A US blog has questioned whether journalists might be influenced by accepting “all expenses paid” fellowships to attend an educational conference on cancer organised by the US National Press Foundation but sponsored by Pfizer.
Pfizer is providing unrestricted funding of $80 000 (£52 000; €62 000) to the US National Press Foundation, a non-profit charitable organisation that provides continuing educational programmes for journalists, to sponsor 15 US journalists to attend the foundation’s four day educational programme on cancer being held in Washington, DC, from 17 to 20 October (http://nationalpress.org/programs-and-resources/program/cancer-issues-2010/).
In his recent Pharmalot blog Ed Silverman, a journalist, asked whether journalists might be influenced by a drug company sponsored but apparently independent educational programme in the way that doctors might be (http://www.pharmalot.com/). “The arrangement is generating a bit of heat in some circles, given sensitivities over perceptions of conflicts of interest,” he said.
Gary Schwitzer, a former professor of journalism at the University of Minnesota, who publishes http://www.healthnewsreview.org/, said he saw the issue in the context of erosion of public confidence in journalists. As for sponsored seminars he said, “Who is paying the bill? This is swept under the carpet.” He recommended that journalists indicate in stories they write that they had attended an all expenses paid seminar sponsored by a drug company.
Charles Ornstein, president of the US Association of Health Care Journalists (http://www.healthjournalism.org/), said that to avoid sponsored programmes journalists could learn from each other through networking and by attending seminars organised by non-profit institutions or universities, such as the US National Institutes of Health and the Centers for Disease Control and Prevention.
He said that healthcare journalists have covered issues of conflict of interest between doctors and drug companies for years and “may have been on the alert when the issue touched them.” He added that the association does not accept funding from commercial organisations with a financial interest in health care.
The association’s rule is stricter than that of the US Accreditation Council for Continuing Medical Education (http://www.accme.org/), which approves continuing medical education for doctors. The council would allow a drug company to fund continuing medical education through an independent organisation if the drug company did not influence the choice of topic or speakers.
Linda Topping Streitfield, director of programmes at the National Press Foundation, said that Pfizer had no role in organising the programme for the cancer meeting, in selecting the topics or speakers, or in selecting the journalists who attend, in line with the foundation’s rules. “We’re proud of the programme and gratified at the reaction of journalists who have attended previous programmes,” she said.
The foundation receives funding from corporate donors, among them major drug companies. Ms Streitfield explained that the same rules applied to all its sponsored programmes: the sponsors are identified and may address journalists at the beginning of the programme, but the foundation controls all aspects of every programme, which will be balanced, fair, and on the record. Journalists invited to participate are selected by the foundation, she said.
Raymond Kerins, vice president for external affairs and communications for Pfizer, told the BMJ that the company wanted to “engage and educate” journalists so they understood the issues. “We want to be part of the solution,” he said. He acknowledged that Pfizer had a major interest in cancer drugs but insisted that the National Press Foundation received an unrestricted educational grant and that Pfizer had “zero impact” on the agenda, focus, choice of speakers, or selection of journalists.
He noted that as newspapers and magazines cut staff, general reporters may cover health and medical news previously covered by specialist reporters, while science reporting is becoming increasingly complex.
Jenny Song, a journalist who participated in a previous conference on cancer organised by the National Press Foundation when working as an editor for a cancer research magazine and who is now with the Waxman Cancer Organization, said, “Never was there any effort to bias me about Pfizer or its products. I never saw any brochures from Pfizer or received anything from them before or after the seminar. No one from Pfizer ever contacted me before or after the seminar either . . . The NPF [National Press Foundation] president, Bob Meyers, spoke openly and frankly with us about Pfizer sponsoring [that] programme.”
**Published in "BMJ"
07 September 2010
Roche, reMYND sign 500 million euro Alzheimer, Parkinson pact
Roche has linked up with Belgium's reMYND to develop therapeutics that could slow down neurodegeneration in Parkinson’s and Alzheimer’s patients.
Specifically, the collaboration will focus on two of reMYND’s pre-clinical small molecule programmes targeting alpha-synuclein and tau related pathologies. The companies say that the compounds are unique because they inhibit α-synuclein and tau neurotoxicity in Parkinson's and Alzheimer's, respectively and as such they are considered disease-modifying, "whilst most currently available treatments only treat the symptoms of the disease".
Cashwise, reMYND, which is a spin-off company of Leuven University, could receive over half a billion euros in milestone payments, as well as double-digit royalties.
Commenting on the agreement, Luca Santarelli, head of Roche CNS said the addition of these programmes "strengthens and complements our existing research". He added: "We believe that they offer a unique approach to combat Parkinson’s and Alzheimer’s disease".
Koen De Witte, managing director of reMYND said that the Alzheimer’s tau programme "represents perhaps a greater potential as it addresses one of the most fundamental aspects of the disease". He added that there is a strong fit between both companies "because we both have a strong biology-driven approach and aim for first-in-class treatments".
Mr De Witte concluded by saying that "Roche’s expertise in diagnostics will be crucial for maximising the chances of success along the long path of clinical development”.
Specifically, the collaboration will focus on two of reMYND’s pre-clinical small molecule programmes targeting alpha-synuclein and tau related pathologies. The companies say that the compounds are unique because they inhibit α-synuclein and tau neurotoxicity in Parkinson's and Alzheimer's, respectively and as such they are considered disease-modifying, "whilst most currently available treatments only treat the symptoms of the disease".
Cashwise, reMYND, which is a spin-off company of Leuven University, could receive over half a billion euros in milestone payments, as well as double-digit royalties.
Commenting on the agreement, Luca Santarelli, head of Roche CNS said the addition of these programmes "strengthens and complements our existing research". He added: "We believe that they offer a unique approach to combat Parkinson’s and Alzheimer’s disease".
Koen De Witte, managing director of reMYND said that the Alzheimer’s tau programme "represents perhaps a greater potential as it addresses one of the most fundamental aspects of the disease". He added that there is a strong fit between both companies "because we both have a strong biology-driven approach and aim for first-in-class treatments".
Mr De Witte concluded by saying that "Roche’s expertise in diagnostics will be crucial for maximising the chances of success along the long path of clinical development”.
Links:
**Published in "Pharma Times"
NIH awards grants to support biomedical research in space
The National Institutes of Health announced today that it has awarded the first new grants under the Biomedical Research on the International Space Station (BioMed-ISS) initiative, a collaborative effort between NIH and NASA. Using a special microgravity environment that Earth-based laboratories cannot replicate, researchers will explore fundamental questions about important health issues, such as how bones and the immune system get weak.
"Through this initiative, the NIH is proud to continue its longstanding partnership with NASA," said NIH Director Francis S. Collins, M.D., Ph.D. "We look forward to working with our NASA colleagues and other members of the ISS team to implement these unique experiments."
The National Laboratory at the ISS provides a virtually gravity-free — or microgravity — environment where the cellular and molecular mechanisms that underlie human diseases can be explored.
Scientists will conduct their experiments under a two-stage mechanism. The first is a ground-based preparatory phase to allow investigators to meet select milestones and technical requirements. The second is an ISS experimental phase that will include preparing the experiments for launch, working with astronauts to conduct them on the ISS, and performing subsequent data analyses on Earth.
"BioMed-ISS offers a novel opportunity for gaining scientific insights that would not otherwise be possible through ground-based means," said Stephen I. Katz, M.D., Ph.D., director of the NIH's National Institute of Arthritis and Musculoskeletal and Skin Diseases, and NIH liaison to NASA. "The beauty of this initiative is that it offers an unprecedented opportunity for benefitting human health on earth, while leveraging the American public’s investment in the ISS."
NIH is hosting three rounds of competition for the BioMed-ISS initiative. The first round of grants for the ground-based phase — totaling an estimated $1,323,000 — has been awarded as follows:
Paola Divieti, M.D., Ph.D., Massachusetts General Hospital/Harvard Medical School, Boston: Weight-bearing activities contribute to the development and maintenance of bone mass, while weightlessness and immobility — as experienced by the astronauts and bedridden and immobilized patients — can result in bone loss and a weakened skeleton. Osteocytes, the most common type of bone cell, are believed to have gravity-sensing abilities. These cells play a key role in bone remodeling, a process that is vital to skeletal health. In studying osteocytes in a gravity-free environment, Divieti aims to uncover new therapeutic targets for osteoporosis and related bone diseases.
Millie Hughes-Fulford, Ph.D., Northern California Institute for Research and Education, San Francisco: The immune system, which protects the body against foreign substances, is suppressed in space. A reduction in the immune response also occurs in the elderly, who, like the astronauts, are at increased risk for infection. As a former astronaut, Hughes-Fulford aims to apply lessons learned from studies of immune cells in microgravity to a new model for investigating the loss of immune response in older women and men.
Declan McCole, Ph.D., University of California, San Diego: Excessive alcohol use is a leading lifestyle-related cause of death in the United States. A major factor in alcohol-related disease stems from the ability of alcohol to compromise the natural barrier function of cells in the gastrointestinal tract, increasing the movement of toxins from the intestines to other organs in the body. Using microgravity three-dimensional cell culture models, McCole plans to generate insights regarding the barrier properties of the intestines, and to explore how the absence of gravity affects alcohol's ability to diminish this barrier.
The NIH Institutes and Centers participating in BioMed-ISS include the National Cancer Institute, the National Center for Research Resources, the National Heart, Lung, and Blood Institute, the National Institute on Aging, the National Institute on Alcohol Abuse and Alcoholism, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute of Biomedical Imaging and Bioengineering, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Neurological Disorders and Stroke.
Information NIH and NASA activities can be found at http://www.niams.nih.gov/News_and_Events/NIH_NASA_Activities/default.asp.
"Through this initiative, the NIH is proud to continue its longstanding partnership with NASA," said NIH Director Francis S. Collins, M.D., Ph.D. "We look forward to working with our NASA colleagues and other members of the ISS team to implement these unique experiments."
The National Laboratory at the ISS provides a virtually gravity-free — or microgravity — environment where the cellular and molecular mechanisms that underlie human diseases can be explored.
Scientists will conduct their experiments under a two-stage mechanism. The first is a ground-based preparatory phase to allow investigators to meet select milestones and technical requirements. The second is an ISS experimental phase that will include preparing the experiments for launch, working with astronauts to conduct them on the ISS, and performing subsequent data analyses on Earth.
"BioMed-ISS offers a novel opportunity for gaining scientific insights that would not otherwise be possible through ground-based means," said Stephen I. Katz, M.D., Ph.D., director of the NIH's National Institute of Arthritis and Musculoskeletal and Skin Diseases, and NIH liaison to NASA. "The beauty of this initiative is that it offers an unprecedented opportunity for benefitting human health on earth, while leveraging the American public’s investment in the ISS."
NIH is hosting three rounds of competition for the BioMed-ISS initiative. The first round of grants for the ground-based phase — totaling an estimated $1,323,000 — has been awarded as follows:
Paola Divieti, M.D., Ph.D., Massachusetts General Hospital/Harvard Medical School, Boston: Weight-bearing activities contribute to the development and maintenance of bone mass, while weightlessness and immobility — as experienced by the astronauts and bedridden and immobilized patients — can result in bone loss and a weakened skeleton. Osteocytes, the most common type of bone cell, are believed to have gravity-sensing abilities. These cells play a key role in bone remodeling, a process that is vital to skeletal health. In studying osteocytes in a gravity-free environment, Divieti aims to uncover new therapeutic targets for osteoporosis and related bone diseases.
Millie Hughes-Fulford, Ph.D., Northern California Institute for Research and Education, San Francisco: The immune system, which protects the body against foreign substances, is suppressed in space. A reduction in the immune response also occurs in the elderly, who, like the astronauts, are at increased risk for infection. As a former astronaut, Hughes-Fulford aims to apply lessons learned from studies of immune cells in microgravity to a new model for investigating the loss of immune response in older women and men.
Declan McCole, Ph.D., University of California, San Diego: Excessive alcohol use is a leading lifestyle-related cause of death in the United States. A major factor in alcohol-related disease stems from the ability of alcohol to compromise the natural barrier function of cells in the gastrointestinal tract, increasing the movement of toxins from the intestines to other organs in the body. Using microgravity three-dimensional cell culture models, McCole plans to generate insights regarding the barrier properties of the intestines, and to explore how the absence of gravity affects alcohol's ability to diminish this barrier.
The NIH Institutes and Centers participating in BioMed-ISS include the National Cancer Institute, the National Center for Research Resources, the National Heart, Lung, and Blood Institute, the National Institute on Aging, the National Institute on Alcohol Abuse and Alcoholism, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute of Biomedical Imaging and Bioengineering, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Neurological Disorders and Stroke.
Information NIH and NASA activities can be found at http://www.niams.nih.gov/News_and_Events/NIH_NASA_Activities/default.asp.
**Published in "NIH News"
NIH study shows how insulin stimulates fat cells to take in glucose
Using high-resolution microscopy, researchers at the National Institutes of Health have shown how insulin prompts fat cells to take in glucose in a rat model. The findings were reported in the Sept. 8 issue of the journal Cell Metabolism.
By studying the surface of healthy, live fat cells in rats, researchers were able to understand the process by which cells take in glucose. Next, they plan to observe the fat cells of people with varying degrees of insulin sensitivity, including insulin resistance — considered a precursor to type 2 diabetes (http://diabetes.niddk.nih.gov). These observations may help identify the interval when someone becomes at risk for developing diabetes.
"What we're doing here is actually trying to understand how glucose transporter proteins called GLUT4 work in normal, insulin-sensitive cells," said Karin G. Stenkula, Ph.D., a researcher at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and a lead author of the paper. "With an understanding of how these transporters in fat cells respond to insulin, we could detect the differences between an insulin-sensitive cell and an insulin-resistant cell, to learn how the response becomes impaired. We hope to identify when a person becomes pre-diabetic, before they go on to develop diabetes."
Glucose, a simple sugar, provides energy for cell functions. After food is digested, glucose is released into the bloodstream. In response, the pancreas secretes insulin, which directs the muscle and fat cells to take in glucose. Cells obtain energy from glucose or convert it to fat for long-term storage.
Like a key fits into a lock, insulin binds to receptors on the cell's surface, causing GLUT4 molecules to come to the cell's surface. As their name implies, glucose transporter proteins act as vehicles to ferry glucose inside the cell.
To get detailed images of how GLUT4 is transported and moves through the cell membrane, the researchers used high-resolution imaging to observe GLUT4 that had been tagged with a fluorescent dye.
The researchers then observed fat cells suspended in a neutral liquid and later soaked the cells in an insulin solution, to determine the activity of GLUT4 in the absence of insulin and in its presence.
In the neutral liquid, the researchers found that individual molecules of GLUT4 as well as GLUT4 clusters were distributed across the cell membrane in equal numbers. Inside the cell, GLUT4 was contained in balloon-like structures known as vesicles. The vesicles transported GLUT4 to the cell membrane and merged with the membrane, a process known as fusion.
After fusion, the individual molecules of GLUT4 are the first to enter the cell membrane, moving at a continuous but relatively infrequent rate. The researchers termed this process fusion with release.
When exposed to insulin, however, the rate of total GLUT4 entry into the cell membrane peaked, quadrupling within three minutes. The researchers saw a dramatic rise in fusion with release — 60 times more often on cells exposed to insulin than on cells not exposed to insulin.
After exposure to insulin, a complex sequence occurred, with GLUT4 shifting from clusters to individual GLUT4 molecules. Based on the total amount of glucose the cells took in, the researchers deduced that glucose was taken into the cell by individual GLUT4 molecules as well as by clustered GLUT4. The researchers also noted that after four minutes, entry of GLUT4 into the cell membrane started to decrease, dropping to levels observed in the neutral liquid in 10 to 15 minutes.
"The magnitude of this change shows just how important the regulation of this process is for the survival of the cell and for the normal function of the whole body," said Joshua Zimmerberg, Ph.D., M.D., the paper's senior author and director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Program in Physical Biology.
The research team next plans to examine the activity of glucose transporters in human fat cells, Zimmerberg said. "Understanding how insulin prepares the cell for glucose uptake may lead to ideas for stimulating this activity when the cells become resistant to insulin."
Stenkula and Samuel W. Cushman, Ph.D., of NIDDK worked with NICHD investigators Vladimir A. Lizunov, Ph.D. and Zimmerberg to complete the research.
**Published in "NIH News"
By studying the surface of healthy, live fat cells in rats, researchers were able to understand the process by which cells take in glucose. Next, they plan to observe the fat cells of people with varying degrees of insulin sensitivity, including insulin resistance — considered a precursor to type 2 diabetes (http://diabetes.niddk.nih.gov). These observations may help identify the interval when someone becomes at risk for developing diabetes.
"What we're doing here is actually trying to understand how glucose transporter proteins called GLUT4 work in normal, insulin-sensitive cells," said Karin G. Stenkula, Ph.D., a researcher at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and a lead author of the paper. "With an understanding of how these transporters in fat cells respond to insulin, we could detect the differences between an insulin-sensitive cell and an insulin-resistant cell, to learn how the response becomes impaired. We hope to identify when a person becomes pre-diabetic, before they go on to develop diabetes."
Glucose, a simple sugar, provides energy for cell functions. After food is digested, glucose is released into the bloodstream. In response, the pancreas secretes insulin, which directs the muscle and fat cells to take in glucose. Cells obtain energy from glucose or convert it to fat for long-term storage.
Like a key fits into a lock, insulin binds to receptors on the cell's surface, causing GLUT4 molecules to come to the cell's surface. As their name implies, glucose transporter proteins act as vehicles to ferry glucose inside the cell.
To get detailed images of how GLUT4 is transported and moves through the cell membrane, the researchers used high-resolution imaging to observe GLUT4 that had been tagged with a fluorescent dye.
The researchers then observed fat cells suspended in a neutral liquid and later soaked the cells in an insulin solution, to determine the activity of GLUT4 in the absence of insulin and in its presence.
In the neutral liquid, the researchers found that individual molecules of GLUT4 as well as GLUT4 clusters were distributed across the cell membrane in equal numbers. Inside the cell, GLUT4 was contained in balloon-like structures known as vesicles. The vesicles transported GLUT4 to the cell membrane and merged with the membrane, a process known as fusion.
After fusion, the individual molecules of GLUT4 are the first to enter the cell membrane, moving at a continuous but relatively infrequent rate. The researchers termed this process fusion with release.
When exposed to insulin, however, the rate of total GLUT4 entry into the cell membrane peaked, quadrupling within three minutes. The researchers saw a dramatic rise in fusion with release — 60 times more often on cells exposed to insulin than on cells not exposed to insulin.
After exposure to insulin, a complex sequence occurred, with GLUT4 shifting from clusters to individual GLUT4 molecules. Based on the total amount of glucose the cells took in, the researchers deduced that glucose was taken into the cell by individual GLUT4 molecules as well as by clustered GLUT4. The researchers also noted that after four minutes, entry of GLUT4 into the cell membrane started to decrease, dropping to levels observed in the neutral liquid in 10 to 15 minutes.
"The magnitude of this change shows just how important the regulation of this process is for the survival of the cell and for the normal function of the whole body," said Joshua Zimmerberg, Ph.D., M.D., the paper's senior author and director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Program in Physical Biology.
The research team next plans to examine the activity of glucose transporters in human fat cells, Zimmerberg said. "Understanding how insulin prepares the cell for glucose uptake may lead to ideas for stimulating this activity when the cells become resistant to insulin."
Stenkula and Samuel W. Cushman, Ph.D., of NIDDK worked with NICHD investigators Vladimir A. Lizunov, Ph.D. and Zimmerberg to complete the research.
**Published in "NIH News"
Cranberry Juice Fights Urinary Tract Infections Quickly
Scientists report that within eight hours of drinking cranberry juice, the juice could help prevent bacteria from developing into an infection in the urinary tract.
Previous studies have suggested that the active compounds in cranberry juice are not destroyed by the digestive system after people drink them, but instead work to fight against bacteria, including E. coli. This latest study, presented at the national meeting of the American Chemical Society in Boston, affirms that and provides evidence of the medicinal value of cranberries.
The new research suggests that the beneficial substances in cranberry juice could reach the urinary tract and prevent bacterial adhesion within eight hours.
Researchers from the Worcester Polytechnic Institute in Massachusetts grew strains of E. coli in urine collected from healthy people before and after they drank cranberry juice cocktail.
How Cranberry Juice Treats Urinary Tract Infections
A mixture of cranberry juice, water, and sweeteners found in cranberry juice cocktail was used for the study because it is the most popular cranberry beverage. The researchers discovered that in petri dishes, cranberry metabolites in the juice prevented E. coli from sticking to other bacteria, limiting its ability to grow and multiply. If E. coli is able to connect with other bacteria, such as the bacteria found in the urinary tract, it forms a layer or "biofilm." This allows the bacteria to multiply and produce an infection.
"A number of controlled clinical trials -- these are carefully designed and conducted scientific studies done in humans -- have concluded that cranberry juice really is effective for preventing urinary tract infections," says study researcher Terri Anne Camesano, PhD, in a news release. "That has important implications, considering the size of the problem and the health care costs involved."
Urinary tract infections are more common among women than men. According to the researchers, one in three women has had a urinary tract infection.
Urinary tract infections can occur anywhere along the urinary tract, which includes the bladder, urethra, and ureter. These infections account for 8 million trips to the doctor's office every year and cost more than $1.6 billion to treat.
Camesano said people should not self-treat urinary tract infections, and anyone who suspects they have an infection should see a doctor, but drinking cranberry juice may be an easy, inexpensive way to help keep E. coli at bay.
In the event of a urinary tract infection, antibiotics are the most common treatment. If left untreated, particularly in children, the elderly, or people with other chronic medical conditions, urinary tract infections can become more severe.
Previous studies have suggested that the active compounds in cranberry juice are not destroyed by the digestive system after people drink them, but instead work to fight against bacteria, including E. coli. This latest study, presented at the national meeting of the American Chemical Society in Boston, affirms that and provides evidence of the medicinal value of cranberries.
The new research suggests that the beneficial substances in cranberry juice could reach the urinary tract and prevent bacterial adhesion within eight hours.
Researchers from the Worcester Polytechnic Institute in Massachusetts grew strains of E. coli in urine collected from healthy people before and after they drank cranberry juice cocktail.
How Cranberry Juice Treats Urinary Tract Infections
A mixture of cranberry juice, water, and sweeteners found in cranberry juice cocktail was used for the study because it is the most popular cranberry beverage. The researchers discovered that in petri dishes, cranberry metabolites in the juice prevented E. coli from sticking to other bacteria, limiting its ability to grow and multiply. If E. coli is able to connect with other bacteria, such as the bacteria found in the urinary tract, it forms a layer or "biofilm." This allows the bacteria to multiply and produce an infection.
"A number of controlled clinical trials -- these are carefully designed and conducted scientific studies done in humans -- have concluded that cranberry juice really is effective for preventing urinary tract infections," says study researcher Terri Anne Camesano, PhD, in a news release. "That has important implications, considering the size of the problem and the health care costs involved."
Urinary tract infections are more common among women than men. According to the researchers, one in three women has had a urinary tract infection.
Urinary tract infections can occur anywhere along the urinary tract, which includes the bladder, urethra, and ureter. These infections account for 8 million trips to the doctor's office every year and cost more than $1.6 billion to treat.
Camesano said people should not self-treat urinary tract infections, and anyone who suspects they have an infection should see a doctor, but drinking cranberry juice may be an easy, inexpensive way to help keep E. coli at bay.
In the event of a urinary tract infection, antibiotics are the most common treatment. If left untreated, particularly in children, the elderly, or people with other chronic medical conditions, urinary tract infections can become more severe.
**Published in Web MD
Un estudio internacional, con presencia española, identifica las bases genéticas que provocan la meningitis
Un estudio internacional y multicéntrico, en el que participan los hospitales Virgen del Rocío de Sevilla, Virgen de las Nieves de Granada, Puerta del Mar de Cádiz, Torrecárdenas de Almería y el Hospital de Jaén, ha identificado ya las variantes genéticas que confieren la susceptibilidad para la enfermedad meningocócica o meningitis, sentando así las bases para el desarrollo de nuevas estrategias de prevención y tratamiento para esta grave enfermedad.
De hecho, la trascendencia de los resultados de esta investigación ha posibilitado su publicación en la revista 'Nature Genetics', especializada en el campo de la genética y una de las de mayor repercusión científica y prestigio a nivel mundial, según ha informado este martes en una nota la Consejería de Salud de la Junta de Andalucía.
Hasta el momento se desconocen los mecanismos exactos que condicionan la variabilidad en la expresión clínica y el pronóstico de la infección meningocócica, es decir, las causas por las que la misma bacteria puede causar la muerte a determinados niños en pocas horas, mientras que a otros ni siquiera les ocasiona síntomas. Sin embargo, y gracias a la investigación realizada por estos profesionales, ahora ha sido posible encontrar una explicación genética, concretamente en dos genes relacionados con el factor H del complemento --un elemento clave en el sistema inmune para la defensa ante las infecciones--, los genes CFH y CFHR3.
Dichos genes explican la posibilidad de contraer la enfermedad meningocócica en las tres cohortes de pacientes estudiadas. El estudio indica que el meningococo secuestra el citado complemento y de este modo se protege de la capacidad defensiva del organismo.
Con este hallazgo se podrá dar un impulso a la investigación de las nuevas vacunas que se están desarrollando. Este nuevo trabajo demuestra igualmente que hay también una base genética relacionada con los genes del factor H del complemento que influyen en nuestra susceptibilidad a la infección. "Este factor es importante, ya que hasta la fecha no existe ninguna vacuna frente al meningococo B, el subtipo que ocasiona más del 80 por ciento de los casos en nuestro país", ha señalado por su parte Jesús de la Cruz, director de la Unidad de Pediatría del Hospital Materno Infantil de Jaén.
"Nuestro estudio sugiere que estas variaciones genéticas en las personas a nivel de los genes reguladores de la activación del complemento, juegan un papel determinante en el hecho que la bacteria se limite a colonizar asintomáticamente nuestra garganta, o bien produzca una enfermedad invasiva. Conocer estas variaciones genéticas será clave en el desarrollo de nuevas vacunas y nuevos tratamientos frente al meningococo B, confirmando su evolución en la dirección correcta", ha incidido.
Se trata del trabajo más amplio realizado hasta la fecha sobre dicha enfermedad y ha consistido en un trabajo de asociación genética con dos estudios de réplica en más de 1.400 niños que sufrieron enfermedad meningocócica. En concreto, este trabajo ha sido desarrollado por el grupo de investigadores ESIGEM, que dirige Federico Martinón, pediatra e investigador del Complejo Hospitalario Universitario de Santiago de Compostela, y Antonio Salas Ellacuriaga, genetista del Instituto de Medicina Legal de Santiago (USC). Además, la publicación de este trabajo se ha realizado en asociación con el 'Meningococcal Genetics Consortium', consorcio sobre enfermedad meningocócica en el que también participan Reino Unido, Austria y Singapur.
--LA ENFERMEDAD MENINGOCÓCICA
La patología meningocócica es la principal causa de muerte por infección de la infancia en los países industrializados. A pesar de los avances en la prevención y tratamiento de esta enfermedad, se estima que causa más de 170.000 muertes al año en el mundo. El patrón de comportamiento clínico y la gravedad del cuadro son impredecibles, lo que unido a su alta tasa de secuelas graves, la convierten en la infección bacteriana más temida. En España, produce en este momento entre 900 y 1.000 casos al año --mayoritariamente niños-- pero cursa con brotes epidémicos como los que acontecieron en los años 80 y después a mediados de los 90 del siglo pasado y que causaron centenares de fallecimientos.
Entre los que sobreviven, al menos un tercio lo hace con mutilaciones o secuelas incapacitantes a pesar de los avances ya realizados en el diagnóstico precoz, el tratamiento y la prevención.
Entre los que sobreviven, al menos un tercio lo hace con mutilaciones o secuelas incapacitantes a pesar de los avances ya realizados en el diagnóstico precoz, el tratamiento y la prevención.
---PROCEDENCIA DE LOS ENFERMOS
Uno de los factores que se han tenido en cuenta en este trabajo ha sido la procedencia del enfermo, ya que se han encontrado diferencias étnicas en la susceptibilidad a la enfermedad meningocócica. En concreto, se ha descubierto una explicación genética al cinturón de la meningitis, y tal y como se señala en el estudio, existe una variante genética protectora de la enfermedad meningocócica. Esta variante es muy común en japoneses y chinos (hasta el 50% la poseen) donde la enfermedad es muy poco frecuente, y sin embargo es muy rara en África (menos del 3% de los africanos la poseen) donde la enfermedad se comporta de forma epidémica.
El grupo ESIGEM mantiene diferentes líneas de trabajo abiertas. Así, se están estudiando nuevas variantes genéticas implicadas en la enfermedad meningocócica, variantes de distinta naturaleza biológica a las estudiadas hasta el momento.
Uno de los factores que se han tenido en cuenta en este trabajo ha sido la procedencia del enfermo, ya que se han encontrado diferencias étnicas en la susceptibilidad a la enfermedad meningocócica. En concreto, se ha descubierto una explicación genética al cinturón de la meningitis, y tal y como se señala en el estudio, existe una variante genética protectora de la enfermedad meningocócica. Esta variante es muy común en japoneses y chinos (hasta el 50% la poseen) donde la enfermedad es muy poco frecuente, y sin embargo es muy rara en África (menos del 3% de los africanos la poseen) donde la enfermedad se comporta de forma epidémica.
El grupo ESIGEM mantiene diferentes líneas de trabajo abiertas. Así, se están estudiando nuevas variantes genéticas implicadas en la enfermedad meningocócica, variantes de distinta naturaleza biológica a las estudiadas hasta el momento.
Nova Line lanza una campaña de educación nutricional en sus 350 centros
La marca de productos de control de peso Nova Line se ha marcado como objetivo para la campaña 2010-2011 promover una alimentación equilibrada y hábitos saludables a las personas preocupadas por su peso y que visiten alguno de sus 350 centros en España.
Asimismo, la firma, propiedad de Nova Diet S.A., ha previsto un plan de formación continua entre su red de asesores nutricionales y entregará material didáctico al consumidor, en forma de manual coleccionable basado en la dieta mediterránea. De este modo, la empresa pretende reformular el concepto del adelgazamiento o la dieta estricta, para configurar un plan personalizada en el que se priorice "educar a la persona en su conducta diaria", ha informado la compañía en un comunicado.
El plan para la presente campaña parte de que en España el 36,7% de la población adulta presenta problemas de sobrepeso, mientras que la obesidad afecta a unos seis millones de personas, según datos del Instituto Nacional de Estadística (INE). De este modo, Nova Diet pretende fomentar la "educación nutricional" y la corrección de los malos hábitos frente a otros métodos más "radicales" de adelgazamiento, centrados en la consecución de objetivos a corto plazo "difíciles de mantener en el tiempo".
La marca Nova Line, de la empresa Nova Diet S.A., no tiene nada que ver con los productos cosméticos de la empresa Nova Line Cosmetics S.L., que fueron retirados del mercado por estar envasados sin la respectiva autorización sanitaria. Frente a informaciones publicadas en fechas anteriores, la compañía aclara que todos los productos Nova Diet, incluida la cosmética y la gama de productos Nova Line, cumplen con los controles de calidad y cuentan con los registros oportunos, además de tener certificados ISO internacionales.
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