La farmacéutica Pfizer Inc ha anunciado en un comunicado que retira alrededor de un millón de paquetes de píldoras para controlar la natalidad en Estados Unidos porque podrían contener una cantidad de anticonceptivos insuficiente para evitar embarazos.
La compañía precisa que las píldoras no suponen un peligro para la salud pero ha instado a las mujeres afectadas a "empezar a usar de inmediato algún tipo de tratamiento anticonceptivo no hormonal". Según Pfizer, el problema afecta a 14 lotes de Lo/Ovral-28 y otros 14 de pastillas de Norgestrel y Ethinyl Esrtadiol.
Las cajas de estos fármacos contienen 28 píldoras, 21 pastillas con anticonceptivo y otras siete como placebo. El problema es que en algunos paquetes se incluyeron más de esas 21 píldoras activas y en otros se incluyeron menos.
En algunos paquetes se incluyeron más de 21 píldoras activas y en otros se incluyeron menos
Un portavoz de la empresa ha asegurado que la confusión se debio tanto a un fallo mecánico como a un error de supervisión ocular. La fecha de caducidad de las cajas van del 31 de julio dde 2013 al 31 de marzo de 2014.
La cifra de un millón de cajas afectadas la precisó en un correo electrónico al margen del comunicado Grace Ann Arnold, portavoz de la empresa, según informa Bloomberg.
Las pastillas supuestamente defectuosas fueron manofacturadas por Pfiser y comercializadas por Akrimax Pharmaceuticals y enviadas a almacenes, clínicas y farmacias de todo el país. En su comunicado Pfizer precisa que los lotes defectuosos se restringieron al mercado de EE UU.
01 February 2012
Websites que facilitan la búsqueda de problemas asociados a miles de fármacos
Dos páginas lanzadas en 2011 han abierto nuevas posibilidades a los pacientes (y sus médicos) que quieren reunir toda la información disponible sobre su tratamiento. Las páginas ordenan y hacen accesible información clave de la FDA.
Los fabricantes de fármacos y de dispositivos médicos tienen la obligación de informar de los problemas que registren en la llamada fase IV, la que se desarrolla una vez el medicamento está en el mercado. En el caso de los pacientes es voluntario. En 2010, según los datos publicados por 'The Wall Street Journal', hubo 759.000 notificaciones de fármacos y 238.000 de dispositivos.
La FDA recopila esta información, pero la falta de referencias claras y unívocas en la base de datos y el sistema de divulgación de las alertas complica el rastreo de la base de datos a los usuarios no especializados. A menudo, además, las enfermedades, los medicamentos (tanto el nombre comercial como el principio activo) y las dosis tienen errores ortográficos.
Adverse Events ha desarrollado un algoritmo que limpia los registros y facilita el acceso a la información a través de una sencilla búsqueda. De esta forma, 200.000 nombres de medicamentos se redujeron a 4.500. El servicio básico es gratuito y el acceso a informe completos costará 10 dólares al mes. La base de datos comprende miles de enfermedades y efectos secundarios desde 2004.
Clarimed ofrece un servicio similar, pero especializado en dispositivos médicos. La página reúne información sobre efectos adversos de 125.000 dispositivos médicos como marcapasos o 'stent'.
Las dos compañías se presentan como una nueva generación de servicios para el paciente informado.
"La mejor manera de producir mejoras en la calidad [de los tratamientos] es hacer las cosas cristalinas y tan transparentes como sea posible", dice al diario económico Nora Illuri, de Clarimed.
Los fabricantes de fármacos y de dispositivos médicos tienen la obligación de informar de los problemas que registren en la llamada fase IV, la que se desarrolla una vez el medicamento está en el mercado. En el caso de los pacientes es voluntario. En 2010, según los datos publicados por 'The Wall Street Journal', hubo 759.000 notificaciones de fármacos y 238.000 de dispositivos.
La FDA recopila esta información, pero la falta de referencias claras y unívocas en la base de datos y el sistema de divulgación de las alertas complica el rastreo de la base de datos a los usuarios no especializados. A menudo, además, las enfermedades, los medicamentos (tanto el nombre comercial como el principio activo) y las dosis tienen errores ortográficos.
Adverse Events ha desarrollado un algoritmo que limpia los registros y facilita el acceso a la información a través de una sencilla búsqueda. De esta forma, 200.000 nombres de medicamentos se redujeron a 4.500. El servicio básico es gratuito y el acceso a informe completos costará 10 dólares al mes. La base de datos comprende miles de enfermedades y efectos secundarios desde 2004.
Clarimed ofrece un servicio similar, pero especializado en dispositivos médicos. La página reúne información sobre efectos adversos de 125.000 dispositivos médicos como marcapasos o 'stent'.
Las dos compañías se presentan como una nueva generación de servicios para el paciente informado.
"La mejor manera de producir mejoras en la calidad [de los tratamientos] es hacer las cosas cristalinas y tan transparentes como sea posible", dice al diario económico Nora Illuri, de Clarimed.
**Publicado en "EL MUNDO"
UCLA researchers indentify a cell-permeable peptide that inhibits hepatitis C
Researchers from UCLA's Jonsson Comprehensive Cancer Center have identified a cell-permeable peptide that inhibits a hepatitis C virus protein and blocks viral replication, which can lead to liver cancer and cirrhosis. This finding by Dr. Samuel French, an assistant professor of pathology and senior author of the study, builds on previous work by the French laboratory that identified two cellular proteins that are important factors in hepatitis C virus infection.
French and his team initially set out to identify the cellular factors involved in hepatitis C replication and, using mass spectrometry, found that heat shock proteins (HSPs) 40 and 70 were important for viral infection. HSP70 was previously known to be involved, but HSP40 was linked for the first time to hepatitis C infection, French said. They further showed that the natural compound Quercetin, which inhibits the synthesis of these proteins, significantly inhibits viral infection in tissue culture.
In this study, published Jan. 30, 2012 in the peer-reviewed journal Hepatology, French and his team demonstrated that the viral non-structural protein 5A (NS5A) directly binds to HSP70 and mapped the site of the NS5A/HSP70 complex on NS5A. While HSP70 was previously shown to bind NS5A in cells, a direct NS5A/HSP70 interaction and complex formation was established in this study. In an effort to stop this interaction, they tested peptides that might inhibit HSP70.
"This is important because we've developed a small peptide that binds to that site and blocks the interaction between the proteins that is important for viral replication," French said. "This is another, potentially highly efficacious way to block replication of hepatitis C."
An estimated 160 million people worldwide are infected with hepatitis C and the conventional treatments -- interferon and ribavirin -- can have significant side effects. A new drug targeting cellular proteins rather than viral proteins would be a valuable addition to the treatment arsenal, French said.
"We were surprised that this peptide works this well," French said. "While its mechanism is different, the activity of this peptide is comparable to other newly developed anti-virals."
The study, done in tissue culture, shows that the peptide gains entry into the cell easily and blocks the cascade of cellular events that allows the virus to replicate, French said. Blocking the HSP70 protein rather than a viral protein also reduces the chance of patients with the hepatitis C virus developing resistance to the peptide.
"There's no direct pressure on the virus, so it is less likely to mutate and develop resistance," French said. "The goal is to achieve a sustained response, essentially a cure, meaning there is no more virus replication. There are a lot of drugs coming out now that are designed to stop hepatitis C replication, but resistance is still an issue. About 10 to 20 percent of patients on the new drugs become resistant. This new peptide may help combat resistance."
Going forward, French and his team are testing variants of the newly discovered peptide to see if they can develop one with an even higher affinity and can decrease the size of the peptide to improve cellular penetration and liver targeting. The new and improved peptides will be tested in animal models.
This peptide "may be a candidate for hepatitis C therapy," the study states. "Considering the potency of the peptide in suppressing viral translation levels, treatment with this peptide may significantly improve the efficacy of conventional treatments in patients who become resistant to conventional therapies."
**Source: University of California, Los Angeles (UCLA), Health Sciences
French and his team initially set out to identify the cellular factors involved in hepatitis C replication and, using mass spectrometry, found that heat shock proteins (HSPs) 40 and 70 were important for viral infection. HSP70 was previously known to be involved, but HSP40 was linked for the first time to hepatitis C infection, French said. They further showed that the natural compound Quercetin, which inhibits the synthesis of these proteins, significantly inhibits viral infection in tissue culture.
In this study, published Jan. 30, 2012 in the peer-reviewed journal Hepatology, French and his team demonstrated that the viral non-structural protein 5A (NS5A) directly binds to HSP70 and mapped the site of the NS5A/HSP70 complex on NS5A. While HSP70 was previously shown to bind NS5A in cells, a direct NS5A/HSP70 interaction and complex formation was established in this study. In an effort to stop this interaction, they tested peptides that might inhibit HSP70.
"This is important because we've developed a small peptide that binds to that site and blocks the interaction between the proteins that is important for viral replication," French said. "This is another, potentially highly efficacious way to block replication of hepatitis C."
An estimated 160 million people worldwide are infected with hepatitis C and the conventional treatments -- interferon and ribavirin -- can have significant side effects. A new drug targeting cellular proteins rather than viral proteins would be a valuable addition to the treatment arsenal, French said.
"We were surprised that this peptide works this well," French said. "While its mechanism is different, the activity of this peptide is comparable to other newly developed anti-virals."
The study, done in tissue culture, shows that the peptide gains entry into the cell easily and blocks the cascade of cellular events that allows the virus to replicate, French said. Blocking the HSP70 protein rather than a viral protein also reduces the chance of patients with the hepatitis C virus developing resistance to the peptide.
"There's no direct pressure on the virus, so it is less likely to mutate and develop resistance," French said. "The goal is to achieve a sustained response, essentially a cure, meaning there is no more virus replication. There are a lot of drugs coming out now that are designed to stop hepatitis C replication, but resistance is still an issue. About 10 to 20 percent of patients on the new drugs become resistant. This new peptide may help combat resistance."
Going forward, French and his team are testing variants of the newly discovered peptide to see if they can develop one with an even higher affinity and can decrease the size of the peptide to improve cellular penetration and liver targeting. The new and improved peptides will be tested in animal models.
This peptide "may be a candidate for hepatitis C therapy," the study states. "Considering the potency of the peptide in suppressing viral translation levels, treatment with this peptide may significantly improve the efficacy of conventional treatments in patients who become resistant to conventional therapies."
**Source: University of California, Los Angeles (UCLA), Health Sciences
Reino Unido: Prohíben un anuncio que borra las arrugas de Rachel Weisz
El regulador de publicidad del Reino Unido ha prohibido un anuncio de una revista de cosméticos francesa L'Oreal que promociona una crema antiarrugas con una fotografía del rostro de la actriz británica Rachel Weisz.
El anuncio a doble página, publicado por primera vez en septiembre, mostró la cara de la actriz en primer plano y en blanco y negro, con una lista de 10 supuestos efectos beneficiosos de la reparación de la crema Revitalift 10.
La parlamentaria liberal demócrata Jo Swinson, que hizo campaña sobre la imagen, ha presentado una demanda contra L'Oreal, acusando a la empresa de haber retocado la imagen, engañando a los consumidores acerca de los efectos del producto.
El regulador ASA (Advertising Standards Authority), si bien reconoce que la foto parecía representar con precisión el brillo y el estado de las arrugas faciales de la actriz, consideró que "la imagen ha sido modificada a fin de cambiar sustancialmente su la piel para que parezca más suave y tersa". ASA ha concluido que el anuncio "exagera el rendimiento del producto" y podría inducir a error al consumidor.
la parlamentaria ha celebrado esta decisión, que prohíbe el uso de nuevo Oréal este anuncio. "La industria de la belleza y la publicidad debe dejar de engañar a los consumidores con imágenes engañosas", ha agregado.
El anuncio a doble página, publicado por primera vez en septiembre, mostró la cara de la actriz en primer plano y en blanco y negro, con una lista de 10 supuestos efectos beneficiosos de la reparación de la crema Revitalift 10.
La parlamentaria liberal demócrata Jo Swinson, que hizo campaña sobre la imagen, ha presentado una demanda contra L'Oreal, acusando a la empresa de haber retocado la imagen, engañando a los consumidores acerca de los efectos del producto.
El regulador ASA (Advertising Standards Authority), si bien reconoce que la foto parecía representar con precisión el brillo y el estado de las arrugas faciales de la actriz, consideró que "la imagen ha sido modificada a fin de cambiar sustancialmente su la piel para que parezca más suave y tersa". ASA ha concluido que el anuncio "exagera el rendimiento del producto" y podría inducir a error al consumidor.
la parlamentaria ha celebrado esta decisión, que prohíbe el uso de nuevo Oréal este anuncio. "La industria de la belleza y la publicidad debe dejar de engañar a los consumidores con imágenes engañosas", ha agregado.
*AFP
Massachusetts General study defines a new genetic subtype of lung cancer
A report from investigators at the Massachusetts General Hospital (MGH) Cancer Center has defined the role of a recently identified gene abnormality in a deadly form of lung cancer. Tumors driven by rearrangements in the ROS1 gene represent 1 to 2 percent of non-small-cell lung cancers (NSCLC), the leading cause of cancer death in the U.S. The researchers show that ROS1-driven tumors can be treated with crizotinib, which also inhibits the growth of tumors driven by an oncogene called ALK, and describe the remarkable response of one patient to crizotinib treatment. "ROS1 encodes a protein that is important for cell growth and survival, and deregulation of ROS1 through chromosomal rearrangement drives the growth of tumors," says Alice Shaw, MD, PhD, of the MGH Cancer Center -- co-lead author of the paper which has been published online in the Journal of Clinical Oncology. "This finding is important because we have drugs that inhibit ROS1 and could lead to the sort of dramatic clinical response we describe in this paper."
The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.
The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.
An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.
"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.
Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.
**Source: Massachusetts General Hospital
The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.
The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.
An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.
"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.
Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.
**Source: Massachusetts General Hospital
Según un estudio el 36% de los varones japoneses se muestra «indiferente o reacio» a mantener relaciones sexuales
Aunque se encuentren en una edad de gran ebullición hormonal, los japoneses de entre 16 y 19 años se muestran poco interesados por el sexo. Eso es al menos lo que se desprende de un estudio publicado por la Asociación de la Planificación Familiar de Japón. Un 36% de los varones entre 16 y 19 años encuestados se muestran indiferentes o reacios a mantener relaciones sexuales. Estos datos significan un incremento de un 19% con respecto a los regsitrados en 2008. Pero la indiferencia se extiende también entre la población femenina. Aunque no aparecen en la encuesta, se deduce que las chicas esto del sexo las deja todavía más frías.
El estudio también ha abordado la vida sexual de las parejas casadas. Aproximadamente el 40% de los casados no habían tenido relaciones sexuales en el último mes, un aumento del 4% de la misma encuesta realizada dos años antes y casi un 10% más que en 2004.
Este tipo de conductas constituyen un verdadero problema en Japón, país que tiene una de las tasas de natalidad más bajas del mundo y una de la poblaciones más envejecidas.
El estudio también ha abordado la vida sexual de las parejas casadas. Aproximadamente el 40% de los casados no habían tenido relaciones sexuales en el último mes, un aumento del 4% de la misma encuesta realizada dos años antes y casi un 10% más que en 2004.
Este tipo de conductas constituyen un verdadero problema en Japón, país que tiene una de las tasas de natalidad más bajas del mundo y una de la poblaciones más envejecidas.
Surprise finding redraws 'map' of blood cell production
A study of the cells that respond to crises in the blood system has yielded a few surprises, redrawing the 'map' of how blood cells are made in the body. The finding, by researchers from the Walter and Eliza Hall Institute, could have wide-ranging implications for understanding blood diseases such as myeloproliferative disorders (that cause excess production of blood cells) as well as used to develop new ways of controlling how blood and clotting cells are produced.
The research team, led by Drs Ashley Ng and Maria Kauppi from the institute's Cancer and Haematology division, investigated subsets of blood 'progenitor' cells and the signals that cause them to expand and develop into mature blood cells. Their results were recently published in the journal Proceedings of the National Academy of Sciences.
Dr Ng describes blood progenitor cells as the 'heavy lifters' of the blood system. "They are the targets for blood cell hormones, called cytokines, which Professor Don Metcalf and colleagues have shown to be critical for regulating blood cell production," Dr Ng said. "In times of stress, such as bleeding, during infection or after chemotherapy, it is really the progenitor cells that respond by replacing lost or damaged blood cells."
Dr Kauppi said the research team was particularly interested in myeloid progenitor cells, which produce megakaryocytes, a type of bone marrow cell that gives rise to blood-clotting platelets. "We used a suite of cell surface markers specific to these progenitor cells that allowed us to isolate and characterise the cells," she said.
The researchers were surprised to find that progenitor cells believed only to be able to produce megakaryocytes were also able to develop into red blood cells.
"We were able to clearly demonstrate that these mouse megakaryocyte progenitor cells have the potential to develop into either megakaryocytes or red blood cells in response to cytokines such as thrombopoietin and erythropoietin, which was quite unexpected," Dr Ng said. "In addition, we discovered that other progenitor populations thought to really only make neutrophils and monocytes [other immune cells], were capable of making red blood cell and platelets really well. In effect, we will have to redraw the map as to how red cells and platelets are made in the bone marrow."
Dr Kauppi said the researchers found they could regulate whether the progenitor cell became a megakaryocyte or a red blood cell by using different combinations of cytokines. "Now that we have properly identified the major cells and determined how they respond to cytokine signals involved in red blood cell and platelet production, the stage is set for understanding how these progenitors are affected in health and disease," she said. "We can also better understand, for instance, how genetic changes may lead to the development of certain blood diseases. "
Dr Ng said the findings would also help researchers discover new ways in which the progenitor cells can be controlled.
"This research is the first step in the future development of treatments for patients with blood diseases," Dr Ng said. "This may occur either by limiting blood cell production when too many are being made, as with myeloproliferative disorders, or stimulating blood production when the blood system is compromised, such as during cancer treatment or infection." Dr Ng said.
The research team, led by Drs Ashley Ng and Maria Kauppi from the institute's Cancer and Haematology division, investigated subsets of blood 'progenitor' cells and the signals that cause them to expand and develop into mature blood cells. Their results were recently published in the journal Proceedings of the National Academy of Sciences.
Dr Ng describes blood progenitor cells as the 'heavy lifters' of the blood system. "They are the targets for blood cell hormones, called cytokines, which Professor Don Metcalf and colleagues have shown to be critical for regulating blood cell production," Dr Ng said. "In times of stress, such as bleeding, during infection or after chemotherapy, it is really the progenitor cells that respond by replacing lost or damaged blood cells."
Dr Kauppi said the research team was particularly interested in myeloid progenitor cells, which produce megakaryocytes, a type of bone marrow cell that gives rise to blood-clotting platelets. "We used a suite of cell surface markers specific to these progenitor cells that allowed us to isolate and characterise the cells," she said.
The researchers were surprised to find that progenitor cells believed only to be able to produce megakaryocytes were also able to develop into red blood cells.
"We were able to clearly demonstrate that these mouse megakaryocyte progenitor cells have the potential to develop into either megakaryocytes or red blood cells in response to cytokines such as thrombopoietin and erythropoietin, which was quite unexpected," Dr Ng said. "In addition, we discovered that other progenitor populations thought to really only make neutrophils and monocytes [other immune cells], were capable of making red blood cell and platelets really well. In effect, we will have to redraw the map as to how red cells and platelets are made in the bone marrow."
Dr Kauppi said the researchers found they could regulate whether the progenitor cell became a megakaryocyte or a red blood cell by using different combinations of cytokines. "Now that we have properly identified the major cells and determined how they respond to cytokine signals involved in red blood cell and platelet production, the stage is set for understanding how these progenitors are affected in health and disease," she said. "We can also better understand, for instance, how genetic changes may lead to the development of certain blood diseases. "
Dr Ng said the findings would also help researchers discover new ways in which the progenitor cells can be controlled.
"This research is the first step in the future development of treatments for patients with blood diseases," Dr Ng said. "This may occur either by limiting blood cell production when too many are being made, as with myeloproliferative disorders, or stimulating blood production when the blood system is compromised, such as during cancer treatment or infection." Dr Ng said.
**Source: Walter and Eliza Hall Institute
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