A survey of patients receiving treatment in a teaching facility found that patients prefer to be informed of trainee participation in their care, and consent rates appear to vary based on scenarios describing increased levels of resident participation, according to a report published Online First by Archives of Surgery, one of the JAMA/Archives journals. According to background in the article, the concept of surgeon-patient interaction prior to surgery can be traced back as far as ancient Greece; however, the formal system of informed consent is more modern. "Currently, no widely accepted guidelines or policies exist for providing information regarding the role of surgical trainees to the patient during the informed consent process," the authors write. "The accepted standard is to provide information that 'a reasonable patient' would want and would need to know to make an informed decision, but this counseling may vary widely by health care professional, setting, and type of surgical procedure."
Christopher R. Porta, M.D., and colleagues from Madigan Army Health System, Tacoma, Wash., conducted an anonymous questionnaire at a tertiary-level U.S. Army hospital and referral center, to evaluate patient perceptions and willingness to participate in surgical resident education and training programs.
The authors distributed 500 surveys, 316 (63.2 percent) of which were returned and included in the study. Most patients indicated no preference for a private hospital versus a teaching hospital, however of those who did, more preferred a teaching hospital to a private facility for overall care (24.9 percent vs. 8.8 percent) and minor surgical procedures (28.2 percent vs. 12 percent), but hospital preference for major surgical procedures was similar (24.7 percent vs. 26.6 percent). Additionally, 91.2 percent of those patients who indicated a facility preference reported that their care in a teaching hospital would be equivalent to or better than that of a private hospital.
Patients also indicated they overwhelmingly preferred to be informed of resident participation in their surgical procedure, regardless of whether it was a major procedure (95.7 percent) or a minor surgery (87.5 percent). A total of 94 percent of respondents indicated they would consent to involvement of a surgical resident, however this decreased to 85 percent for a surgical intern and 79.9 percent for medical student involvement. When provided with specific scenarios involving trainee participation, 57.6 percent of patients consented to having a junior resident act as the first assistant, 25.6 percent consented to the resident acting as the operation surgeon with direct staff observation, and 18.2 percent consented to resident participation without direct staff observation.
The authors conclude that their findings show, "patients routinely would prefer to be informed regarding details of trainee participation in their care, and that this information would significantly affect their willingness to consent." However, they also note, "Although most patients express an overall willingness to participate in surgical education, wide variations can be observed in the actual consent rates for specific training situations. This decreased willingness to consent and the potential effect on training programs must be considered when discussing policy initiatives aimed at improving informed consent."
**Source: JAMA and Archives Journals
20 September 2011
The cellular intricacies of cystic fibrosis
When researchers discovered the primary genetic defect that causes cystic fibrosis (CF) back in 1989, they opened up a new realm of research into treatment and a cure for the disease. Since then, scientists have been able to clone the defective gene and study its effects in animals. Now researchers at the University of North Carolina at Chapel Hill have developed a technique for observing the defects at work in human tissue donated by patients with CF. This technique has yielded an extraordinary view of the cellular intricacies of CF, which Martina Gentzsch, assistant professor of cell and developmental biology, will discuss at the 7th International Symposium on Aldosterone and the ENaC/Degenerin Family of Ion Channels, being held September 18-22 in Pacific Grove, Calif. The meeting is sponsored by the American Physiological Society. Her poster presentation is entitled, "The Cystic Fibrosis Transmembrane Conductance Regulator Inhibits Proteolytic Stimulation of ENaC."
Ion Transport Processes in CF
Cystic fibrosis is caused by a mutation in the gene that encodes a protein called cystic fibrosis transmembrane conductance regulator (CFTR), which functions as a chloride channel at the surface of airways and moves chloride out of the cells. CFTR also regulates another protein called epithelial sodium channel (ENaC), which is responsible for transporting sodium into cells. Thus far, scientists have been able to establish that when the CFTR mutation is present, ENaC becomes overactive and causes the cells in the lungs to absorb too much sodium. Water follows the sodium from the cells' surfaces into the cells, and as a result, the airways become dry and mucous becomes thick and sticky, leading to infections in the lungs.
To observe how CFTR regulates ENaC, Dr. Gentzsch and her team took cells from healthy lung tissue and CF lung tissue and maintained them in a liquid medium. The cells' surfaces were exposed to air, which prompted the cells to grow and behave as though they were still inside human lungs. Then the team studied proteolytic cleavage of ENaC, a process in which the ENaC protein is cut by enzymes called proteases at specific sites on the protein. This limited cleavage causes ENaC to become active. When the team analyzed the cells' behavior, they found that ENaC was more likely to have undergone cleavage in cells from CF tissue.
According to Dr. Gentzsch, these observations prompted two questions. First, what role does CFTR play in regulating ENaC cleavage? Second, why is ENaC cleavage not regulated in CF?
"CFTR binds to ENaC, so our initial thought was that close contact of ENaC to CFTR protects ENaC from being cleaved. But another possibility is that CFTR is responsible for suppressing ENaC cleavage and activation," said Dr. Gentzsch. In other words, the absence of a normally functioning CFTR protein may cause ENaC overactivity. Because there is more cleavage when the CFTR mutation is present, it implies that healthy CFTR prevents ENaC cleavage and activation, but defective CFTR does not.
Either way, Dr. Gentzsch feels that both CFTR and ENaC should be considered when developing therapies for CF. "Successful treatments should address both decreased CFTR function and increased salt absorption caused by ENaC overactivity."
**Source: American Physiological Society
Ion Transport Processes in CF
Cystic fibrosis is caused by a mutation in the gene that encodes a protein called cystic fibrosis transmembrane conductance regulator (CFTR), which functions as a chloride channel at the surface of airways and moves chloride out of the cells. CFTR also regulates another protein called epithelial sodium channel (ENaC), which is responsible for transporting sodium into cells. Thus far, scientists have been able to establish that when the CFTR mutation is present, ENaC becomes overactive and causes the cells in the lungs to absorb too much sodium. Water follows the sodium from the cells' surfaces into the cells, and as a result, the airways become dry and mucous becomes thick and sticky, leading to infections in the lungs.
To observe how CFTR regulates ENaC, Dr. Gentzsch and her team took cells from healthy lung tissue and CF lung tissue and maintained them in a liquid medium. The cells' surfaces were exposed to air, which prompted the cells to grow and behave as though they were still inside human lungs. Then the team studied proteolytic cleavage of ENaC, a process in which the ENaC protein is cut by enzymes called proteases at specific sites on the protein. This limited cleavage causes ENaC to become active. When the team analyzed the cells' behavior, they found that ENaC was more likely to have undergone cleavage in cells from CF tissue.
According to Dr. Gentzsch, these observations prompted two questions. First, what role does CFTR play in regulating ENaC cleavage? Second, why is ENaC cleavage not regulated in CF?
"CFTR binds to ENaC, so our initial thought was that close contact of ENaC to CFTR protects ENaC from being cleaved. But another possibility is that CFTR is responsible for suppressing ENaC cleavage and activation," said Dr. Gentzsch. In other words, the absence of a normally functioning CFTR protein may cause ENaC overactivity. Because there is more cleavage when the CFTR mutation is present, it implies that healthy CFTR prevents ENaC cleavage and activation, but defective CFTR does not.
Either way, Dr. Gentzsch feels that both CFTR and ENaC should be considered when developing therapies for CF. "Successful treatments should address both decreased CFTR function and increased salt absorption caused by ENaC overactivity."
**Source: American Physiological Society
Scientists disarm HIV in step towards vaccine
Researchers have found a way to prevent HIV from damaging the immune system, in a new lab-based study published in the journal Blood. The research, led by scientists at Imperial College London and Johns Hopkins University, could have important implications for the development of HIV vaccines. HIV/AIDS is the third biggest cause of death in low income countries, killing around 1.8 million people a year worldwide. An estimated 2.6 million people became infected with HIV in 2009.
The research shows that HIV is unable to damage the immune system if cholesterol is removed from the virus's membrane. Usually, when a person becomes infected, the body's innate immune response provides an immediate defence. However, some researchers believe that HIV causes the innate immune system to overreact and that this weakens the immune system's next line of defence, known as the adaptive immune response.
In the new study, the researchers removed cholesterol from the membrane surrounding the virus and found that this stopped HIV from triggering the innate immune response. This led to a stronger adaptive response, orchestrated by immune cells called T cells. These results support the idea that HIV overstimulates the innate response and that this weakens the immune system.
Dr Adriano Boasso, first author of the study, from Imperial College London, said: "HIV is very sneaky. It evades the host's defences by triggering overblown responses that damage the immune system. It's like revving your car in first gear for too long. Eventually the engine blows out.
"This may be one reason why developing a vaccine has proven so difficult. Most vaccines prime the adaptive response to recognise the invader, but it's hard for this to work if the virus triggers other mechanisms that weaken the adaptive response."
HIV takes its membrane from the cell that it infects. This membrane contains cholesterol, which helps to keep it fluid. The fluidity of the membrane enables the virus to interact with particular types of cell. Cholesterol in the cell membrane is not connected to cholesterol in the blood, which is a risk factor for heart disease but is not linked to HIV.
Normally, a subset of immune cells called plasmacytoid dendritic cells (pDCs) recognise HIV quickly and react by producing signalling molecules called interferons. These signals activate various processes which are initially helpful, but which damage the immune system if switched on for too long.
In collaboration with researchers at Johns Hopkins University, the University of Milan and Innsbruck University, Dr Boasso's group at Imperial have discovered that if cholesterol is removed from HIV's envelope, it can no longer activate pDCs. As a consequence, T cells, which orchestrate the adaptive response, can fight the virus more effectively.
The researchers removed cholesterol using varying concentrations of beta-cyclodextrin (bCD), a derivative of starch that binds cholesterol. Using high levels of bCD they produced a virus with a large hole in its envelope. This permeabilised virus was not infectious and could not activate pDCs, but was still recognised by T cells. Dr Boasso and his colleagues are now looking to investigate whether this inactivated virus could be developed into a vaccine.
"It's like an army that has lost its weapons but still has flags, so another army can recognise it and attack it," he said.
The research was funded by the Wellcome Trust and the National Institutes of Health.
**Source: Imperial College London
The research shows that HIV is unable to damage the immune system if cholesterol is removed from the virus's membrane. Usually, when a person becomes infected, the body's innate immune response provides an immediate defence. However, some researchers believe that HIV causes the innate immune system to overreact and that this weakens the immune system's next line of defence, known as the adaptive immune response.
In the new study, the researchers removed cholesterol from the membrane surrounding the virus and found that this stopped HIV from triggering the innate immune response. This led to a stronger adaptive response, orchestrated by immune cells called T cells. These results support the idea that HIV overstimulates the innate response and that this weakens the immune system.
Dr Adriano Boasso, first author of the study, from Imperial College London, said: "HIV is very sneaky. It evades the host's defences by triggering overblown responses that damage the immune system. It's like revving your car in first gear for too long. Eventually the engine blows out.
"This may be one reason why developing a vaccine has proven so difficult. Most vaccines prime the adaptive response to recognise the invader, but it's hard for this to work if the virus triggers other mechanisms that weaken the adaptive response."
HIV takes its membrane from the cell that it infects. This membrane contains cholesterol, which helps to keep it fluid. The fluidity of the membrane enables the virus to interact with particular types of cell. Cholesterol in the cell membrane is not connected to cholesterol in the blood, which is a risk factor for heart disease but is not linked to HIV.
Normally, a subset of immune cells called plasmacytoid dendritic cells (pDCs) recognise HIV quickly and react by producing signalling molecules called interferons. These signals activate various processes which are initially helpful, but which damage the immune system if switched on for too long.
In collaboration with researchers at Johns Hopkins University, the University of Milan and Innsbruck University, Dr Boasso's group at Imperial have discovered that if cholesterol is removed from HIV's envelope, it can no longer activate pDCs. As a consequence, T cells, which orchestrate the adaptive response, can fight the virus more effectively.
The researchers removed cholesterol using varying concentrations of beta-cyclodextrin (bCD), a derivative of starch that binds cholesterol. Using high levels of bCD they produced a virus with a large hole in its envelope. This permeabilised virus was not infectious and could not activate pDCs, but was still recognised by T cells. Dr Boasso and his colleagues are now looking to investigate whether this inactivated virus could be developed into a vaccine.
"It's like an army that has lost its weapons but still has flags, so another army can recognise it and attack it," he said.
The research was funded by the Wellcome Trust and the National Institutes of Health.
**Source: Imperial College London
Un estudio japonés indica que el riesgo de demencia se duplica con la diabetes
Mayor riesgo cardiovascular y ahora también más probabilidades de demencia. Según un estudio publicado en 'Neurology', las personas con diabetes son dos veces más propensas al deterioro cognitivo que aquellas que tienen niveles normales de azúcar.
Entre los estudios realizados hasta la fecha, algunos confirman la diabetes como un factor de riesgo independiente de cualquier tipo de demencia, otros sólo encuentran asociación con la enfermedad de Alzheimer y otros no confirman ninguna relación. Con el objetivo de resolver esta disparidad de resultados, señalan los autores de la actual investigación, "hemos realizado un análisis prospectivo con un total de 1.017 japoneses (a partir de los 60 años) durante 15 años (de 1988 a 2003)".
Se sometieron a pruebas de tolerancia a la glucosa para determinar si tenían diabetes y además, en el transcurso del estudio, también fueron monitorizados para evaluar su función cognitiva a través de técnicas de neuroimagen.
"El desarrollo de este tipo de estudios tan largos resulta muy difícil de hacer. Se trata de un buen trabajo que refuerza la hipótesis que vincula la intolerancia a la glucosa con el deterioro cognitivo", señala Ambrosio Miralles, jefe de sección de Neurología del Hospital Infanta Sofía de Madrid. Una de las pocas limitaciones que tiene, añade, es que las clasificaciones que utilizan para diagnosticar la demencia y la diabetes son de hace más de 20 años.
En total, 232 pacientes desarrollaron demencia (105 con Alzheimer, 65 con demencia vascular y 62 con otros tipos de demencia). Según las conclusiones de esta investigación, los individuos con diabetes tenían un riesgo casi del doble de sufrir deterioro cognitivo en los siguientes 15 años.
Los investigadores también valoraron la influencia que podían tener otros factores de riesgo, como la hipertensión, el colesterol, el índice de masa corporal, la actividad física, el tabaco o el consumo de alcohol, pero los resultados continuaron en la misma línea. "Las probabilidades de demencia seguían siendo más altas para las personas con diabetes y también para aquellas que no tenían esta enfermedad, pero sí un estado inicial de intolerancia a la glucosa".
La razón, tal y como explican los expertos, basándose en estudios previos, estriba en que "las personas con diabetes tienen alta cantidad de un tipo de toxinas que favorecen la formación de placas amiloide y ovillos característicos del Alzheimer". Otra de las hipótesis, apunta el neurólogo español, es que altos niveles de azúcar pueden producir daños vasculares responsables de la demencia vascular.
La asociación entre este último tipo de deterioro cognitivo y la diabetes se mostró más débil en este estudio, "puede deberse a los pocos casos que observamos de demencia vascular". En cualquier caso, añaden los autores, aunque queda claro su papel como factor independiente, "la diabetes, a través de otros desencadenantes como la hipertensión, sí que incrementa las probabilidades de esta alteración".
-Factor de riesgo modificable
Este hallazgo "subraya la necesidad de considerar la diabetes como un factor de riesgo independiente para todos los tipos de demencia y, probablemente también de la vascular", asegura el principal autor de la investigación, Yutaka Kiyohara, de la Universidad de Kyushu (Fukuoka, Japón). "Se trata de una alteración muy común que afecta cada vez a más personas".
Según la Encuesta Europea sobre Calidad de Vida de estos pacientes -presentada en el Congreso Europeo de Diabetes que se celebra estos días en Lisboa (Portugal)-, hasta un 40% de los afectados no tiene controlada su enfermedad.
"Están tratados, pero no controlados", explica Olga González, médico adjunto del servicio de Endocrinología del Hospital Ramón y Cajal de Madrid, que participa estos días en dicho congreso. "Bien por un cambio de tratamiento, a la hora de subir las dosis, por un mal cumplimiento de la dieta o la medicación o por la inercia de muchos médicos que a veces tardan varios años (una media de 2,3) en cambiar de fármaco".
Dado el riesgo cardiovascular que entraña y las probabilidades de demencia que conlleva, aseveran los investigadores japoneses, controlar la diabetes es ahora más importante que nunca.
**publicado en "EL MUNDO"
Entre los estudios realizados hasta la fecha, algunos confirman la diabetes como un factor de riesgo independiente de cualquier tipo de demencia, otros sólo encuentran asociación con la enfermedad de Alzheimer y otros no confirman ninguna relación. Con el objetivo de resolver esta disparidad de resultados, señalan los autores de la actual investigación, "hemos realizado un análisis prospectivo con un total de 1.017 japoneses (a partir de los 60 años) durante 15 años (de 1988 a 2003)".
Se sometieron a pruebas de tolerancia a la glucosa para determinar si tenían diabetes y además, en el transcurso del estudio, también fueron monitorizados para evaluar su función cognitiva a través de técnicas de neuroimagen.
"El desarrollo de este tipo de estudios tan largos resulta muy difícil de hacer. Se trata de un buen trabajo que refuerza la hipótesis que vincula la intolerancia a la glucosa con el deterioro cognitivo", señala Ambrosio Miralles, jefe de sección de Neurología del Hospital Infanta Sofía de Madrid. Una de las pocas limitaciones que tiene, añade, es que las clasificaciones que utilizan para diagnosticar la demencia y la diabetes son de hace más de 20 años.
En total, 232 pacientes desarrollaron demencia (105 con Alzheimer, 65 con demencia vascular y 62 con otros tipos de demencia). Según las conclusiones de esta investigación, los individuos con diabetes tenían un riesgo casi del doble de sufrir deterioro cognitivo en los siguientes 15 años.
Los investigadores también valoraron la influencia que podían tener otros factores de riesgo, como la hipertensión, el colesterol, el índice de masa corporal, la actividad física, el tabaco o el consumo de alcohol, pero los resultados continuaron en la misma línea. "Las probabilidades de demencia seguían siendo más altas para las personas con diabetes y también para aquellas que no tenían esta enfermedad, pero sí un estado inicial de intolerancia a la glucosa".
La razón, tal y como explican los expertos, basándose en estudios previos, estriba en que "las personas con diabetes tienen alta cantidad de un tipo de toxinas que favorecen la formación de placas amiloide y ovillos característicos del Alzheimer". Otra de las hipótesis, apunta el neurólogo español, es que altos niveles de azúcar pueden producir daños vasculares responsables de la demencia vascular.
La asociación entre este último tipo de deterioro cognitivo y la diabetes se mostró más débil en este estudio, "puede deberse a los pocos casos que observamos de demencia vascular". En cualquier caso, añaden los autores, aunque queda claro su papel como factor independiente, "la diabetes, a través de otros desencadenantes como la hipertensión, sí que incrementa las probabilidades de esta alteración".
-Factor de riesgo modificable
Este hallazgo "subraya la necesidad de considerar la diabetes como un factor de riesgo independiente para todos los tipos de demencia y, probablemente también de la vascular", asegura el principal autor de la investigación, Yutaka Kiyohara, de la Universidad de Kyushu (Fukuoka, Japón). "Se trata de una alteración muy común que afecta cada vez a más personas".
Según la Encuesta Europea sobre Calidad de Vida de estos pacientes -presentada en el Congreso Europeo de Diabetes que se celebra estos días en Lisboa (Portugal)-, hasta un 40% de los afectados no tiene controlada su enfermedad.
"Están tratados, pero no controlados", explica Olga González, médico adjunto del servicio de Endocrinología del Hospital Ramón y Cajal de Madrid, que participa estos días en dicho congreso. "Bien por un cambio de tratamiento, a la hora de subir las dosis, por un mal cumplimiento de la dieta o la medicación o por la inercia de muchos médicos que a veces tardan varios años (una media de 2,3) en cambiar de fármaco".
Dado el riesgo cardiovascular que entraña y las probabilidades de demencia que conlleva, aseveran los investigadores japoneses, controlar la diabetes es ahora más importante que nunca.
**publicado en "EL MUNDO"
Mammography use up for US immigrants
While mammography rates have improved among foreign-born women residing in the United States, these women are still less likely to have undergone breast cancer screening than native-born U.S. women. These study results were presented at the Fourth AACR Conference on The Science of Cancer Health Disparities, held Sept. 18-21, 2011, in Washington, D.C.
Researchers at Pennsylvania State University believe that lack of access to health insurance and a regular source of health care are important factors related to the lower percentage of mammography screening among U.S. immigrants.
"There is progress, overall, in use of mammography among foreign-born women in the United States, but there is still a lot of work to do to improve their use of recommended breast cancer screening," said the study's lead researcher Nengliang (Aaron) Yao, a doctoral student in health policy and administration.
Yao and colleagues used data from the 2000 and 2008 National Health Interview Survey, conducted by the National Center for Health Statistics and administered by the U.S. Census Bureau, to look at mammography screening among immigrants and factors associated with use. Information on immigrants' legal status was not included in the survey.
Screening rates among immigrants increased from about 60.2 percent in 2000 to 65.5 percent in 2008, and disparities in the use of mammography between immigrants and native women narrowed from 11.2 percent in 2000 to 3.4 percent in 2008.
Immigrants who resided in the United States a decade or longer had markedly higher mammography rates compared to those who had been in the country less than a decade (64.7 percent versus 39.3 percent in 2000; 67.9 percent versus 55.7 percent in 2008).
Insurance coverage played an important role in predicting who would receive screening. By 2008, immigrant women with public insurance had odds of receiving a mammogram that were twice those of uninsured immigrant women, Yao said, and those with private insurance had odds more than 2.5 times higher than uninsured women.
In addition, having a regular source of health care also became a more important predictor of mammography use over time. In 2008, women with a regular source of care had odds of receiving screening that were more than twice as high as those for women without a regular source of care.
Yao added that there has been an increase in "culturally and linguistically appropriate subsidized programs," such as those developed by the CDC's National Breast and Cervical Cancers Early Detection Program that encourage foreign-born women to seek a mammogram, which may have led to increased use of the test.
"As much progress as we have made, we still need to improve access to mammography screening for immigrant women, as well as for women overall," he said.
*Source: American Association for Cancer Research
Researchers at Pennsylvania State University believe that lack of access to health insurance and a regular source of health care are important factors related to the lower percentage of mammography screening among U.S. immigrants.
"There is progress, overall, in use of mammography among foreign-born women in the United States, but there is still a lot of work to do to improve their use of recommended breast cancer screening," said the study's lead researcher Nengliang (Aaron) Yao, a doctoral student in health policy and administration.
Yao and colleagues used data from the 2000 and 2008 National Health Interview Survey, conducted by the National Center for Health Statistics and administered by the U.S. Census Bureau, to look at mammography screening among immigrants and factors associated with use. Information on immigrants' legal status was not included in the survey.
Screening rates among immigrants increased from about 60.2 percent in 2000 to 65.5 percent in 2008, and disparities in the use of mammography between immigrants and native women narrowed from 11.2 percent in 2000 to 3.4 percent in 2008.
Immigrants who resided in the United States a decade or longer had markedly higher mammography rates compared to those who had been in the country less than a decade (64.7 percent versus 39.3 percent in 2000; 67.9 percent versus 55.7 percent in 2008).
Insurance coverage played an important role in predicting who would receive screening. By 2008, immigrant women with public insurance had odds of receiving a mammogram that were twice those of uninsured immigrant women, Yao said, and those with private insurance had odds more than 2.5 times higher than uninsured women.
In addition, having a regular source of health care also became a more important predictor of mammography use over time. In 2008, women with a regular source of care had odds of receiving screening that were more than twice as high as those for women without a regular source of care.
Yao added that there has been an increase in "culturally and linguistically appropriate subsidized programs," such as those developed by the CDC's National Breast and Cervical Cancers Early Detection Program that encourage foreign-born women to seek a mammogram, which may have led to increased use of the test.
"As much progress as we have made, we still need to improve access to mammography screening for immigrant women, as well as for women overall," he said.
*Source: American Association for Cancer Research
Londres: Termina con éxito la separación de dos bebés sudaneses unidos por la cabeza
Los médicos del hospital londinense Great Ormond Street han conseguido separar con éxito a dos niñas siamesas sudanesas de once meses de edad que estaban unidas por la cabeza, según informó este lunes el diario británico «The Guardian».
Ritag y Rital Gaboura han sido sometidas a cuatro operaciones de alto riesgo, dos en mayo, una en julio y la última el pasado 15 de agosto. Las dos niñas habían nacido mediante cesárea el 22 de septiembre de 2010 en Jartum, capital de Sudán, y fueron trasladadas el pasado mes de abril en un avión a Londres gracias al apoyo de la organización caritativa Facing the World.
Los nacimientos de bebés unidos por la cabeza («craneópagos») suceden en uno de cada 2,5 millones de nacimientos. La operación de separación es particularmente peligrosa por la gran cantidad de sangre que fluye entre los dos cerebros.
No obstante, si no se opera los riesgos son también grandes, dado que la sangre casi nunca circula de forma uniforme y cabe la posibilidad de que el corazón del hermano más fuerte acabe succionando la sangre del otro.
Según Facing the World, la tasa de supervivencia de este tipo de siameses después de la infancia es de uno por cada diez millones, El corazón de Ritag, añadió, ya había empezado a sufrir problemas graves cuando la familia llegó a Reino Unido.
«La supervivencia de los gemelos en estas condiciones es extremadamente escasa», declaró el cirujano jefe, David Dunaway. «La operación presentaba innumerables problemas y todos éramos conscientes de nuestra responsabilidad ante la familia y ante las dos pequeñas», agregó.
Las operaciones, pese a su éxito y pese a que no presentó complicaciones especiales, pueden dejar secuelas neurológicas, pero los expertos esperan que Rital y Ritag gocen de buena salud.
«Dentro de algunos días, las gemelas regresarán a la planta normal y jugarán como siempre», declaró Sarah Driver-Jowitt, de Facing the World. Los dos padres -cuyas identidades no han sido reveladas- regresarán pronto a casa «con dos niñas sanas y separadas», manifestó.
Ritag y Rital Gaboura han sido sometidas a cuatro operaciones de alto riesgo, dos en mayo, una en julio y la última el pasado 15 de agosto. Las dos niñas habían nacido mediante cesárea el 22 de septiembre de 2010 en Jartum, capital de Sudán, y fueron trasladadas el pasado mes de abril en un avión a Londres gracias al apoyo de la organización caritativa Facing the World.
Los nacimientos de bebés unidos por la cabeza («craneópagos») suceden en uno de cada 2,5 millones de nacimientos. La operación de separación es particularmente peligrosa por la gran cantidad de sangre que fluye entre los dos cerebros.
No obstante, si no se opera los riesgos son también grandes, dado que la sangre casi nunca circula de forma uniforme y cabe la posibilidad de que el corazón del hermano más fuerte acabe succionando la sangre del otro.
Según Facing the World, la tasa de supervivencia de este tipo de siameses después de la infancia es de uno por cada diez millones, El corazón de Ritag, añadió, ya había empezado a sufrir problemas graves cuando la familia llegó a Reino Unido.
«La supervivencia de los gemelos en estas condiciones es extremadamente escasa», declaró el cirujano jefe, David Dunaway. «La operación presentaba innumerables problemas y todos éramos conscientes de nuestra responsabilidad ante la familia y ante las dos pequeñas», agregó.
Las operaciones, pese a su éxito y pese a que no presentó complicaciones especiales, pueden dejar secuelas neurológicas, pero los expertos esperan que Rital y Ritag gocen de buena salud.
«Dentro de algunos días, las gemelas regresarán a la planta normal y jugarán como siempre», declaró Sarah Driver-Jowitt, de Facing the World. Los dos padres -cuyas identidades no han sido reveladas- regresarán pronto a casa «con dos niñas sanas y separadas», manifestó.
**AGENCIAS Y FOTO DE "REUTERS"
To ditch dessert, feed the brain
If the brain goes hungry, Twinkies look a lot better, a study led by researchers at Yale University and the University of Southern California has found. Brain imaging scans show that when glucose levels drop, an area of the brain known to regulate emotions and impulses loses the ability to dampen desire for high-calorie food, according to the study published online September 19 in The Journal of Clinical Investigation.
"Our prefrontal cortex is a sucker for glucose," said Rajita Sinha, the Foundations Fund Professor of Psychiatry, and professor in the Department of Neurobiology and the Yale Child Study Center, one of the senior authors of the research.
The Yale team manipulated glucose levels intravenously and monitored changes in blood sugar levels while subjects were shown pictures of high-calorie food, low-calorie food and non-food as they underwent fMRI scans.
When glucose levels drop, an area of the brain called the hypothalamus senses the change. Other regions called the insula and striatum associated with reward are activated, inducing a desire to eat, the study found. The most pronounced reaction to reduced glucose levels was seen in the prefrontal cortex. When glucose is lowered, the prefrontal cortex seemed to lose its ability to put the brakes upon increasingly urgent signals to eat generated in the striatum. This weakened response was particularly striking in the obese when shown high-calorie foods.
"This response was quite specific and more dramatic in the presence of high-calorie foods," Sinha said.
"Our results suggest that obese individuals may have a limited ability to inhibit the impulsive drive to eat, especially when glucose levels drop below normal," commented Kathleen Page, assistant professor of medicine at the University of Southern California and one of the lead authors of the paper.
A similarly robust response to high-calorie food was also seen in the striatum, which became hyperactive when glucose was reduced. However, the levels of the stress hormone cortisol seemed to play a more significant role than glucose in activating the brain's reward centers, note the researchers. Sinha suggests that the stress associated with glucose drops may play a key role in activating the striatum.
"The key seems to be eating healthy foods that maintain glucose levels," Sinha said. "The brain needs its food."
"Our prefrontal cortex is a sucker for glucose," said Rajita Sinha, the Foundations Fund Professor of Psychiatry, and professor in the Department of Neurobiology and the Yale Child Study Center, one of the senior authors of the research.
The Yale team manipulated glucose levels intravenously and monitored changes in blood sugar levels while subjects were shown pictures of high-calorie food, low-calorie food and non-food as they underwent fMRI scans.
When glucose levels drop, an area of the brain called the hypothalamus senses the change. Other regions called the insula and striatum associated with reward are activated, inducing a desire to eat, the study found. The most pronounced reaction to reduced glucose levels was seen in the prefrontal cortex. When glucose is lowered, the prefrontal cortex seemed to lose its ability to put the brakes upon increasingly urgent signals to eat generated in the striatum. This weakened response was particularly striking in the obese when shown high-calorie foods.
"This response was quite specific and more dramatic in the presence of high-calorie foods," Sinha said.
"Our results suggest that obese individuals may have a limited ability to inhibit the impulsive drive to eat, especially when glucose levels drop below normal," commented Kathleen Page, assistant professor of medicine at the University of Southern California and one of the lead authors of the paper.
A similarly robust response to high-calorie food was also seen in the striatum, which became hyperactive when glucose was reduced. However, the levels of the stress hormone cortisol seemed to play a more significant role than glucose in activating the brain's reward centers, note the researchers. Sinha suggests that the stress associated with glucose drops may play a key role in activating the striatum.
"The key seems to be eating healthy foods that maintain glucose levels," Sinha said. "The brain needs its food."
**Source: Yale University
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