies of colorectal biopsy samples are part of a larger effort to identify a portfolio of measurements that together can gauge someone's risk of getting colon cancer, says Roberd Bostick, MD, MPH, professor of epidemiology at Emory's Rollins School of Public Health.
"We want to have the equivalent of measuring cholesterol or high blood pressure, but for colon cancer instead of heart disease," Bostick says. "These measurements will describe the climate of risk in the colon rather than spotting individual tumors or cells that may become tumors."
More about Bostick's plans for developing non-invasive blood or urine tests for colon cancer risk is available in an Emory Health Sciences Magazine article.
Another abstract from Bostick and his colleagues (565) demonstrates in a 200-patient case-control study that high levels of calcium and vitamin D together are associated with increased levels of E-cadherin, which moderates colon cells' movement and proliferation.
A third abstract on the same case-control study (5504) shows that high levels of iron in the diet are linked to low levels of APC, a protein whose absence in colon cancer cells leads to their runaway growth.
Bostick and his colleagues are participating in a ten-year multi-center study of the effects of increased vitamin D and calcium and biomarker-guided treatment of colon cancer recurrence. The study involves almost 2,500 people nationwide who have regular colonoscopies.
The Bostick team's research is funded by the National Cancer Institute and the Wilson and Anne Franklin Foundation.
Source: Ashante Dobbs
Emory University
воскресенье, 2 октября 2011 г.
Genome Mapping Technique Speeds Process Of Finding Specific Genes
A Purdue University scientist was part of a global team that has demonstrated a specialized mapping technique that could speed work in genomic fields by quickly finding genetic associations that shape an organism's observable characteristics.
Using plants from 93 different Arabidopsis thaliana populations, a team led by the Gregor Mendel Institute of Plant Biology in Austria was able to find genetic associations among multiple phenotypes, or traits, suggesting that the same genes or closely related genes controlled those traits. David E. Salt, a Purdue professor of plant biology and co-author of a Nature paper on the study released Wednesday (March 24), said the ability to find these types of genetic links could speed scientists' ability to find and isolate genes and understand their function.
"This may show that multiple phenotypes are being controlled by a specific region of the genome," Salt said. "It helps us understand the mechanisms."
A traditional search for a gene responsible for a particular characteristic requires using plants that have been phenotyped, or identified by characteristics. They are then crossed with others, and the offspring are phenotyped.
Scientists then check for similarities in offsprings' genes with the desired trait. The process can be painstaking and time consuming because many thousands of individuals may need to be checked, Salt said.
Genome-wide association mapping compares the sequence of DNA in genomes of many individual plants or animals to find similarities that narrow the scope of the search for a particular gene.
"We can look for a region in the genome that is in common among the individuals," Salt said. "For plant biologists, it's a much more efficient way of getting to genes. And for animal biologists, where making test crosses is more difficult, this is critical."
In this study, specific differences in DNA, called single nucleotide polymorphisms, or SNPs, were compared at 250,000 sites across the genomes of many individuals. The genomes were matched up against specific traits for each individual in order to find SNPs that are associated with the trait of interest. If scientists were looking for plants that produce high seed yields, for example, they would compare the genomes of plants that have a range of seed yields. The places where the genomes match in individuals with high seed yields are possible locations of sought-after genes.
Genome-wide association mapping is a faster process because fewer plants - usually in the hundreds - need to be grown and phenotyped. Finding genetic associations among multiple phenotypes could reveal more information about how those characteristics might be connected.
Of the 107 phenotypes used in the research, Salt was responsible for phenotyping the plants for 18 characteristics, which focused on nutrient and micronutrient content. He said the next step in the research would be to test those associations to determine the genes responsible for particular plant characteristics.
The National Institutes of Health funded the research.
Writer: Brian Wallheimer
Source:
Brian Wallheimer
Purdue University
Using plants from 93 different Arabidopsis thaliana populations, a team led by the Gregor Mendel Institute of Plant Biology in Austria was able to find genetic associations among multiple phenotypes, or traits, suggesting that the same genes or closely related genes controlled those traits. David E. Salt, a Purdue professor of plant biology and co-author of a Nature paper on the study released Wednesday (March 24), said the ability to find these types of genetic links could speed scientists' ability to find and isolate genes and understand their function.
"This may show that multiple phenotypes are being controlled by a specific region of the genome," Salt said. "It helps us understand the mechanisms."
A traditional search for a gene responsible for a particular characteristic requires using plants that have been phenotyped, or identified by characteristics. They are then crossed with others, and the offspring are phenotyped.
Scientists then check for similarities in offsprings' genes with the desired trait. The process can be painstaking and time consuming because many thousands of individuals may need to be checked, Salt said.
Genome-wide association mapping compares the sequence of DNA in genomes of many individual plants or animals to find similarities that narrow the scope of the search for a particular gene.
"We can look for a region in the genome that is in common among the individuals," Salt said. "For plant biologists, it's a much more efficient way of getting to genes. And for animal biologists, where making test crosses is more difficult, this is critical."
In this study, specific differences in DNA, called single nucleotide polymorphisms, or SNPs, were compared at 250,000 sites across the genomes of many individuals. The genomes were matched up against specific traits for each individual in order to find SNPs that are associated with the trait of interest. If scientists were looking for plants that produce high seed yields, for example, they would compare the genomes of plants that have a range of seed yields. The places where the genomes match in individuals with high seed yields are possible locations of sought-after genes.
Genome-wide association mapping is a faster process because fewer plants - usually in the hundreds - need to be grown and phenotyped. Finding genetic associations among multiple phenotypes could reveal more information about how those characteristics might be connected.
Of the 107 phenotypes used in the research, Salt was responsible for phenotyping the plants for 18 characteristics, which focused on nutrient and micronutrient content. He said the next step in the research would be to test those associations to determine the genes responsible for particular plant characteristics.
The National Institutes of Health funded the research.
Writer: Brian Wallheimer
Source:
Brian Wallheimer
Purdue University
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