Ha perdido cuatro kilos en apenas un mes. A sus 75 años no quiere comer porque «no tiene ganas», y apenas sale de casa. Sufre lo que los expertos denominan «anorexia senil». Según Alberto López Rocha, presidente de la Sociedad Española de Médicos de Residencias (Semer) «provoca una disminución del apetito que en la mayoría de los casos se debe a causas sociales, fisiológicas o psicológicas». Y esta última es importante, pues «en la actualidad todavía hay un millón y medio de mayores de 65 años que viven solos y que tienen que enfrentarse a barreras arquitectónicas». Y eso no sólo quita las ganas de comer, sino que, además, les hace desconfiados. «No se fían de las personas que ponen a su disposición para ayudarles, por ejemplo, a hacer la compra, y como ellos no pueden bajar a por ella, terminan consumiendo «monoalimentos». Otro factor psicológico es la depresión y los estados de tristeza en los que se ven inmersos y que de forma indirecta repercuten en su alimentación.
No obstante, no hay que confundir este trastorno con la denominada hiporexia, que, tal y como aclara Fernando Gómez-Busto, miembro del grupo de nutrición de la Sociedad Española de Geriatría y Gerontología «es poco apetito». No es como la anorexia de envejecimiento, que se caracteriza por una disminución gradual de la ingesta en respuesta cambios corporales, a las menores necesidades energéticas, y a la menor actividad física». Entre los 20 y los 80 años, esta disminución se calcula, entre 600 Kcal/ día (mujeres) y 1.300 Kcal/ día (hombres) especialmente entre los 60 y 70 años y después de los 80. En cuanto al balance nutricional del paciente se produce «una disminución de la ingesta de proteínas y lípidos. Entre los micronutrientes, disminuye principalmente la ingesta de vitaminas A y D, calcio, folatos y magnesio», matiza Gómez-Busto.
Otro factor es la impactación fecal. «El 50 por ciento de los mayores sufre estreñimiento, lo que hace que tengas aún menos ganas de comer», señala el presidente de la Semer. La pérdida de peso también puede ser consecuencia de una mala dentición, alteraciones del gusto, infecciones o prótesis, así como de la demencia o enfermedades neurodegenerativas.RiesgoCuando el anciano deja de comer, el peligro principal es la desnutrición, que se asocia a pérdida de masa muscular y «mayor riesgo de caídas, menor capacidad inmunológica y mayor aumento de fragilidad».
Según los expertos, este problema está presente en entre el 1 y el 8 por ciento de los mayores que viven en sus domicilios. «Entre los ancianos hospitalizados y los ingresados en centros geriátricos, que tienen mayores problemas de enfermedad y dependencia, estas cifras son bastante más elevadas», dice el miembro de la Sociedad Española de Geriatría y Gerontología. Algo que corrobora López Rocha, pues, a su juicio «el 37 por ciento de los españoles mayores de 70 años que está hospitalizado muestra síntomas de desnutrición producida por dicha anorexia».
Para hacer frente al trastorno hay que acudir al médico de cabecera para que descarte otras patologías como, una enfermedad tumoral. En casa, hacer los platos más atractivos, ya que muchas veces el problema es que al no poder masticar, ingieren purés, cuyo aspecto no despierta las ganas de comer. Otra clave es tener cuidado con las siestas y, en lugar de que duerman nada más comer, es preferible que den un paseo.
**Publicado en "LA RAZON"
16 January 2012
New 'smart' nanotherapeutics can deliver drugs directly to the pancreas
A research collaboration between the Wyss Institute for Biologically Inspired Engineering at Harvard University and Children's Hospital Boston has developed "smart" injectable nanotherapeutics that can be programmed to selectively deliver drugs to the cells of the pancreas. Although this nanotechnology will need significant additional testing and development before being ready for clinical use, it could potentially improve treatment for Type I diabetes by increasing therapeutic efficacy and reducing side effects. The approach was found to increase drug efficacy by 200-fold in in vitro studies based on the ability of these nanomaterials to both protect the drug from degradation and concentrate it at key target sites, such as regions of the pancreas that contain the insulin-producing cells. The dramatic increase in efficacy also means that much smaller amounts of drugs would be needed for treatment, opening the possibility of significantly reduced toxic side effects, as well as lower treatment costs.
The research was led by Wyss Institute Founding Director Donald Ingber M.D., Ph.D. and Kaustabh Ghosh, Ph.D., a former postdoctoral fellow at Children's Hospital Boston. Their findings appear in the current issue of Nano Letters. Ingber is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Children's Hospital Boston, and Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. Ghosh is now an Assistant Professor of Bioengineering at the University of California, Riverside. Wyss Institute Postdoctoral Fellows, Umai Kanapathipillai and Netanel Korin, also contributed to the work, as did Jason McCarthy, Assistant Professor in Radiology at Harvard Medical School and an Assistant in Chemistry at Massachusetts General Hospital.
Type I diabetes, which often strikes children and young adults, is a debilitating disease in which the body's immune system progressively destroys the cells in the pancreas that produce insulin. According to the Juvenile Diabetes Research Foundation, as many as 3 million Americans have the disease and some 30,000 new cases are diagnosed every year. The risk of developing Type I diabetes, which can lead to serious health complications such as kidney failure and blindness, can be predicted with 90 percent accuracy. But therapeutic intervention for people identified as high risk has been limited because many systemic treatments are barred from clinical use due to the severe side effects they produce when used at the high doses required to achieve a therapeutic response.
"The consequences of Type I diabetes are felt in both the people who live with the disease and in the terrible strain that treatment costs put on the economy," said Ingber. "In keeping with our vision at the Wyss Institute, we hope that the programmable nanotherapy we have developed here will have a major positive impact on people's lives in the future."
Using nanoparticles that can be programmed to deliver drug or stem cell therapies to specific disease sites is an excellent alternative to systemic treatments because improved responses can be obtained with significantly lower therapeutic doses and hence, fewer side effects. To date, such nanotherapeutics have been developed primarily to treat cancer, since they can home in on the tumor via its leaky blood vessels. The challenge has been to develop ways to selectively deliver drugs to treat other diseases in which the tissues of interest are not as easily targeted. The research team addressed this problem by using a unique homing peptide molecule to create "smart" nanoparticles that can seek out and bind to the capillary blood vessels in the islets of the pancreas that feed the insulin-producing cells most at risk during disease onset.
*Source: Wyss Institute for Biologically Inspired Engineering at Harvard
The research was led by Wyss Institute Founding Director Donald Ingber M.D., Ph.D. and Kaustabh Ghosh, Ph.D., a former postdoctoral fellow at Children's Hospital Boston. Their findings appear in the current issue of Nano Letters. Ingber is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Children's Hospital Boston, and Professor of Bioengineering at Harvard's School of Engineering and Applied Sciences. Ghosh is now an Assistant Professor of Bioengineering at the University of California, Riverside. Wyss Institute Postdoctoral Fellows, Umai Kanapathipillai and Netanel Korin, also contributed to the work, as did Jason McCarthy, Assistant Professor in Radiology at Harvard Medical School and an Assistant in Chemistry at Massachusetts General Hospital.
Type I diabetes, which often strikes children and young adults, is a debilitating disease in which the body's immune system progressively destroys the cells in the pancreas that produce insulin. According to the Juvenile Diabetes Research Foundation, as many as 3 million Americans have the disease and some 30,000 new cases are diagnosed every year. The risk of developing Type I diabetes, which can lead to serious health complications such as kidney failure and blindness, can be predicted with 90 percent accuracy. But therapeutic intervention for people identified as high risk has been limited because many systemic treatments are barred from clinical use due to the severe side effects they produce when used at the high doses required to achieve a therapeutic response.
"The consequences of Type I diabetes are felt in both the people who live with the disease and in the terrible strain that treatment costs put on the economy," said Ingber. "In keeping with our vision at the Wyss Institute, we hope that the programmable nanotherapy we have developed here will have a major positive impact on people's lives in the future."
Using nanoparticles that can be programmed to deliver drug or stem cell therapies to specific disease sites is an excellent alternative to systemic treatments because improved responses can be obtained with significantly lower therapeutic doses and hence, fewer side effects. To date, such nanotherapeutics have been developed primarily to treat cancer, since they can home in on the tumor via its leaky blood vessels. The challenge has been to develop ways to selectively deliver drugs to treat other diseases in which the tissues of interest are not as easily targeted. The research team addressed this problem by using a unique homing peptide molecule to create "smart" nanoparticles that can seek out and bind to the capillary blood vessels in the islets of the pancreas that feed the insulin-producing cells most at risk during disease onset.
*Source: Wyss Institute for Biologically Inspired Engineering at Harvard
Researchers find first major gene mutation associated with hereditary prostate cancer risk
After a 20-year quest to find a genetic driver for prostate cancer that strikes men at younger ages and runs in families, researchers have identified a rare, inherited mutation linked to a significantly higher risk of the disease. A report on the discovery, published in the January 12, 2012 issue of the New England Journal of Medicine, was led by investigators at the Johns Hopkins University School of Medicine and the University of Michigan Health System. The research team found that men who inherit this mutation have a 10 to 20 times higher risk of developing prostate cancer.
While accounting for only a small fraction of all prostate cancer cases, the discovery may provide important clues about how this common cancer develops and help to identify a subset ofmen who might benefit from additional or earlier screening. This year, an estimated 240,000 men in the United States will be diagnosed with prostate cancer.
"This is the first major genetic variant associated with inherited prostate cancer," says Kathleen A. Cooney, M.D., professor of internal medicine and urology at the U-M Medical School, one of the study's two senior authors.
"It's what we've been looking for over the past 20 years," adds William B. Isaacs, Ph.D., professor of urology and oncology at the Johns Hopkins University School of Medicine, the study's other senior author. "It's long been clear that prostate cancer can run in families, but pinpointing the underlying genetic basis has been challenging and previous studies have provided inconsistent results."
For this study, the researchers collaborated with John Carpten, Ph.D., at the Translational Genomics Research Institute (TGen) in Phoenix, Arizona, who used the latest technology to sequence the DNA of more than 200 genes in a human chromosome region known as 17q21-22.
Cooney, working with Ethan Lange, Ph.D., of the University of North Carolina on the U-M Prostate Cancer Genetics Project, was the first to identify 17q21-22 as a region of interest.
Researchers started with samples from the youngest patients with prostate cancer in 94 families who had participated in studies at U-M and Johns Hopkins. Each of those families had multiple cases of the disease among close relatives, such as between fathers and sons or among brothers.
Members of four different families were found to have the same mutation in the HOXB13 gene, which plays an important role in the development of the prostate during the fetal stage and its function later in life. The mutation was carried by all 18 men with prostate cancer in these four families.
The researchers collaborated with Jianfeng Xu, Ph.D., and Lilly Zheng, Ph.D., at Wake Forest University to look for the same HOXB13 gene mutation among 5,100 men who had been treated for prostate cancer at either Johns Hopkins or U-M. The mutation was found in 1.4 percent -- or 72 of the men. It turned out that those men were much more likely to have at least one first-degree relative, a father or brother, who also had been diagnosed. The researchers also looked for the mutation in a control group of 1,400 men without prostate cancer, and only one of those men carried the mutation. In addition, the researchers studied men who were specifically enrolled in studies of early-onset or familial prostate cancer.
"We found that the mutation was significantly more common in men with a family history and early diagnosis compared with men diagnosed later, after age 55, without a family history. The difference was 3.1 percent versus 0.62 percent, Cooney says.
"We had never seen anything like this before. It all came together to suggest that this single change may account for at least a portion of the hereditary form of the disease," says study co-author Patrick Walsh, M.D., professor of urology at Johns Hopkins, who is one of the pioneers in prostate cancer treatment. In the 1980s, Walsh was one of the first to publish a study showing that the risk of prostate cancer was higher among men with close relatives who also had the disease.
The researchers say with further study, it may be possible one day to have genetic test for inherited prostate cancer in much the same way that tests are available to look for BRCA1 and BRCA2 mutations that greatly increase a woman's chance of developing breast and/or ovarian cancer.
"We need to continue studying this variant and look at larger groups of men. Our next step will be to develop a mouse model with this mutation to see if it causes prostate cancer," says Isaacs. He adds, "Future DNA sequencing may also identify additional rare variants that contribute to prostate cancer risk in families."
This particular mutation was found in families of European descent, while two different mutations on the HOXB13 gene were identified in families of African descent. Since only seven of the 94 families studied were of African descent, more research will be required before the significance of those mutations is known. African-American men are more likely to be diagnosed with prostate cancer at younger ages and have a more aggressive form of the disease.
Cooney says patients with questions about prostate cancer screening, particularly if the disease runs in their families, are encouraged to speak with their doctor.
*Source: Johns Hopkins Medical Institutions
While accounting for only a small fraction of all prostate cancer cases, the discovery may provide important clues about how this common cancer develops and help to identify a subset ofmen who might benefit from additional or earlier screening. This year, an estimated 240,000 men in the United States will be diagnosed with prostate cancer.
"This is the first major genetic variant associated with inherited prostate cancer," says Kathleen A. Cooney, M.D., professor of internal medicine and urology at the U-M Medical School, one of the study's two senior authors.
"It's what we've been looking for over the past 20 years," adds William B. Isaacs, Ph.D., professor of urology and oncology at the Johns Hopkins University School of Medicine, the study's other senior author. "It's long been clear that prostate cancer can run in families, but pinpointing the underlying genetic basis has been challenging and previous studies have provided inconsistent results."
For this study, the researchers collaborated with John Carpten, Ph.D., at the Translational Genomics Research Institute (TGen) in Phoenix, Arizona, who used the latest technology to sequence the DNA of more than 200 genes in a human chromosome region known as 17q21-22.
Cooney, working with Ethan Lange, Ph.D., of the University of North Carolina on the U-M Prostate Cancer Genetics Project, was the first to identify 17q21-22 as a region of interest.
Researchers started with samples from the youngest patients with prostate cancer in 94 families who had participated in studies at U-M and Johns Hopkins. Each of those families had multiple cases of the disease among close relatives, such as between fathers and sons or among brothers.
Members of four different families were found to have the same mutation in the HOXB13 gene, which plays an important role in the development of the prostate during the fetal stage and its function later in life. The mutation was carried by all 18 men with prostate cancer in these four families.
The researchers collaborated with Jianfeng Xu, Ph.D., and Lilly Zheng, Ph.D., at Wake Forest University to look for the same HOXB13 gene mutation among 5,100 men who had been treated for prostate cancer at either Johns Hopkins or U-M. The mutation was found in 1.4 percent -- or 72 of the men. It turned out that those men were much more likely to have at least one first-degree relative, a father or brother, who also had been diagnosed. The researchers also looked for the mutation in a control group of 1,400 men without prostate cancer, and only one of those men carried the mutation. In addition, the researchers studied men who were specifically enrolled in studies of early-onset or familial prostate cancer.
"We found that the mutation was significantly more common in men with a family history and early diagnosis compared with men diagnosed later, after age 55, without a family history. The difference was 3.1 percent versus 0.62 percent, Cooney says.
"We had never seen anything like this before. It all came together to suggest that this single change may account for at least a portion of the hereditary form of the disease," says study co-author Patrick Walsh, M.D., professor of urology at Johns Hopkins, who is one of the pioneers in prostate cancer treatment. In the 1980s, Walsh was one of the first to publish a study showing that the risk of prostate cancer was higher among men with close relatives who also had the disease.
The researchers say with further study, it may be possible one day to have genetic test for inherited prostate cancer in much the same way that tests are available to look for BRCA1 and BRCA2 mutations that greatly increase a woman's chance of developing breast and/or ovarian cancer.
"We need to continue studying this variant and look at larger groups of men. Our next step will be to develop a mouse model with this mutation to see if it causes prostate cancer," says Isaacs. He adds, "Future DNA sequencing may also identify additional rare variants that contribute to prostate cancer risk in families."
This particular mutation was found in families of European descent, while two different mutations on the HOXB13 gene were identified in families of African descent. Since only seven of the 94 families studied were of African descent, more research will be required before the significance of those mutations is known. African-American men are more likely to be diagnosed with prostate cancer at younger ages and have a more aggressive form of the disease.
Cooney says patients with questions about prostate cancer screening, particularly if the disease runs in their families, are encouraged to speak with their doctor.
*Source: Johns Hopkins Medical Institutions
"Adelgazar haciendo el amor" según el nutricionista Pierre Durand
La empuja contra la pared. Los latidos aumentan. La sostiene con fuerza por las nalgas y la eleva. El ritmo cardíaco se dispara. Hace fuerza con las piernas mientras ella, izada en el aire, se aferra a su cuerpo enlazando las piernas alrededor de su cintura. Y si aguantan así entre 15 y 25 minutos, no sólo disfrutarán del sexo más apasionado, sino que además quemarán unas 500 calorías cada uno. Así lo afirma Pierre Durand, nutricionista y autor de la obra «Adelgazar haciendo el amor», en la que detalla las posturas más eficientes para perder peso.
-Antes de...
Y los preliminares también cuentan. Mientras le quitas la ropa a la pareja, tú te quitas 120 y un buen beso representa 60 calorías, a las que se añaden 20 durante una sesión de caricias. Una vez metidos en faena, el experto señala que, en general, las posturas en las que la pareja está de pie son las que contribuyen a quemar más calorías, ya que se trabajan todos los músculos del cuerpo para mantener el equilibrio y el esfuerzo es mayor para realizar los movimientos propios del coito. Para los escépticos, esta técnica tiene su ciencia, ya que la vasodilatación de las zonas genitales erógenas ayuda a perder calorías.
-De rodillas
Esta postura consume, pero no es la única. Otra de las más completas es en la que ambos están de rodillas, él tras ella con el cuerpo hacia atrás apoyado sobre las manos, y ella con el cuerpo arqueado. Pero si lo que se prefiere es bajar «barriga», en el caso de la mujer, ésta puede tumbarse boca arriba y subir las piernas para apoyarlas en el hombro de la pareja, que estará de rodillas y al penetrarla estará fortaleciendo sus cuádriceps. No obstante, y pese a lo complicadas que puedan parecer para algunos ciertas posturas, Durand explicó a este semanario que «cualquiera puede conseguirlo, y lo de las sesiones es flexible. No estamos hablando de matemáticas sino de seres humanos y no hay dos personas iguales». Ahora bien, lo que siempre suma es el orgasmo que acaba con unas 27 calorías. De hecho, según matizan los expertos, es un excelente ejercicio cardiovascular. «Acelera brevemente el compás cardíaco hasta alcanzar un ritmo comparable al que produce correr», especifica Durand. En cuanto al tiempo, que nadie tema, porque no se trata de maratones ni de estar pendientes constantemente del reloj. Y es que si la pareja tiene que estar pendiente del reloj, estaríamos hablando de gimnasia y no de erotismo. Por ello, cada uno puede proceder según sus habilidades y posibilidades. De hecho, a ritmo mucho más suave y en posturas más clásicas que no requieren demasiado esfuerzo, se pueden quemar, según la experta en deporte Terri Walsh, «unas 125 calorías tras 30 minutos».
Pero no basta con practicar sexo. Hay que acompañarlo con unas recetas saludables que se incluyen después de cada sesión amatoria. Lo que no es del todo incompatible con las escenas eróticas a lo «Nueve semanas y media». Se puede usar a la pareja como plato para saborear yogur, sorbetes de fresa, nata... Siempre que sea «light».
**Publicado en "LA RAZON"
NIH study shows 32 million Americans have autoantibodies that target their own tissues
More than 32 million people in the United States have autoantibodies, which are proteins made by the immune system that target the body's tissues and define a condition known as autoimmunity, a study shows. The first nationally representative sample looking at the prevalence of the most common type of autoantibody, known as antinuclear antibodies (ANA), found that the frequency of ANA is highest among women, older individuals, and African-Americans. The study was conducted by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. Researchers in Gainesville at the University of Florida also participated.
Earlier studies have shown that ANA can actually develop many years before the clinical appearance of autoimmune diseases, such as type 1 diabetes, lupus, and rheumatoid arthritis. ANA are frequently measured biomarkers for detecting autoimmune diseases, but the presence of autoantibodies does not necessarily mean a person will get an autoimmune disease. Other factors, including drugs, cancer, and infections, are also known to cause autoantibodies in some people.
"Previous estimates of ANA prevalence have varied widely and were conducted in small studies not representative of the general population," said Frederick Miller, M.D., Ph.D., an author of the study and acting clinical director at NIEHS. "Having this large data set that is representative of the general U.S. population and includes nearly 5,000 individuals provides us with an accurate estimate of ANA and may allow new insights into the etiology of autoimmune diseases." The findings appear online in the Jan. 11 issue of the Journal Arthritis and Rheumatism.
Miller, who studies the causes of autoimmune diseases, explains that the body's immune system makes large numbers of proteins called antibodies to help the body fight off infections. In some cases, however, antibodies are produced that are directed against one's own tissues. These are referred to as autoantibodies.
A multi-disciplinary team of researchers evaluated blood serum samples using a technique called immunofluorescence to detect ANA in 4,754 individuals from the 1994-2004 National Health and Nutrition Examination Survey (NHANES). The overall prevalence of ANA in the population was 13.8 percent, and was found to be modestly higher in African-Americans compared to whites. ANA generally increased with age and was higher in women than in men, with the female to male ratio peaking at 40-49 years of age and then declining in older age groups.
"The peak of autoimmunity in females compared to males during the 40-49 age bracket is suggestive of the effects that the hormones estrogen and progesterone might be playing on the immune system," said Linda Birnbaum, Ph.D., director of NIEHS and an author on the paper.
The paper also found that the prevalence of ANA was lower in overweight and obese individuals than persons of normal weight. "This finding is interesting and somewhat unexpected," said Edward Chan, Ph.D., an author on the study and professor of the Department of Oral Biology at the University of Florida.
"It raises the likelihood that fat tissues can secrete proteins that inhibit parts of the immune system and prevent the development of autoantibodies, but we will need to do more research to understand the role that obesity might play in the development of autoimmune diseases," said Minoru Satoh, M.D., Ph.D., another author on the study and associate professor of rheumatology and clinical immunology at the University of Florida.
The researchers say the paper should serve as a useful baseline for future studies looking at changes in ANA prevalence over time and the factors associated with ANA development. The paper is the first in a series analyzing this data from the NHANES dataset, and exploring possible environmental associations with ANA.
**Source: National Institute of Environmental Health Sciences (NIEHS)
Earlier studies have shown that ANA can actually develop many years before the clinical appearance of autoimmune diseases, such as type 1 diabetes, lupus, and rheumatoid arthritis. ANA are frequently measured biomarkers for detecting autoimmune diseases, but the presence of autoantibodies does not necessarily mean a person will get an autoimmune disease. Other factors, including drugs, cancer, and infections, are also known to cause autoantibodies in some people.
"Previous estimates of ANA prevalence have varied widely and were conducted in small studies not representative of the general population," said Frederick Miller, M.D., Ph.D., an author of the study and acting clinical director at NIEHS. "Having this large data set that is representative of the general U.S. population and includes nearly 5,000 individuals provides us with an accurate estimate of ANA and may allow new insights into the etiology of autoimmune diseases." The findings appear online in the Jan. 11 issue of the Journal Arthritis and Rheumatism.
Miller, who studies the causes of autoimmune diseases, explains that the body's immune system makes large numbers of proteins called antibodies to help the body fight off infections. In some cases, however, antibodies are produced that are directed against one's own tissues. These are referred to as autoantibodies.
A multi-disciplinary team of researchers evaluated blood serum samples using a technique called immunofluorescence to detect ANA in 4,754 individuals from the 1994-2004 National Health and Nutrition Examination Survey (NHANES). The overall prevalence of ANA in the population was 13.8 percent, and was found to be modestly higher in African-Americans compared to whites. ANA generally increased with age and was higher in women than in men, with the female to male ratio peaking at 40-49 years of age and then declining in older age groups.
"The peak of autoimmunity in females compared to males during the 40-49 age bracket is suggestive of the effects that the hormones estrogen and progesterone might be playing on the immune system," said Linda Birnbaum, Ph.D., director of NIEHS and an author on the paper.
The paper also found that the prevalence of ANA was lower in overweight and obese individuals than persons of normal weight. "This finding is interesting and somewhat unexpected," said Edward Chan, Ph.D., an author on the study and professor of the Department of Oral Biology at the University of Florida.
"It raises the likelihood that fat tissues can secrete proteins that inhibit parts of the immune system and prevent the development of autoantibodies, but we will need to do more research to understand the role that obesity might play in the development of autoimmune diseases," said Minoru Satoh, M.D., Ph.D., another author on the study and associate professor of rheumatology and clinical immunology at the University of Florida.
The researchers say the paper should serve as a useful baseline for future studies looking at changes in ANA prevalence over time and the factors associated with ANA development. The paper is the first in a series analyzing this data from the NHANES dataset, and exploring possible environmental associations with ANA.
**Source: National Institute of Environmental Health Sciences (NIEHS)
Surprising results from smoke inhalation study
A Loyola University Chicago Stritch School of Medicine study includes some unexpected findings about the immune systems of smoke-inhalation patients. Contrary to expectations, patients who died from their injuries had lower inflammatory responses in their lungs than patients who survived.
"Perhaps a better understanding of this early pulmonary immune dysfunction will allow for therapies that further improve outcomes in burn care," researchers reported.
The study is published in the January/February issue of the Journal of Burn Care & Research. First author of the study is Christopher S. Davis, MD, MPH, a research resident in Loyola's Burn & Shock Trauma Institute. Corresponding author is Elizabeth J. Kovacs, PhD, director of research of the Burn & Shock Trauma Institute.
Researchers followed 60 burn patients in Loyola's Burn Center. As expected, patients with the worst combined burn and smoke-inhalation injuries required more time on the ventilator, in the intensive care unit and in the hospital. They also were more likely to die, although this finding fell just short of being statistically significant.
Also according to expectations, patients who died were older and had larger injuries than patients who survived.
But the immune system findings were unexpected. Researchers measured concentrations of 28 immune system modulators in fluid collected from the lungs of patients within 14 hours of burn and smoke-inhalation injuries.
These modulators are proteins produced by leukocytes (white blood cells) and other cells, including those that line the airway. Some of the modulators recruit leukocytes to areas of tissue damage or activate them to begin the repair process that follows tissue injury.
Based on studies conducted at Loyola and other centers, researchers had expected to find higher concentrations of modulators in patients who died, because sicker patients tend to have more active inflammatory responses. But researchers found just the opposite: patients who died had lower concentrations of these modulators in their lungs.
Why do some patients mount robust immune responses in the lungs while others do not? The reason may be due to age, genetics, differences in patients' underlying health conditions or anything that might disrupt the balance between too much and too little inflammation, Davis said.
Survival of burn patients has significantly improved since the 1950s, due to advancements such as better wound care and improved prevention and treatment of infections. But progress has somewhat stalled in the last 10 years.
The immune response to injury "remains incompletely understood and additional effort is required to further improve survival of the burn-injured patient," researchers wrote.
The study was presented at the 2011 meeting of the American Burn Association, where it won the 2011 Carl A. Moyer Resident Award for the best study submitted by a resident physician.
Other co-authors of the study are Richard L. Gamelli, MD, FACS, director of the Burn & Shock Trauma Institute; Joslyn M. Albright, MD, chief resident in the Department of Surgery; Stewart R. Carter, MD, research resident; Luis Ramirez, BA, laboratory technician; and Hajwa Kim, MA, MS. All are from Loyola except Kim, who is at the University of Illinois at Chicago.
The study was funded by grants from the National Institutes of Health, Department of Defense, International Association of Fire Fighters and the Dr. Ralph and Marian C. Falk Medical Research Trust.
Loyola's Burn Center is one of the busiest in the Midwest, treating more than 600 patients annually in the hospital, and another 3,500 patients each year in its clinic. It is one of only two centers in Illinois that have received verification by the American Burn Association.
The study is among the results of research over the last several years conducted in Loyola's Burn Center and Burn & Shock Trauma Institute, which is investigating the lung's response to burn and inhalation injuries.
**Source: Loyola University Health System
"Perhaps a better understanding of this early pulmonary immune dysfunction will allow for therapies that further improve outcomes in burn care," researchers reported.
The study is published in the January/February issue of the Journal of Burn Care & Research. First author of the study is Christopher S. Davis, MD, MPH, a research resident in Loyola's Burn & Shock Trauma Institute. Corresponding author is Elizabeth J. Kovacs, PhD, director of research of the Burn & Shock Trauma Institute.
Researchers followed 60 burn patients in Loyola's Burn Center. As expected, patients with the worst combined burn and smoke-inhalation injuries required more time on the ventilator, in the intensive care unit and in the hospital. They also were more likely to die, although this finding fell just short of being statistically significant.
Also according to expectations, patients who died were older and had larger injuries than patients who survived.
But the immune system findings were unexpected. Researchers measured concentrations of 28 immune system modulators in fluid collected from the lungs of patients within 14 hours of burn and smoke-inhalation injuries.
These modulators are proteins produced by leukocytes (white blood cells) and other cells, including those that line the airway. Some of the modulators recruit leukocytes to areas of tissue damage or activate them to begin the repair process that follows tissue injury.
Based on studies conducted at Loyola and other centers, researchers had expected to find higher concentrations of modulators in patients who died, because sicker patients tend to have more active inflammatory responses. But researchers found just the opposite: patients who died had lower concentrations of these modulators in their lungs.
Why do some patients mount robust immune responses in the lungs while others do not? The reason may be due to age, genetics, differences in patients' underlying health conditions or anything that might disrupt the balance between too much and too little inflammation, Davis said.
Survival of burn patients has significantly improved since the 1950s, due to advancements such as better wound care and improved prevention and treatment of infections. But progress has somewhat stalled in the last 10 years.
The immune response to injury "remains incompletely understood and additional effort is required to further improve survival of the burn-injured patient," researchers wrote.
The study was presented at the 2011 meeting of the American Burn Association, where it won the 2011 Carl A. Moyer Resident Award for the best study submitted by a resident physician.
Other co-authors of the study are Richard L. Gamelli, MD, FACS, director of the Burn & Shock Trauma Institute; Joslyn M. Albright, MD, chief resident in the Department of Surgery; Stewart R. Carter, MD, research resident; Luis Ramirez, BA, laboratory technician; and Hajwa Kim, MA, MS. All are from Loyola except Kim, who is at the University of Illinois at Chicago.
The study was funded by grants from the National Institutes of Health, Department of Defense, International Association of Fire Fighters and the Dr. Ralph and Marian C. Falk Medical Research Trust.
Loyola's Burn Center is one of the busiest in the Midwest, treating more than 600 patients annually in the hospital, and another 3,500 patients each year in its clinic. It is one of only two centers in Illinois that have received verification by the American Burn Association.
The study is among the results of research over the last several years conducted in Loyola's Burn Center and Burn & Shock Trauma Institute, which is investigating the lung's response to burn and inhalation injuries.
**Source: Loyola University Health System
La actividad sexual disminuye con la edad las mujeres, pero no la satisfacción según un estudio
¿Quién ha dicho que con los años, las mujeres están sexualmente menos satisfechas? Porque no están en lo cierto. Todo lo contrario. Los datos de una última investigación confirman que la complacencia sexual aumenta con la edad. Pero más importante aún: esta se alcanza incluso sin la existencia de deseo previo o de relaciones sexuales con penetración.
Elizabeth Barrett-Conor, de la Universidad de California (EEUU), es la autora del nuevo ensayo en el que han participado 806 mujeres residentes en la comunidad Rancho Bernardino, un suburbio de San Diego. La edad de todas ellas: de 40 a 100 años.
Desde la creación de la mencionada comunidad (1972-1974), todas las participantes del estudio han recibido un seguimiento anual para conocer su estado vital. Cada dos años se analizaban, además, las condiciones específicas y los comportamientos potencialmente relacionadas con el envejecimiento saludable.
En el caso concreto de las mujeres, los científicos preguntaron a las participantes sobre su salud física y emocional, si tenían la menopausia, si usaban terapias sustitutivas de estrógenos, si tenían pareja estable y su actividad sexual reciente. Se indagó, asimismo, en su función sexual: deseo, excitación, lubricación, dolor y satisfacción.
Los datos revelan que las probabilidades de actividad sexual se reducían con la edad. La mitad de las participantes había tenido encuentros íntimos en el último mes, de las cuales el 80% era con su pareja estable. "Un 67% de las mujeres sexualmente activas alcanzaba el orgasmo", según publica el último 'The American Journal of Medicine'.
-Sin deseo
Más referencias de interés son las que hacen alusión a que el 40% de las mujeres dijo que nunca o casi nunca sentía deseo sexual, y un tercio de las participantes sexualmente activas reconoció que su libido era baja. "A pesar de existir una correlación entre el deseo sexual y otros dominios de la función sexual, apenas una de cada cinco mujeres sexualmente activas confesó tener mucho deseo sexual", confiesa la autora principal del ensayo.
A Francisca Molero, directora del Instituto de Sexología de Barcelona y vicepresidenta de la Federación Española de Sociedades de Sexología, los resultados del estudio no le sorprenden pese a que las creencias populares sean otras.
En declaraciones al ELMUNDO.es argumenta que la satisfacción sexual no "tiene por qué estar ligada necesariamente al deseo espontáneo, más bien está relacionada con la calidad emocional, con comunicación y cercanía de la pareja".
Para esta especialista que las mujeres de más edad se sientan más complacidas con el sexo que las más jóvenes puede deberse a que "a ciertas edades como en la cuarentena la mujer sufre un cambio de rol, le sucede en casa porque los hijos ya son mayores, pero también en el trabajo y con la pareja. Además, empiezan los cambios físicos, se gana peso, y todavía existe una gran preocupación social por la imagen corporal. Todo ello hace que el 'sexo' pueda pasar temporalmente a un segundo plano. Pero cuando este momento pasa, la mujer empieza a vivir de otra forma".
Uno de los errores tradicionales es pensar que "ellas necesitan sentir deseo para iniciar relaciones sexuales y estar satisfechas. A diferencia de los hombres, y sobre todo en las relaciones estables, las mujeres no siempre inician las relaciones desde el deseo sexual espontáneo. En ellas suele aparecer en las etapas de enamoramiento o en las situaciones en que las sorprenden (una cena, un viaje...). El deseo suele aparecer después de la excitación. El que no exista previamente no significa que no puedan iniciar un encuentro sexual".
-Satisfacción orgásmica
Pese a que la edad avanzada se considera un predictor de una baja satisfacción sexual, el porcentaje de mujeres sexualmente satisfechas del estudio en realidad aumentó con la edad. Alrededor de la mitad de las mujeres mayores de 80 años casi siempre o siempre reconoció estar satisfechas sexualmente. Entre éstas, las que eran sexualmente activas tenían tasas de satisfacción orgásmica similares a las de las mujeres más jóvenes.
"En este estudio, la actividad sexual no siempre tenía el propósito de la satisfacción sexual a través del coito. Las que no eran sexualmente activas podrían haber logrado satisfacción sexual a través del tocamiento, las caricias u otras actividades íntimas desarrolladas en el transcurso de una relación", detallan los investigadores.
"La cercanía emocional y física con la pareja podría ser más importante que experimentar un orgasmo. Llevar a cabo un abordaje más positivo de la salud sexual femenina destinado a valorar su satisfacción podría ser más beneficioso para las mujeres que un enfoque limitado a la actividad sexual o las disfunciones", agregan.
De la misma opinión se muestra la doctora Molero que comenta que son "muchas las mujeres que consultan porque piensan que no sentir deseo es un problema. Hay que normalizar las cosas, ser más positivos. Sólo cuando la carencia del mismo causa angustia elevada e interfiere en la vida diaria estamos hablando de una disfunción. En el resto de casos, no hay un problema".
**Publicado en "EL MUNDO"
Elizabeth Barrett-Conor, de la Universidad de California (EEUU), es la autora del nuevo ensayo en el que han participado 806 mujeres residentes en la comunidad Rancho Bernardino, un suburbio de San Diego. La edad de todas ellas: de 40 a 100 años.
Desde la creación de la mencionada comunidad (1972-1974), todas las participantes del estudio han recibido un seguimiento anual para conocer su estado vital. Cada dos años se analizaban, además, las condiciones específicas y los comportamientos potencialmente relacionadas con el envejecimiento saludable.
En el caso concreto de las mujeres, los científicos preguntaron a las participantes sobre su salud física y emocional, si tenían la menopausia, si usaban terapias sustitutivas de estrógenos, si tenían pareja estable y su actividad sexual reciente. Se indagó, asimismo, en su función sexual: deseo, excitación, lubricación, dolor y satisfacción.
Los datos revelan que las probabilidades de actividad sexual se reducían con la edad. La mitad de las participantes había tenido encuentros íntimos en el último mes, de las cuales el 80% era con su pareja estable. "Un 67% de las mujeres sexualmente activas alcanzaba el orgasmo", según publica el último 'The American Journal of Medicine'.
-Sin deseo
Más referencias de interés son las que hacen alusión a que el 40% de las mujeres dijo que nunca o casi nunca sentía deseo sexual, y un tercio de las participantes sexualmente activas reconoció que su libido era baja. "A pesar de existir una correlación entre el deseo sexual y otros dominios de la función sexual, apenas una de cada cinco mujeres sexualmente activas confesó tener mucho deseo sexual", confiesa la autora principal del ensayo.
A Francisca Molero, directora del Instituto de Sexología de Barcelona y vicepresidenta de la Federación Española de Sociedades de Sexología, los resultados del estudio no le sorprenden pese a que las creencias populares sean otras.
En declaraciones al ELMUNDO.es argumenta que la satisfacción sexual no "tiene por qué estar ligada necesariamente al deseo espontáneo, más bien está relacionada con la calidad emocional, con comunicación y cercanía de la pareja".
Para esta especialista que las mujeres de más edad se sientan más complacidas con el sexo que las más jóvenes puede deberse a que "a ciertas edades como en la cuarentena la mujer sufre un cambio de rol, le sucede en casa porque los hijos ya son mayores, pero también en el trabajo y con la pareja. Además, empiezan los cambios físicos, se gana peso, y todavía existe una gran preocupación social por la imagen corporal. Todo ello hace que el 'sexo' pueda pasar temporalmente a un segundo plano. Pero cuando este momento pasa, la mujer empieza a vivir de otra forma".
Uno de los errores tradicionales es pensar que "ellas necesitan sentir deseo para iniciar relaciones sexuales y estar satisfechas. A diferencia de los hombres, y sobre todo en las relaciones estables, las mujeres no siempre inician las relaciones desde el deseo sexual espontáneo. En ellas suele aparecer en las etapas de enamoramiento o en las situaciones en que las sorprenden (una cena, un viaje...). El deseo suele aparecer después de la excitación. El que no exista previamente no significa que no puedan iniciar un encuentro sexual".
-Satisfacción orgásmica
Pese a que la edad avanzada se considera un predictor de una baja satisfacción sexual, el porcentaje de mujeres sexualmente satisfechas del estudio en realidad aumentó con la edad. Alrededor de la mitad de las mujeres mayores de 80 años casi siempre o siempre reconoció estar satisfechas sexualmente. Entre éstas, las que eran sexualmente activas tenían tasas de satisfacción orgásmica similares a las de las mujeres más jóvenes.
"En este estudio, la actividad sexual no siempre tenía el propósito de la satisfacción sexual a través del coito. Las que no eran sexualmente activas podrían haber logrado satisfacción sexual a través del tocamiento, las caricias u otras actividades íntimas desarrolladas en el transcurso de una relación", detallan los investigadores.
"La cercanía emocional y física con la pareja podría ser más importante que experimentar un orgasmo. Llevar a cabo un abordaje más positivo de la salud sexual femenina destinado a valorar su satisfacción podría ser más beneficioso para las mujeres que un enfoque limitado a la actividad sexual o las disfunciones", agregan.
De la misma opinión se muestra la doctora Molero que comenta que son "muchas las mujeres que consultan porque piensan que no sentir deseo es un problema. Hay que normalizar las cosas, ser más positivos. Sólo cuando la carencia del mismo causa angustia elevada e interfiere en la vida diaria estamos hablando de una disfunción. En el resto de casos, no hay un problema".
**Publicado en "EL MUNDO"
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