In a mouse study, scientists at Mayo Clinic Florida have demonstrated the feasibility of a promising new strategy for treating human type 2 diabetes, which affects more than 200 million people worldwide. In type 2 diabetes, the body stops responding efficiently to insulin, a hormone that controls blood sugar. To compensate for the insensitivity to insulin, many diabetes drugs work by boosting insulin levels; for example, by injecting more insulin or by increasing the amount of insulin secreted from the pancreas. The new study, published in the June 9 issue of PLoS ONE, showed that a different approach could also be effective for treating diabetes — namely, blocking the breakdown of insulin, after it is secreted from the pancreas.
"Insulin levels in the blood reflect the balance between how much is secreted and how fast it is broken down," says the study's lead researcher, Malcolm A. Leissring, Ph.D., from Mayo Clinic's Department of Neuroscience. "Blocking the breakdown of insulin is simply an alternative method for achieving the same goal as many existing diabetes therapies."
The researchers tested this idea by studying mice in which insulin-degrading enzyme (IDE) was "knocked out," or deleted genetically. IDE is a molecular "machine" that normally chews up the insulin hormone, breaking it down into smaller pieces. Levels of insulin in the blood are controlled, in part, by this process.
Compared to normal mice, IDE knockout mice had more insulin overall, weighed less, and were more efficient at controlling their blood sugar. They were, in effect, "super mice" with respect to their ability to lower their blood sugar after a meal, the process that is disrupted in diabetes, explains Dr. Leissring.
These findings suggest that drugs that inhibit IDE could be useful in treating diabetes. Dr. Leissring's team is actively working to develop such drugs. As reported in a separate study in PLoS ONE last year, Dr. Leissring and colleagues developed the first potent and selective inhibitors of IDE. The Mayo team has now developed more drug-like IDE inhibitors that they are preparing to test in animal models of diabetes.
"The reason we studied IDE knockout mice was to help us understand whether IDE inhibitors would be useful for treating diabetes," says Samer Abdul-Hay, Ph.D., first author on the study. But the IDE knockout mice are not a perfect model of how a drug will perform, he notes. "They are actually a better model of overdosing on an IDE inhibitor. We would never want a drug that inhibits IDE 100 percent in all tissues throughout life."
The effect of deleting all IDE in the mice was so strong, in fact, that the effect eventually backfired, the researchers say. Despite being "super mice" when young, as the IDE knockout mice aged, they slowly became resistant to the elevated insulin, gained weight, and lost control of their blood sugar. As a result, the older mice developed classic type 2 diabetes.
"The finding that older IDE knockout mice develop diabetes has confused a lot of people," says Dr. Leissring. "It's an example of too much of a good thing becoming bad for you." Drugs that inhibit IDE only partially or only transiently would not be expected to cause diabetes, he says. "Deleting all IDE is overkill."
The researchers say the Mayo study also has interesting implications for understanding how diabetes starts. "Deleting IDE produces elevated insulin levels — a condition known as hyperinsulinemia. Diabetes is usually believed to cause hyperinsulinemia, not the other way around," Dr. Leissring says. Nevertheless, in the IDE knockout mice, chronic hyperinsulinemia seemed to actually cause diabetes. As they aged, the mice appeared to adapt to the chronically high insulin levels, for example, by reducing the number of receptors for insulin in their tissues. "These adaptations make the mice less sensitive to insulin, which is the exact cause of type 2 diabetes."
Whether these findings apply to humans is unclear, Dr. Leissring cautions. He says these novel findings "represent early, but exciting days" in a new avenue of diabetes research. Dr. Leissring was recently awarded a five-year career development grant from the American Diabetes Association, which will help support this line of research.
**Source: Mayo Clinic
10 June 2011
Cancer protein discovery may aid radiation therapy
Farber Cancer Institute have uncovered a new role for a key cancer protein, a finding that could pave the way for more-effective radiation treatment of a variety of tumors. Many cancers are driven in part by elevated levels of cyclin D1, which allow the cells to escape growth controls and proliferate abnormally. In the new research, reported in the June 9 issue of Nature, researchers discovered that cyclin D1 also helps cancer cells to quickly repair DNA damage caused by radiation treatments, making the tumors resistant to the therapy.
Based on this finding, the researchers made cancer cells more sensitive to several cancer drugs and to radiation by using a molecular tool to lower the cancer cells' cyclin D1 levels, said Peter Sicinski, MD, PhD, senior author of the report and a professor of genetics at Dana-Farber.
"This is the first time a cell cycle protein has been shown to be directly involved in DNA repair," said Siwanon Jirawatnotai, PhD, the lead author of the paper. "If we could come up with a strategy to inhibit cyclin D1, it might be very useful in treating a variety of cancers."
The gene for cyclin D1 is the second most-overexpressed gene found in human cancers, including breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer. Cyclin D1's normal function in cellular growth control is to temporarily remove a molecular brake, allowing the cell to manufacture more DNA in preparation for cell division. When cyclin D1 is mutated or is overactivated by external growth signals, the cell may run out of control and proliferate in a malignant fashion.
The findings came in a series of experiments by Jirawatnotai, a post-doctoral fellow in the Sicinski lab. With the goal of uncovering details of cyclin D1's function in human cancer cells, Jirawatnotai broke open four types of cancer cells, isolated the cyclin D1 protein, and searched for other proteins with which it interacted.
The experiment netted more than 132 partner proteins, most of them part of the cell cycle protein mechanism in which cyclin D1 is a major player. But unexpectedly, the scientists also observed that the cyclin D1 protein was binding to a cluster of DNA repair proteins, most importantly RAD51. The RAD51 protein is an enzyme that rushes to broken parts of the cancer cell's DNA instructions and repairs the damage, including damage caused by radiation therapy administered to stop cancer cells' division and growth. In another experiment, it was observed that cyclin D1 was recruited along with RAD51 to the DNA damage site.
"This was a surprise," said Jirawatnotai. "This finding showed that cyclin D1 has an unexpected function in repairing broken DNA." In additional experiments, he used a molecular tool, RNA interference (RNAi) to drastically reduce the level of cyclin D1 in the cancer cells. "When you lower D1 levels, you get poorer repair," he said.
When cancer cells with reduced cyclin D1 protein levels were administered to mice, the resulting tumor proved to be more sensitive to radiation than those grown from cells with overexpressed cyclin D1.
Currently, cyclin D1 is thought to be responsible for driving cancer cell proliferation. Agents that target cyclin D1 are currently in clinical trials, with the goal of reducing cancer cell growth. The new findings strongly suggest that targeting cyclin D1 may increase susceptibility of human cancers to radiation, said the scientists, and this discovery may encourage targeting cyclin D1 even in these cancers whose cells do not depend on cyclin D1 for proliferation.
"Our results potentially change the way we think about cyclin D1 and cancer and may encourage targeting cyclin D1 in a very large pool of human cancers which do not need cyclin D1 for proliferation, but may still depend on cyclin D1 for DNA repair," said Jirawatnotai, who also holds a faculty position at the Mahidol University in Bangkok, Thailand.
**Source: Dana-Farber Cancer Institute
Based on this finding, the researchers made cancer cells more sensitive to several cancer drugs and to radiation by using a molecular tool to lower the cancer cells' cyclin D1 levels, said Peter Sicinski, MD, PhD, senior author of the report and a professor of genetics at Dana-Farber.
"This is the first time a cell cycle protein has been shown to be directly involved in DNA repair," said Siwanon Jirawatnotai, PhD, the lead author of the paper. "If we could come up with a strategy to inhibit cyclin D1, it might be very useful in treating a variety of cancers."
The gene for cyclin D1 is the second most-overexpressed gene found in human cancers, including breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer. Cyclin D1's normal function in cellular growth control is to temporarily remove a molecular brake, allowing the cell to manufacture more DNA in preparation for cell division. When cyclin D1 is mutated or is overactivated by external growth signals, the cell may run out of control and proliferate in a malignant fashion.
The findings came in a series of experiments by Jirawatnotai, a post-doctoral fellow in the Sicinski lab. With the goal of uncovering details of cyclin D1's function in human cancer cells, Jirawatnotai broke open four types of cancer cells, isolated the cyclin D1 protein, and searched for other proteins with which it interacted.
The experiment netted more than 132 partner proteins, most of them part of the cell cycle protein mechanism in which cyclin D1 is a major player. But unexpectedly, the scientists also observed that the cyclin D1 protein was binding to a cluster of DNA repair proteins, most importantly RAD51. The RAD51 protein is an enzyme that rushes to broken parts of the cancer cell's DNA instructions and repairs the damage, including damage caused by radiation therapy administered to stop cancer cells' division and growth. In another experiment, it was observed that cyclin D1 was recruited along with RAD51 to the DNA damage site.
"This was a surprise," said Jirawatnotai. "This finding showed that cyclin D1 has an unexpected function in repairing broken DNA." In additional experiments, he used a molecular tool, RNA interference (RNAi) to drastically reduce the level of cyclin D1 in the cancer cells. "When you lower D1 levels, you get poorer repair," he said.
When cancer cells with reduced cyclin D1 protein levels were administered to mice, the resulting tumor proved to be more sensitive to radiation than those grown from cells with overexpressed cyclin D1.
Currently, cyclin D1 is thought to be responsible for driving cancer cell proliferation. Agents that target cyclin D1 are currently in clinical trials, with the goal of reducing cancer cell growth. The new findings strongly suggest that targeting cyclin D1 may increase susceptibility of human cancers to radiation, said the scientists, and this discovery may encourage targeting cyclin D1 even in these cancers whose cells do not depend on cyclin D1 for proliferation.
"Our results potentially change the way we think about cyclin D1 and cancer and may encourage targeting cyclin D1 in a very large pool of human cancers which do not need cyclin D1 for proliferation, but may still depend on cyclin D1 for DNA repair," said Jirawatnotai, who also holds a faculty position at the Mahidol University in Bangkok, Thailand.
**Source: Dana-Farber Cancer Institute
Hormone test helps predict success in IVF
Given how much patients invest in in vitro fertilization (IVF), both financially and emotionally, tools to inform couples about what they might expect during their treatment can be welcome. A study by researchers at Brown University and Women & Infants Hospital shows that as the IVF cycle is beginning, a blood test for levels of a hormone called AMH, or antimullerian hormone, can help predict the number of eggs that will be harvested. "Clinicians can measure AMH before or during ovarian stimulation to counsel couples about their likelihood of success," said Geralyn Lambert-Messerlian, professor of pathology and laboratory medicine in the Warren Alpert Medical School of Brown University and a researcher in the Division of Medical Screening and Special Testing at Women & Infants Hospital. She co-authored a paper that will be published in an upcoming issue of the American Journal of Obstetrics and Gynecology. It appeared in advance online last month.
Lead author Andrew Blazar, a physician at Women & Infants' Division of Reproductive Endocrinology and Infertility, said the finding could be useful for adjusting IVF preparations on the fly, for instance by adjusting how much follicle stimulation hormone women are receiving in the week or so before eggs are extracted for fertilization.
"The main thrust of the paper is that you can do this test even after you have begun the preparations for initiating an IVF cycle, so it allows you to modify your treatment, at least in theory, so that your probability of success would be improved," said Blazar, who is also a clinical associate professor of obstetrics and gynecology at the Alpert Medical School. "Though not proven, this approach seems like a logical way to use this new information.
"What I'm hoping is that eventually it will turn out that you can now do this test in the same cycle and not wait until you have to do another cycle, which would be a considerable advantage to your patient," he said.
The research was partly supported by Beckman Coulter Inc., which makes the assay the team used for measuring AMH in blood samples.
AMH predicts eggs, pregnancy
AMH is made by small follicles in the ovary and helps regulate their growth. AMH levels in the blood are an indicator of how many follicles a woman has at the time of the hormone measurement.
In their research, Blazar and Lambert-Messerlian's team measured AMH levels in 190 IVF patients, ages 22 to 44, both at the beginning and end of their preparatory course of follicle stimulation hormone treatment. They counted the eggs that were eventually harvested and then performed blood tests and later an ultrasound to confirm pregnancy.
The researchers found that women with low AMH levels in the first test (less than one nanogram per milliliter) on average yielded only about six eggs, while women who had more than three times as much AMH provided about 20 eggs on average.
In this study, AMH similarly predicted whether pregnancy became established. Only about a quarter of women with less than one nanogram of AMH were pregnant five to six weeks after the IVF procedure. Among women with more than three nanograms, three in five were pregnant at that stage.
Lambert-Messerlian cautioned that most other studies have not found an association of AMH levels and pregnancy success though delivery.
Blazar noted that because some women with low AMH levels were still able to establish pregnancies, he wouldn't recommend that all such women necessarily forgo an upcoming IVF procedure.
**Source: Brown University
Lead author Andrew Blazar, a physician at Women & Infants' Division of Reproductive Endocrinology and Infertility, said the finding could be useful for adjusting IVF preparations on the fly, for instance by adjusting how much follicle stimulation hormone women are receiving in the week or so before eggs are extracted for fertilization.
"The main thrust of the paper is that you can do this test even after you have begun the preparations for initiating an IVF cycle, so it allows you to modify your treatment, at least in theory, so that your probability of success would be improved," said Blazar, who is also a clinical associate professor of obstetrics and gynecology at the Alpert Medical School. "Though not proven, this approach seems like a logical way to use this new information.
"What I'm hoping is that eventually it will turn out that you can now do this test in the same cycle and not wait until you have to do another cycle, which would be a considerable advantage to your patient," he said.
The research was partly supported by Beckman Coulter Inc., which makes the assay the team used for measuring AMH in blood samples.
AMH predicts eggs, pregnancy
AMH is made by small follicles in the ovary and helps regulate their growth. AMH levels in the blood are an indicator of how many follicles a woman has at the time of the hormone measurement.
In their research, Blazar and Lambert-Messerlian's team measured AMH levels in 190 IVF patients, ages 22 to 44, both at the beginning and end of their preparatory course of follicle stimulation hormone treatment. They counted the eggs that were eventually harvested and then performed blood tests and later an ultrasound to confirm pregnancy.
The researchers found that women with low AMH levels in the first test (less than one nanogram per milliliter) on average yielded only about six eggs, while women who had more than three times as much AMH provided about 20 eggs on average.
In this study, AMH similarly predicted whether pregnancy became established. Only about a quarter of women with less than one nanogram of AMH were pregnant five to six weeks after the IVF procedure. Among women with more than three nanograms, three in five were pregnant at that stage.
Lambert-Messerlian cautioned that most other studies have not found an association of AMH levels and pregnancy success though delivery.
Blazar noted that because some women with low AMH levels were still able to establish pregnancies, he wouldn't recommend that all such women necessarily forgo an upcoming IVF procedure.
**Source: Brown University
New animal study shows promise for development of Parkinson's disease drug
Few treatments for Parkinson's disease (PD) restore function for extended periods. In a new study published today in the inaugural issue issue of the Journal of Parkinson's Disease, an international group of researchers report that platelet-derived growth factor-BB (PDGF-BB) restored function in rodents and shows promise as a clinical candidate drug for treatment of PD. Parkinson's disease is the second most common neurodegenerative disorder, affecting 1% of the population over the age of 65. It is characterized by loss of brain cells (neurons) from the mid-brain which use the neurotransmitter dopamine to help control voluntary movements. Investigators from NeuroNova AB, Stockholm, Sweden, the Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden, The Parkinson's Institute, Sunnyvale, CA, USA, and Motac Neuroscience Ltd, Manchester, UK, found that behavioral, tissue and biochemical changes in experimental models of Parkinson's disease in rodents could be counteracted by infusion of PDGF-BB. This could offer an alternative strategy to restore function in PD.
"In animal models of nigrostriatal injury, a two weeks treatment with platelet-derived growth factor-BB resulted in long-lasting restoration of striatal dopamine transporter binding sites and expression of nigral tyrosine hydroxylase," commented Anders Haegerstrand, MD, PhD, Chief Scientific Officer, NeuroNova AB, Stockholm, Sweden."It also normalized amphetamine-induced rotational behavior in 6-hydroxydopamine lesioned rats. Platelet-derived growth factor-BB promoted proliferation of neural progenitor cells in the subventricular zone. The effects on dopaminergic neurons and functional recovery could be blocked by co-infusion with a proliferation inhibitor, indicating a link between the proliferative and anti-parkinsonian effects. Based on the current data, we consider platelet-derived growth factor-BB a clinical candidate drug for treatment of Parkinson's disease."
**Source: IOS Press
"In animal models of nigrostriatal injury, a two weeks treatment with platelet-derived growth factor-BB resulted in long-lasting restoration of striatal dopamine transporter binding sites and expression of nigral tyrosine hydroxylase," commented Anders Haegerstrand, MD, PhD, Chief Scientific Officer, NeuroNova AB, Stockholm, Sweden."It also normalized amphetamine-induced rotational behavior in 6-hydroxydopamine lesioned rats. Platelet-derived growth factor-BB promoted proliferation of neural progenitor cells in the subventricular zone. The effects on dopaminergic neurons and functional recovery could be blocked by co-infusion with a proliferation inhibitor, indicating a link between the proliferative and anti-parkinsonian effects. Based on the current data, we consider platelet-derived growth factor-BB a clinical candidate drug for treatment of Parkinson's disease."
**Source: IOS Press
Un estudio explica cómo la nicotina actúa de efecto inhibidor del apetito
Dejar de fumar es bueno para la salud, pero también acarrea ciertas incomodidades entre las que destaca, sin duda, el aumento de peso... Por lo menos, hasta ahora. Según un estudio que publica la revista Science, se ha descubierto el proceso por el cual la nicotina fortalece la sensación de saciedad, algo que si se copia en las en los tratamientos antitabaco, podría convertirse en un hito que evitaría la obesidad tras abandonar los humos de este hábito.
"Desafortunadamente al fumar pierdes peso, lo que hace que muchas personas preocupadas por su aspecto decidan seguir fumando para no engordar", comenta Marina R. Picciotto, profesora del departamento de Psiquitria de la Universidad de Yale (Connecticut, EEUU) y directora de esta investigación. "Es por esto por lo que estos resultados son tan interesantes, ya que se puede animar a estos fumadores a abandonar definitivamente este hábito sin riesgo a que engorden", apunta.
Hasta ahora era conocido que la nicotina inhibía el apetito, pero ¿qué proceso desencadena esta reacción? El estudio de la profesora Picciotto ha descubierto que la 'culpa' de esta situación se debe a que la nicotina activa una serie de neuronas que están directamente relacionadas con la sensación de saciedad.
"El hipotálamo es un área del cerebro que integra las señales procedentes de nuestro intestino y se encarga de 'decir' si necesitamos más alimentos o ya tenemos suficientes calorías", explica Picciotto. "Lo que hemos averiguado, a través del trabajo con ratones, es que la nicotina estimula una serie de receptores superficiales que, a su vez, activan una serie de neuronas que se encuentran en esta zona del cerebro, las pro-opiomelanocortinas (POMC), que conducen directamente a la supresión del apetito".
Según explica a ELMUNDO.es Yann Mineur, uno de los autores de este descubrimiento, este dato "ayuda a comprender los mecanismos relacionados con la adicción, el peso y el tabaquismo,con lo que se puede buscar medidas terapéuticas basadas en agentes nicotínicos, es decir, productos químicos con efectos parecidos a la nicotina, que eliminen el aumento de peso tras dejar de fumar".
"Desafortunadamente al fumar pierdes peso, lo que hace que muchas personas preocupadas por su aspecto decidan seguir fumando para no engordar", comenta Marina R. Picciotto, profesora del departamento de Psiquitria de la Universidad de Yale (Connecticut, EEUU) y directora de esta investigación. "Es por esto por lo que estos resultados son tan interesantes, ya que se puede animar a estos fumadores a abandonar definitivamente este hábito sin riesgo a que engorden", apunta.
Hasta ahora era conocido que la nicotina inhibía el apetito, pero ¿qué proceso desencadena esta reacción? El estudio de la profesora Picciotto ha descubierto que la 'culpa' de esta situación se debe a que la nicotina activa una serie de neuronas que están directamente relacionadas con la sensación de saciedad.
"El hipotálamo es un área del cerebro que integra las señales procedentes de nuestro intestino y se encarga de 'decir' si necesitamos más alimentos o ya tenemos suficientes calorías", explica Picciotto. "Lo que hemos averiguado, a través del trabajo con ratones, es que la nicotina estimula una serie de receptores superficiales que, a su vez, activan una serie de neuronas que se encuentran en esta zona del cerebro, las pro-opiomelanocortinas (POMC), que conducen directamente a la supresión del apetito".
Según explica a ELMUNDO.es Yann Mineur, uno de los autores de este descubrimiento, este dato "ayuda a comprender los mecanismos relacionados con la adicción, el peso y el tabaquismo,con lo que se puede buscar medidas terapéuticas basadas en agentes nicotínicos, es decir, productos químicos con efectos parecidos a la nicotina, que eliminen el aumento de peso tras dejar de fumar".
-Nuevas medidas terapéuticas
Para Juan Antonio Riesco, miembro del Centro de Investigación en Red de Enfermedades Respiratorias e integrante de la Unidad Antitabaco de la Comunidad de Madrid, ésta es una novedad "muy importante, puesto que ese hándicap de la hipotética ganancia de peso es una excusa muy común entre aquellos que todavía no se deciden a dejar el tabaco".
Dependiendo del caso, lo normal es ganar entre tres a siete kilos al dejar de fumar, pero para Riesco "es algo hipotético porque no todo el mundo engorda tras dejar de fumar y, además, se tiende a que con el paso del tiempo -meses o años, según el paciente- el cuerpo vuelva a recuperar el equilibrio en su peso".
"Todo el mundo tiene un determinado metabolismo basal. Cuando los fumadores comienzan con esta práctica, lo que hacen es introducir una serie de sustancias de la nicotina en el metabolismo, con lo que se favorece el gasto energético de nuestro cuerpo de una forma no natural", explica Riesco, "por lo que si se suprime la nicotina, disminuye nuestro gasto de energía y se produce esa ganancia", comenta.
Hasta ahora, un control de la dieta, el ejercicio físico y algunos fármacos trataban de eliminar o, al menos, aminorar, el aumento de peso cuando se dejaba de fumar, pero según afirma Picciotto "se podría avanzar en esos tratamientos con el desarrollo de fármacos que controlen esto de forma rápida y segura. En última instancia incluso, nos gustaría también ayudar a los no fumadores que están luchando contra la obesidad a través de componentes con efectos parecidos a la nicotina".
Para Juan Antonio Riesco, miembro del Centro de Investigación en Red de Enfermedades Respiratorias e integrante de la Unidad Antitabaco de la Comunidad de Madrid, ésta es una novedad "muy importante, puesto que ese hándicap de la hipotética ganancia de peso es una excusa muy común entre aquellos que todavía no se deciden a dejar el tabaco".
Dependiendo del caso, lo normal es ganar entre tres a siete kilos al dejar de fumar, pero para Riesco "es algo hipotético porque no todo el mundo engorda tras dejar de fumar y, además, se tiende a que con el paso del tiempo -meses o años, según el paciente- el cuerpo vuelva a recuperar el equilibrio en su peso".
"Todo el mundo tiene un determinado metabolismo basal. Cuando los fumadores comienzan con esta práctica, lo que hacen es introducir una serie de sustancias de la nicotina en el metabolismo, con lo que se favorece el gasto energético de nuestro cuerpo de una forma no natural", explica Riesco, "por lo que si se suprime la nicotina, disminuye nuestro gasto de energía y se produce esa ganancia", comenta.
Hasta ahora, un control de la dieta, el ejercicio físico y algunos fármacos trataban de eliminar o, al menos, aminorar, el aumento de peso cuando se dejaba de fumar, pero según afirma Picciotto "se podría avanzar en esos tratamientos con el desarrollo de fármacos que controlen esto de forma rápida y segura. En última instancia incluso, nos gustaría también ayudar a los no fumadores que están luchando contra la obesidad a través de componentes con efectos parecidos a la nicotina".
**Publicado en "EL MUNDO"
FARMAMUNDI DESTINA A ASISTENCIA SANITARIA EL 86% DE LOS FONDOS PARA HAITÍ
Farmamundi ha destinado el 86 por ciento de los fondos recaudados para Haití a brindar asistencia sanitaria a más de 44.000 haitianos damnificados por el terremoto de los distritos de Puerto Príncipe, Jacmel y Léogane, entre otras zonas.Concretamente, Farmamundi y sus socios locales realizaron seis intervenciones de emergencia y post-emergencia. De los 497.700 euros recaudados, el 74 por ciento fue de origen privado (250 euros de donación media) y el resto aportaciones públicas. El 36 por ciento de las donaciones se destinó a la provisión de alimentos, un 33 por ciento al suministro de medicamentos, el 17 por ciento fue para brindar atención médica y el 14 por ciento restante para la cobertura de necesidades de albergue. Estas aportaciones están permitiendo a la ONG mantener durante unos meses la Atención Primaria en salud, ante el repunte del brote de cólera en zonas rurales de la provincia de Léogane.
Además de las ayudas de carácter privado para esta campaña, la ONG consiguió financiación pública e institucional para proyectos de acción humanitaria y emergencias de la Obra Social Caja de Ahorros de Navarra (CAN), Obra Social Bancaja y Agencia Extremeña de Cooperación Internacional para el Desarrollo (AEXCID), así como de convenios firmados con la Agencia Catalana de Cooperació al Desenvolupament (ACCD), la Fundación Axencia Humanitaria de Galicia (FAHG), la Generalitat Valenciana y del Fondo de Ayuda Humanitaria y de Emergencias de Farmamundi (FAHE).
Según comunicó la ONG, durante 2010, se desarrollaron seis intervenciones de post-emergencia, en las que se han invertido 332.885 euros: La primera, en los distritos de Jacmel y Jimaní. Primera actuación con el Colectivo de Salud Popular (COSALUP), que benefició a más de 7.000 personas con el suministro de medicamentos esenciales, material médico y logístico, la provisión de alimentos y agua potable y la realización de operativos médicos. También con COSALUP, se realizaron 12 jornadas médicas en la Provincia Independencia en República Dominicana, donde se atendió a 1.628 personas. La tercera actuación correspondió a las localidades de Puerto Príncipe, Croix-des-Bouquets y Petion-Ville y en Jacmel, donde la ONG haitiana Movimiento Socio Cultural de los Trabajadores Haitianos (MOSCHTA), equipó con medicamentos y material sanitario a los operativos médicos responsables.
También con MOSCHTA, se intensificó la atención de emergencia en campamentos de Puerto Príncipe, Léogane y Grand Goave. En la localidad de Cabaret, entre los meses de julio y agosto, en coordinación con el Centre de Formation et Developpement Communautaire (CEFODEC) se ofreció asistencia a un total de 2.814 personas que tuvieron acceso a medicamentos y monitoreo psicológico, a través de 24 operativos médicos. También se distribuyeron 1.661 kits alimenticios a 415 familias. Por último, entre octubre y diciembre de 2010 y con el apoyo del Institut pour le Developement Integral d´Haiti (IDIH), se desarrolló otra actuación socio-sanitaria de emergencia en la comuna Bon Repos del municipio de Croix-des-Bouquets, donde se atendieron a 12.000 damnificados y 238 familias recibieron asistencia alimenticia mediante el reparto de 932 kits de alimentos.
Además de las ayudas de carácter privado para esta campaña, la ONG consiguió financiación pública e institucional para proyectos de acción humanitaria y emergencias de la Obra Social Caja de Ahorros de Navarra (CAN), Obra Social Bancaja y Agencia Extremeña de Cooperación Internacional para el Desarrollo (AEXCID), así como de convenios firmados con la Agencia Catalana de Cooperació al Desenvolupament (ACCD), la Fundación Axencia Humanitaria de Galicia (FAHG), la Generalitat Valenciana y del Fondo de Ayuda Humanitaria y de Emergencias de Farmamundi (FAHE).
Según comunicó la ONG, durante 2010, se desarrollaron seis intervenciones de post-emergencia, en las que se han invertido 332.885 euros: La primera, en los distritos de Jacmel y Jimaní. Primera actuación con el Colectivo de Salud Popular (COSALUP), que benefició a más de 7.000 personas con el suministro de medicamentos esenciales, material médico y logístico, la provisión de alimentos y agua potable y la realización de operativos médicos. También con COSALUP, se realizaron 12 jornadas médicas en la Provincia Independencia en República Dominicana, donde se atendió a 1.628 personas. La tercera actuación correspondió a las localidades de Puerto Príncipe, Croix-des-Bouquets y Petion-Ville y en Jacmel, donde la ONG haitiana Movimiento Socio Cultural de los Trabajadores Haitianos (MOSCHTA), equipó con medicamentos y material sanitario a los operativos médicos responsables.
También con MOSCHTA, se intensificó la atención de emergencia en campamentos de Puerto Príncipe, Léogane y Grand Goave. En la localidad de Cabaret, entre los meses de julio y agosto, en coordinación con el Centre de Formation et Developpement Communautaire (CEFODEC) se ofreció asistencia a un total de 2.814 personas que tuvieron acceso a medicamentos y monitoreo psicológico, a través de 24 operativos médicos. También se distribuyeron 1.661 kits alimenticios a 415 familias. Por último, entre octubre y diciembre de 2010 y con el apoyo del Institut pour le Developement Integral d´Haiti (IDIH), se desarrolló otra actuación socio-sanitaria de emergencia en la comuna Bon Repos del municipio de Croix-des-Bouquets, donde se atendieron a 12.000 damnificados y 238 familias recibieron asistencia alimenticia mediante el reparto de 932 kits de alimentos.
09 June 2011
International Statement on Hormone Replacement Therapy
A new evaluation of the evidence for Hormone Replacement Therapy (HRT) confirms that treatment needs to be tailored to the individual woman, but that most women going through the menopause need have few worries about safety. These findings are published in the peer-reviewed journal Climacteric and will be made available at the 13th World Congress on Menopause, in Rome, on 10th June (see: http://www.imsroma2011.com/)
The publication of the first Women’s Health Initiative (WHI) report in 2002 raised alarms about the safe use of HRT. However, recent and more detailed interpretations of the WHI study, plus additional work from other sources, has indicated that any risks of HRT are small, and those which exist are mostly associated with older women – not mainly those going through the menopause. Because of this recent evidence, the International Menopause Society (IMS) is updating its recommendations on the use of HRT.
-The main findings are
That a woman’s decision to take or to stay on HRT is not a simple yes or no, but needs to be agreed with her physician in the light of individual circumstances and as part of an overall health strategy.
Most women who have menopausal symptoms will benefit, and most menopausal women have little to fear from adverse effects of HRT.
Each woman is different, and her decision to take HRT will carry different benefits and risks, depending on such things as severity of symptoms, age and family history. As a woman grows older, her risks seem to increase, and so women long past the menopause should take greater care
-General Recommendations in the report
The report says that a woman’s decision to take HRT should be discussed with her physician, and should be reviewed annually. Taking HRT should be part of an overall health strategy, to include factors such as diet, exercise, stopping smoking and safe levels of alcohol consumption. Like all medicines, HRT should only be prescribed where there is a clear indication of potential benefit. A woman should use the lowest effective dose of HRT that improves her symptoms, but the decision on how long to take HRT should be discussed with her physician. Some side-effects (risks) rise as a woman gets older, so it is important that a woman continues to consult with her physician.
-Benefits
HRT is the best remedy for menopausal symptoms such as hot flushes and vaginal atrophy. These can have a severe affect on the quality of life of women going through the menopause. HRT also protects against osteoporosis and has beneficial effects on skin and joints, and there is some evidence that HRT protects against cardiovascular disease, especially in younger women (younger than 60), and colon cancer. Recent evidence from the WHI shows that in these younger women who have had a hysterectomy, estrogen therapy protects against cardiovascular disease, and has no effect on breast cancer risk.
-Risks
Women take HRT for the benefits it can give, but each woman needs to consider the potential risks, and whether they apply to her. As stated previously, the risks and benefits depend on the individual. Women who have had a hysterectomy benefit from taking HRT, in terms of reduced risk of breast cancer and cardiovascular disease.
Women taking combined HRT (estrogen and progesterone) to help them go through the menopause have slightly increased risks of breast cancer. Breast cancer is a major concern for women (although cardiovascular disease, see above, kills many more than breast cancer), and woman who are concerned, at risk, or have a family history of breast cancer, should probably not take HRT.
HRT is associated with a higher risk of stroke in women over 60. Women who wish to take HRT but who may be at increased risk of stroke might consider transdermal HRT, which does not seem to increase the risk of stroke
-On balance
On balance, HRT should be considered safe for most women going through the menopause (bear in mind that no medicine is completely safe), and the vast majority of woman who suffer from menopausal symptoms will benefit from taking HRT.
The risks associated with HRT are small, but tend to increase as a woman gets older.
A woman’s decision to take, or to stay on, HRT, should be made in consultation with her physician as part of an overall health strategy
-Dr Roger Lobo (Columbia University, New York), one of the authors of the report, said:
“This report sets out the current thinking of doctors who actually treat women going through the menopause. After the publication of the first Women’s Health Initiative report in 2002, Hormone Replacement Therapy got a very bad press, but the pendulum has been swinging back towards a greater acceptance of HRT use. Even the WHI researchers are now saying that HRT can be a good decision if the circumstances are right. This is partly because of new findings, but mainly because the original results have been better interpreted, indicating that there are few risks taking HRT during and just after the menopause – which is when it is needed most. The bottom line is that most doctors nowadays should feel comfortable about prescribing HRT to most women going through the menopause. Like all medicines, you need to look at individual circumstances before deciding to take it”.
-Co-author Professor Rod Baber (University of Sydney, Australia), commenting, said:
“This report was finalised before we saw the recent paper from the WHI which showed that HRT for women in the 50-59 age group who have had a hysterectomy is quite beneficial. For example, there was no overall increase in any adverse events or breast cancer in this group, but of course these women were able to experience the beneficial effects of HRT, including a lesser risk of cardiovascular disease and osteoporosis. There are some small risks associated with HRT use, but these risks vary from person to person and need to be kept in context. The message is, discuss HRT use with your doctor”.
-Co-author Dr David Sturdee (Solihull, UK), President of the IMS said:
“As any woman who has undergone a difficult menopause knows, the symptoms which can affect women during the menopause can really be quite undermining, and we shouldn’t undervalue the negative effect this can have on a woman or on her relationships. HRT is the best option to treat these symptoms. It is vitally important that women going through premature menopause should be given the opportunity to use HRT at least until the average age of the menopause (51y) to maintain their quality of life and to minimise long term risks such as osteoporosis, cardiovascular disease and Alzheimers. The benefits far outweigh the risks in this age group. We are not saying that HRT is right for everyone, but that every woman whose quality of life is affected should have the option to consider the benefits and risks to her of taking HRT”.
The publication of the first Women’s Health Initiative (WHI) report in 2002 raised alarms about the safe use of HRT. However, recent and more detailed interpretations of the WHI study, plus additional work from other sources, has indicated that any risks of HRT are small, and those which exist are mostly associated with older women – not mainly those going through the menopause. Because of this recent evidence, the International Menopause Society (IMS) is updating its recommendations on the use of HRT.
-The main findings are
That a woman’s decision to take or to stay on HRT is not a simple yes or no, but needs to be agreed with her physician in the light of individual circumstances and as part of an overall health strategy.
Most women who have menopausal symptoms will benefit, and most menopausal women have little to fear from adverse effects of HRT.
Each woman is different, and her decision to take HRT will carry different benefits and risks, depending on such things as severity of symptoms, age and family history. As a woman grows older, her risks seem to increase, and so women long past the menopause should take greater care
-General Recommendations in the report
The report says that a woman’s decision to take HRT should be discussed with her physician, and should be reviewed annually. Taking HRT should be part of an overall health strategy, to include factors such as diet, exercise, stopping smoking and safe levels of alcohol consumption. Like all medicines, HRT should only be prescribed where there is a clear indication of potential benefit. A woman should use the lowest effective dose of HRT that improves her symptoms, but the decision on how long to take HRT should be discussed with her physician. Some side-effects (risks) rise as a woman gets older, so it is important that a woman continues to consult with her physician.
-Benefits
HRT is the best remedy for menopausal symptoms such as hot flushes and vaginal atrophy. These can have a severe affect on the quality of life of women going through the menopause. HRT also protects against osteoporosis and has beneficial effects on skin and joints, and there is some evidence that HRT protects against cardiovascular disease, especially in younger women (younger than 60), and colon cancer. Recent evidence from the WHI shows that in these younger women who have had a hysterectomy, estrogen therapy protects against cardiovascular disease, and has no effect on breast cancer risk.
-Risks
Women take HRT for the benefits it can give, but each woman needs to consider the potential risks, and whether they apply to her. As stated previously, the risks and benefits depend on the individual. Women who have had a hysterectomy benefit from taking HRT, in terms of reduced risk of breast cancer and cardiovascular disease.
Women taking combined HRT (estrogen and progesterone) to help them go through the menopause have slightly increased risks of breast cancer. Breast cancer is a major concern for women (although cardiovascular disease, see above, kills many more than breast cancer), and woman who are concerned, at risk, or have a family history of breast cancer, should probably not take HRT.
HRT is associated with a higher risk of stroke in women over 60. Women who wish to take HRT but who may be at increased risk of stroke might consider transdermal HRT, which does not seem to increase the risk of stroke
-On balance
On balance, HRT should be considered safe for most women going through the menopause (bear in mind that no medicine is completely safe), and the vast majority of woman who suffer from menopausal symptoms will benefit from taking HRT.
The risks associated with HRT are small, but tend to increase as a woman gets older.
A woman’s decision to take, or to stay on, HRT, should be made in consultation with her physician as part of an overall health strategy
-Dr Roger Lobo (Columbia University, New York), one of the authors of the report, said:
“This report sets out the current thinking of doctors who actually treat women going through the menopause. After the publication of the first Women’s Health Initiative report in 2002, Hormone Replacement Therapy got a very bad press, but the pendulum has been swinging back towards a greater acceptance of HRT use. Even the WHI researchers are now saying that HRT can be a good decision if the circumstances are right. This is partly because of new findings, but mainly because the original results have been better interpreted, indicating that there are few risks taking HRT during and just after the menopause – which is when it is needed most. The bottom line is that most doctors nowadays should feel comfortable about prescribing HRT to most women going through the menopause. Like all medicines, you need to look at individual circumstances before deciding to take it”.
-Co-author Professor Rod Baber (University of Sydney, Australia), commenting, said:
“This report was finalised before we saw the recent paper from the WHI which showed that HRT for women in the 50-59 age group who have had a hysterectomy is quite beneficial. For example, there was no overall increase in any adverse events or breast cancer in this group, but of course these women were able to experience the beneficial effects of HRT, including a lesser risk of cardiovascular disease and osteoporosis. There are some small risks associated with HRT use, but these risks vary from person to person and need to be kept in context. The message is, discuss HRT use with your doctor”.
-Co-author Dr David Sturdee (Solihull, UK), President of the IMS said:
“As any woman who has undergone a difficult menopause knows, the symptoms which can affect women during the menopause can really be quite undermining, and we shouldn’t undervalue the negative effect this can have on a woman or on her relationships. HRT is the best option to treat these symptoms. It is vitally important that women going through premature menopause should be given the opportunity to use HRT at least until the average age of the menopause (51y) to maintain their quality of life and to minimise long term risks such as osteoporosis, cardiovascular disease and Alzheimers. The benefits far outweigh the risks in this age group. We are not saying that HRT is right for everyone, but that every woman whose quality of life is affected should have the option to consider the benefits and risks to her of taking HRT”.
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