Decreased nanobacteria levels and symptoms of nanobacteria-associated interstitial cystitis/painful bladder syndrome after tetracycline treatment
Urological Research Institute of PLA, Southwest Hospital, Third Military Medical University,
Chongqing, 400038, People's Republic of China.
This study was designed to detect whether nanobacteria (NB) reside in urine and bladder
tissue samples of patients with interstitial cystitis/painful bladder syndrome (IC/PBS) and
whether antibiotic therapy targeting these organisms is effective in reducing NB levels and
IC/PBS symptoms.
Twenty-seven IC/PBS patients underwent cystoscopy. Bladder biopsies and urine samples
were obtained and cultured for NB, which were identified by indirect immunofluorescent
staining and transmission electron microscopy.
Eleven bladder samples showed growth of microbes that were identified to be similar to NB.
Homologous study of the 16S ribosomal RNA gene suggested that the NB could be the
pathogen. For enrolled 11 patients, NB levels decreased dramatically after tetracycline
treatment, and they reported significant reduction in the severity of IC/PBS symptoms.
A high prevalence of NB was observed in female IC/PBS, and anti-NB treatment effectively
improved the symptoms, which suggest that NB may cause some cases of IC/PBS.
Written by:
Zhang QH, Shen XC, Zhou ZS, Chen ZW, Lu GS, Song B. Are you the author?
Reference:
Int Urogynecol J Pelvic Floor Dysfunct. 2009 Sep 17. Epub ahead of print.
doi:10.1007/s00192-009-0994-7
PubMed Abstract
PMID:19760079
Wednesday, October 14, 2009
Thursday, October 8, 2009
CONSORTIUM OF RESEARCHERS DISCOVER RETROVIRAL LINK TO CHRONIC FATIGUE SYNDROME
From an NIH press release. A very important new finding that a virus may be linked to Chronic Fatigue Syndrome. - BRH
CONSORTIUM OF RESEARCHERS DISCOVER RETROVIRAL LINK TO CHRONIC FATIGUE SYNDROME
Scientists have discovered a potential retroviral link to chronic fatigue syndrome, known as CFS, a debilitating disease that affects millions of people in the United States. Researchers from the Whittemore Peterson Institute (WPI), located at the University of Nevada, Reno, the National Cancer Institute (NCI), part of the National Institutes of Health, and the Cleveland Clinic, report this finding online Oct. 8, 2009, issue of Science.
"We now have evidence that a retrovirus named XMRV is frequently present in the blood of patients with CFS. This discovery could be a major step in the discovery of vital treatment options for millions of patients," said Judy Mikovits, Ph.D., director of research for WPI and leader of the team that discovered this association. Researchers cautioned however, that this finding shows there is an association between XMRV and CFS but does not prove that XMRV causes CFS.
The scientists provide a new hypothesis for a retrovirus link with CFS. The virus, XMRV, was first identified by Robert H. Silverman, Ph.D., professor in the Department of Cancer Biology at the Cleveland Clinic Lerner Research Institute, in men who had a specific immune system defect that reduced their ability to fight viral infections.
"The discovery of XMRV in two major diseases, prostate cancer and now chronic fatigue syndrome, is very exciting. If cause-and-effect is established, there would be a new opportunity for prevention and treatment of these diseases," said Silverman, a co-author on the CFS paper.
Commonality of an immune system defect in patients with CFS and prostate cancer led researchers to look for the virus in their blood samples. In this study, WPI scientists identified XMRV in the blood of 68 of 101 (67 percent) CFS patients. In contrast, they found that eight of 218 healthy people (3.7 percent) contained XMRV DNA. The research team not only found that blood cells contained XMRV but also expressed XMRV proteins at high levels and produced infectious viral particles. A clinically validated test to detect XMRV antibodies in patients' plasma is currently under development.
These results were also supported by the observation of retrovirus particles in patient samples when examined using transmission electron microscopy. The data demonstrate the first direct isolation of infectious XMRV from humans.
"These compelling data allow the development of a hypothesis concerning a cause of this complex and misunderstood disease, since retroviruses are a known cause of neurodegenerative diseases and cancer in man," said Francis Ruscetti, Ph.D., Laboratory of Experimental Immunology, NCI.
Retroviruses like XMRV have also been shown to activate a number of other latent viruses. This could explain why so many different viruses, such as Epstein-Barr virus, which was causally linked to Burkitt's and other lymphomas in the 1970s, have been associated with CFS. It is important to note that retroviruses, like XMRV, are not airborne.
"The scientific evidence that a retrovirus is implicated in CFS opens a new world of possibilities for so many people," said Annette Whittemore, founder and president of WPI and mother of a CFS patient. "Scientists can now begin the important work of translating this discovery into medical care for individuals with XMRV related diseases."
Dan Peterson, M.D., medical director of WPI added, "Patients with CFS deal with a myriad of health issues as their quality of life declines. I'm excited about the possibility of providing patients, who are positive for XMRV, a definitive diagnosis, and hopefully very soon, a range of effective treatments options."
The Whittemore Peterson Institute for Neuro Immune Disease exists to bring discovery, knowledge, and effective treatments to patients with illnesses that are caused by acquired dysregulation of both the immune system and the nervous system, often resulting in lifelong disease and disability. www.wpinstitute.org.
The Lerner Research Institute is home to Cleveland Clinic's laboratory, translational and clinical research. Its mission: to promote human health by investigating in the laboratory and the clinic the causes of disease and discovering novel approaches to prevention and treatments; to train the next generation of biomedical researchers; and to foster productive collaborations with those providing clinical care. More than 1,200 people in 11 departments work in research programs focusing on cardiovascular, cancer, neurologic, musculoskeletal, allergic and immunologic, eye, metabolic, and infectious disease. The Institute also is an integral part of the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University.
The National Cancer Institute (NCI) leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit.
-------------------------------
REFERENCE: Lombardi VC, Ruscetti FW, Gupta JD, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, and Mikovits JA. Detection of Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome. Online October 8, 2009. Science.
--------------------
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Thursday, October 8, 2009, 2 p.m. EDT
CONTACTS:
NCI Office of Media Relations, 301-496-6641,
Whittemore Peterson Institute, Frankie Vigil, 775-336-4555,
Cleveland Clinic Corp. Communications, Megan F. Pruce, 216-445-7452,
![Reblog this post [with Zemanta]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_uT9YhMcSafLtGicA2ULOQ_fqF0_NaZB0_cmdsqRJznpKKuJLu3KQB85E3Q0fenmR_UIct1Th_2dfTi-_w_uM4Gl5-wY9N5lVdmmS5MKWhUpuoMkOSLtjH3vYCUxi8j9a8ii2OvuKQ_dVRnPruFIsct=s0-d)
CONSORTIUM OF RESEARCHERS DISCOVER RETROVIRAL LINK TO CHRONIC FATIGUE SYNDROME
Scientists have discovered a potential retroviral link to chronic fatigue syndrome, known as CFS, a debilitating disease that affects millions of people in the United States. Researchers from the Whittemore Peterson Institute (WPI), located at the University of Nevada, Reno, the National Cancer Institute (NCI), part of the National Institutes of Health, and the Cleveland Clinic, report this finding online Oct. 8, 2009, issue of Science.
"We now have evidence that a retrovirus named XMRV is frequently present in the blood of patients with CFS. This discovery could be a major step in the discovery of vital treatment options for millions of patients," said Judy Mikovits, Ph.D., director of research for WPI and leader of the team that discovered this association. Researchers cautioned however, that this finding shows there is an association between XMRV and CFS but does not prove that XMRV causes CFS.
The scientists provide a new hypothesis for a retrovirus link with CFS. The virus, XMRV, was first identified by Robert H. Silverman, Ph.D., professor in the Department of Cancer Biology at the Cleveland Clinic Lerner Research Institute, in men who had a specific immune system defect that reduced their ability to fight viral infections.
"The discovery of XMRV in two major diseases, prostate cancer and now chronic fatigue syndrome, is very exciting. If cause-and-effect is established, there would be a new opportunity for prevention and treatment of these diseases," said Silverman, a co-author on the CFS paper.
Commonality of an immune system defect in patients with CFS and prostate cancer led researchers to look for the virus in their blood samples. In this study, WPI scientists identified XMRV in the blood of 68 of 101 (67 percent) CFS patients. In contrast, they found that eight of 218 healthy people (3.7 percent) contained XMRV DNA. The research team not only found that blood cells contained XMRV but also expressed XMRV proteins at high levels and produced infectious viral particles. A clinically validated test to detect XMRV antibodies in patients' plasma is currently under development.
These results were also supported by the observation of retrovirus particles in patient samples when examined using transmission electron microscopy. The data demonstrate the first direct isolation of infectious XMRV from humans.
"These compelling data allow the development of a hypothesis concerning a cause of this complex and misunderstood disease, since retroviruses are a known cause of neurodegenerative diseases and cancer in man," said Francis Ruscetti, Ph.D., Laboratory of Experimental Immunology, NCI.
Retroviruses like XMRV have also been shown to activate a number of other latent viruses. This could explain why so many different viruses, such as Epstein-Barr virus, which was causally linked to Burkitt's and other lymphomas in the 1970s, have been associated with CFS. It is important to note that retroviruses, like XMRV, are not airborne.
"The scientific evidence that a retrovirus is implicated in CFS opens a new world of possibilities for so many people," said Annette Whittemore, founder and president of WPI and mother of a CFS patient. "Scientists can now begin the important work of translating this discovery into medical care for individuals with XMRV related diseases."
Dan Peterson, M.D., medical director of WPI added, "Patients with CFS deal with a myriad of health issues as their quality of life declines. I'm excited about the possibility of providing patients, who are positive for XMRV, a definitive diagnosis, and hopefully very soon, a range of effective treatments options."
The Whittemore Peterson Institute for Neuro Immune Disease exists to bring discovery, knowledge, and effective treatments to patients with illnesses that are caused by acquired dysregulation of both the immune system and the nervous system, often resulting in lifelong disease and disability. www.wpinstitute.org.
The Lerner Research Institute is home to Cleveland Clinic's laboratory, translational and clinical research. Its mission: to promote human health by investigating in the laboratory and the clinic the causes of disease and discovering novel approaches to prevention and treatments; to train the next generation of biomedical researchers; and to foster productive collaborations with those providing clinical care. More than 1,200 people in 11 departments work in research programs focusing on cardiovascular, cancer, neurologic, musculoskeletal, allergic and immunologic, eye, metabolic, and infectious disease. The Institute also is an integral part of the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University.
The National Cancer Institute (NCI) leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
-------------------------------
REFERENCE: Lombardi VC, Ruscetti FW, Gupta JD, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, and Mikovits JA. Detection of Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome. Online October 8, 2009. Science.
--------------------
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Thursday, October 8, 2009, 2 p.m. EDT
CONTACTS:
NCI Office of Media Relations, 301-496-6641,
Whittemore Peterson Institute, Frankie Vigil, 775-336-4555,
Cleveland Clinic Corp. Communications, Megan F. Pruce, 216-445-7452,
Wednesday, October 7, 2009
PROSTATE TUMORS CAN CHANGE THE FUNCTION OF IMMUNE CELLS IN MICE
From an NIH press release:
PROSTATE TUMORS CAN CHANGE THE FUNCTION OF IMMUNE CELLS IN MICE
Researchers have discovered that prostate tumors in mice can cause immune cells known as CD8+ T cells to change their function from cells that have antitumor activity to cells that suppress immune responses. This finding, by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, has important implications for the design of immune-based therapies for cancer. The new study, available online, appears in the Oct. 15, 2009, issue of the Journal of Immunology.
"The conversion of CD8+ T cells into suppressor cells may be one of the mechanisms by which tumors restrict the immune system's ability to control tumor growth," said Arthur A. Hurwitz, Ph.D., head of the Tumor Immunity and Tolerance Group at NCI's Center for Cancer Research. "Studying this process in mice may help explain why some cancer patients have an initial response from their immune-based therapy, but this response fails with time."
In mice and humans, when the immune system encounters a pathogen or other foreign invader, it responds by mounting an immune response. Part of this response involves the recruitment and activation of CD8+ T cells, which are also called cytotoxic T cells or killer T cells, to help destroy the invader. CD8+ T cells also play a role in immune responses against tumor cells. Other T cells, known as CD4+ T regulatory cells, work to suppress CD8+ T cell activity. Immune suppression by these regulatory T cells helps prevent the body from attacking its own cells. A high level of CD4+ T regulatory cells is also associated with poor prognosis of some cancers. Moreover, research in mice has shown that blocking the immune suppressive activity of these regulatory T cells enhances the body's immunity against tumors, causing tumor growth to slow and improving the antitumor immune responses elicited by cancer vaccines.
Recent evidence in mice has suggested that CD8+ T cells can develop suppressive activities similar to those of CD4+ T regulatory cells. In addition, CD8+ suppressor cells have been found in cancer patients. The presence of these suppressor cells could explain earlier findings by Hurwitz's team that prostate tumor-specific CD8+ T cells injected into prostate tumor-bearing mice migrate to the tumors but then become unresponsive, or tolerized, to the tumor cells. It remained unclear, however, whether the suppressive CD8+ T cells have suppressor activity before they reach the tumor or whether they are converted into suppressor cells by the tumor.
In the new research, Hurwitz's team found that CD8+ T cells acquire immune suppressive functions after they enter the mouse tumor microenvironment, which encompasses nearby noncancerous cells and immune cells in addition to tumor cells. The researchers found that tumor-specific CD8+ T cells isolated from the tumors were able to suppress the proliferative capacity of nonspecific T cells, whereas tumor-specific CD8+ T cells isolated from lymph nodes of the mice were unable to do so.
This anti-proliferative activity appeared to be caused, in part, by substances secreted by the CD8+ T cells after they had been converted to suppressor cells. One of these substances, TGF-beta, is a protein that controls cell proliferation and differentiation and plays a role in cancer and other diseases. TGF-beta is thought to be involved in the immune-suppressive activity of CD4+ T-regulatory cells.
Next, the team investigated whether the conversion of tumor-specific CD8+ T cells to suppressor cells could be prevented. To do this, they administered tumor-specific CD4+ and CD8+ T cells to prostate tumor-bearing mice. Some CD4+ T cells act as helper cells and enhance the activity of other immune cells, including CD8+ T cells. The researchers found that, under these conditions, CD8+ T cells isolated from the prostate tumors no longer suppressed the proliferation of other T cells. Moreover, these cells produced less TGF-beta than cells that were not exposed to CD4+ T cells.
The researchers propose that activated CD4+ T cells that enter tumors may secrete factors that support the CD8+ T cell antitumor functions, or may help other immune cells located in the tumor block the processes by which CD8+ T cells acquire their suppressive activity.
Future work by this team will focus on defining the mechanisms by which tumor-specific CD8+ T cells gain their suppressive functions upon entering the mouse tumor microenvironment. "It is important to understand how these cells become suppressive and how they mediate suppression to find approaches to block these processes," said Hurwitz. "This will enhance our ability to generate more effective antitumor T cell responses in mice, which then might be translated to human."
For more information on Dr. Hurwitz's research, please go to.
NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit.
------------------------------------
REFERENCE:
Shafer-Weaver, KA, Anderson, MJ, Stagliano K, Malyguine, A, Greenberg, NM, and Hurwitz AA. Cutting Edge: Tumor-Specific CD8+ T Cells Infiltrating Prostatic Tumors Are Induced to Become Suppressor Cells. J Immunol. Oct. 15, 2009. Vol. 183, No. 8.
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
For Immediate Release: Wednesday, October 7, 2009
CONTACT: NCI Office of Media Relations, 301-496-6641,
![Reblog this post [with Zemanta]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_sni7B9YQ1tR5PoCtgWzokVLGC-Gj2kQnoIZxJVrpqTR6Vp05UjZb8U-OUlPRaDHKOtURu1fY78Dgk5N1T_TXtg0OSf7hOIeMR1K12tSWr09KQVYrIzZJ5_ND5dbqWChT4V2-enroPRd1y-q8nznZkE=s0-d)
PROSTATE TUMORS CAN CHANGE THE FUNCTION OF IMMUNE CELLS IN MICE
Researchers have discovered that prostate tumors in mice can cause immune cells known as CD8+ T cells to change their function from cells that have antitumor activity to cells that suppress immune responses. This finding, by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, has important implications for the design of immune-based therapies for cancer. The new study, available online, appears in the Oct. 15, 2009, issue of the Journal of Immunology.
"The conversion of CD8+ T cells into suppressor cells may be one of the mechanisms by which tumors restrict the immune system's ability to control tumor growth," said Arthur A. Hurwitz, Ph.D., head of the Tumor Immunity and Tolerance Group at NCI's Center for Cancer Research. "Studying this process in mice may help explain why some cancer patients have an initial response from their immune-based therapy, but this response fails with time."
In mice and humans, when the immune system encounters a pathogen or other foreign invader, it responds by mounting an immune response. Part of this response involves the recruitment and activation of CD8+ T cells, which are also called cytotoxic T cells or killer T cells, to help destroy the invader. CD8+ T cells also play a role in immune responses against tumor cells. Other T cells, known as CD4+ T regulatory cells, work to suppress CD8+ T cell activity. Immune suppression by these regulatory T cells helps prevent the body from attacking its own cells. A high level of CD4+ T regulatory cells is also associated with poor prognosis of some cancers. Moreover, research in mice has shown that blocking the immune suppressive activity of these regulatory T cells enhances the body's immunity against tumors, causing tumor growth to slow and improving the antitumor immune responses elicited by cancer vaccines.
Recent evidence in mice has suggested that CD8+ T cells can develop suppressive activities similar to those of CD4+ T regulatory cells. In addition, CD8+ suppressor cells have been found in cancer patients. The presence of these suppressor cells could explain earlier findings by Hurwitz's team that prostate tumor-specific CD8+ T cells injected into prostate tumor-bearing mice migrate to the tumors but then become unresponsive, or tolerized, to the tumor cells. It remained unclear, however, whether the suppressive CD8+ T cells have suppressor activity before they reach the tumor or whether they are converted into suppressor cells by the tumor.
In the new research, Hurwitz's team found that CD8+ T cells acquire immune suppressive functions after they enter the mouse tumor microenvironment, which encompasses nearby noncancerous cells and immune cells in addition to tumor cells. The researchers found that tumor-specific CD8+ T cells isolated from the tumors were able to suppress the proliferative capacity of nonspecific T cells, whereas tumor-specific CD8+ T cells isolated from lymph nodes of the mice were unable to do so.
This anti-proliferative activity appeared to be caused, in part, by substances secreted by the CD8+ T cells after they had been converted to suppressor cells. One of these substances, TGF-beta, is a protein that controls cell proliferation and differentiation and plays a role in cancer and other diseases. TGF-beta is thought to be involved in the immune-suppressive activity of CD4+ T-regulatory cells.
Next, the team investigated whether the conversion of tumor-specific CD8+ T cells to suppressor cells could be prevented. To do this, they administered tumor-specific CD4+ and CD8+ T cells to prostate tumor-bearing mice. Some CD4+ T cells act as helper cells and enhance the activity of other immune cells, including CD8+ T cells. The researchers found that, under these conditions, CD8+ T cells isolated from the prostate tumors no longer suppressed the proliferation of other T cells. Moreover, these cells produced less TGF-beta than cells that were not exposed to CD4+ T cells.
The researchers propose that activated CD4+ T cells that enter tumors may secrete factors that support the CD8+ T cell antitumor functions, or may help other immune cells located in the tumor block the processes by which CD8+ T cells acquire their suppressive activity.
Future work by this team will focus on defining the mechanisms by which tumor-specific CD8+ T cells gain their suppressive functions upon entering the mouse tumor microenvironment. "It is important to understand how these cells become suppressive and how they mediate suppression to find approaches to block these processes," said Hurwitz. "This will enhance our ability to generate more effective antitumor T cell responses in mice, which then might be translated to human."
For more information on Dr. Hurwitz's research, please go to
NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
------------------------------------
REFERENCE:
Shafer-Weaver, KA, Anderson, MJ, Stagliano K, Malyguine, A, Greenberg, NM, and Hurwitz AA. Cutting Edge: Tumor-Specific CD8+ T Cells Infiltrating Prostatic Tumors Are Induced to Become Suppressor Cells. J Immunol. Oct. 15, 2009. Vol. 183, No. 8.
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
For Immediate Release: Wednesday, October 7, 2009
CONTACT: NCI Office of Media Relations, 301-496-6641,
Thursday, September 24, 2009
Thursday, September 3, 2009
NIBIB SCIENTISTS COMBINE MICROSCOPY METHODS TO INCREASE IMAGING EFFICIENCY IN CELL STRUCTURE STUDIES
This is an excellent new advance in microscopy. - BRH
NIBIB SCIENTISTS COMBINE MICROSCOPY METHODS TO INCREASE IMAGING EFFICIENCY IN CELL STRUCTURE STUDIES
New Method Produces High-Resolution Images of Thicker Specimen Samples
Scientists in the National Institute of Biomedical Imaging and Bioengineering (NIBIB) Laboratory of Bioengineering and Physical Science have developed a new technique that allows researchers to visualize fine details of cell structure three-dimensionally in thick sections, thus providing greater insight into how cells are organized and how they function. The work is described in a report published online this week in Nature Methods.
The new electron tomography method, referred to as BF STEM tomography, lets researchers image samples that are more than three times the thickness of typical samples.
Electron tomography is carried out at the nanoscale on individual cells. Conventionally, high-resolution imaging of biological specimens has been accomplished by cutting cells into thin sections (300 nanometers or less) and imaging each section separately. Although reconstructing an entire structure from thin sections is laborious, thin sections are used because images of thicker sections typically are blurred. Serial BF STEM tomography accomplishes the same work using fewer yet thicker specimen sections, leading to faster reconstruction of intact organelles, intracellular pathogens, and even entire mammalian cells.
Drs. Alioscka Sousa, Martin Hohmann-Marriott, Richard Leapman and colleagues in NIBIB, in collaboration with Dr. Joshua Zimmerberg and colleagues in the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), demonstrated feasibility and advantages of BF-STEM tomography in a study of red blood cells infected with Plasmodium falciparum, a parasite that causes malaria. High-resolution 3D reconstructions of entire cells were generated by serially imaging just a few thick sections. The intricate system of red blood cell and parasite membranes, as well as several organelles, can be seen in detail.
"We believe that the new technique, which was conceived by Dr. Sousa on the project team, will lead to improved 3D visualization of larger internal structures in mammalian cells at a nanoscale. And it will complement cryo electron tomography and super-resolution optical imaging approaches," according to Dr. Leapman.
Most high-performance electron microscopes can readily be equipped to utilize the BF STEM tomography approach. "This exciting new method, with its ability to provide nanoscale structural details over three dimensions, has the potential for broad application in cell biology," says NIBIB Director Roderic Pettigrew. "This should open new vistas in the understanding of the interplay between cellular structure and function, and is a great example of NIBIB-supported research that moves medical science forward through technological innovation."
This work was supported by the Intramural Research Programs of the NIBIB and the NICHD at the National Institutes of Health. In addition, Dr. Hohmann-Marriott received support through the Joint NIST/NIBIB Postdoctoral Associateship Program of the National Research Council, USA.
NIBIB, a component of NIH, is dedicated to improving health by bridging the physical and biological sciences to develop and apply new biomedical technologies. Additional information and publications are available at.
The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit.
------------
REFERENCE: Nanoscale 3D cellular imaging by axial scanning transmission electron tomography. Martin F Hohmann-Marriott, Alioscka A Sousa, Afrouz A Azari, Svetlana Glushakova, Guofeng Zhang, Joshua Zimmerberg & Richard D Leapman. Published online: 30 August 2009 | doi:10.1038/nmeth.1367.
##
This NIH News Release is available online at:
.
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Biomedical Imaging and Bioengineering (NIBIB)
For Immediate Release: Thursday, September 3, 2009
CONTACT: Cheryl Fee, 301-451-6772, ![Reblog this post [with Zemanta]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_vsfZw_QxgjNSLKAAz-_SU7FKY8J2uGoWgGpQUSt6P2S1yRbALQY5nrRbgoGW9Mg_AIq3pZi59s3EXwFttPM9Z6pyz_b2jLqronrqYvTm6KO0X1yBfKA_QHfsTuFUffSp45CbMnM43qFf3O3wD6e4c=s0-d)
NIBIB SCIENTISTS COMBINE MICROSCOPY METHODS TO INCREASE IMAGING EFFICIENCY IN CELL STRUCTURE STUDIES
New Method Produces High-Resolution Images of Thicker Specimen Samples
Scientists in the National Institute of Biomedical Imaging and Bioengineering (NIBIB) Laboratory of Bioengineering and Physical Science have developed a new technique that allows researchers to visualize fine details of cell structure three-dimensionally in thick sections, thus providing greater insight into how cells are organized and how they function. The work is described in a report published online this week in Nature Methods.
The new electron tomography method, referred to as BF STEM tomography, lets researchers image samples that are more than three times the thickness of typical samples.
Electron tomography is carried out at the nanoscale on individual cells. Conventionally, high-resolution imaging of biological specimens has been accomplished by cutting cells into thin sections (300 nanometers or less) and imaging each section separately. Although reconstructing an entire structure from thin sections is laborious, thin sections are used because images of thicker sections typically are blurred. Serial BF STEM tomography accomplishes the same work using fewer yet thicker specimen sections, leading to faster reconstruction of intact organelles, intracellular pathogens, and even entire mammalian cells.
Drs. Alioscka Sousa, Martin Hohmann-Marriott, Richard Leapman and colleagues in NIBIB, in collaboration with Dr. Joshua Zimmerberg and colleagues in the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), demonstrated feasibility and advantages of BF-STEM tomography in a study of red blood cells infected with Plasmodium falciparum, a parasite that causes malaria. High-resolution 3D reconstructions of entire cells were generated by serially imaging just a few thick sections. The intricate system of red blood cell and parasite membranes, as well as several organelles, can be seen in detail.
"We believe that the new technique, which was conceived by Dr. Sousa on the project team, will lead to improved 3D visualization of larger internal structures in mammalian cells at a nanoscale. And it will complement cryo electron tomography and super-resolution optical imaging approaches," according to Dr. Leapman.
Most high-performance electron microscopes can readily be equipped to utilize the BF STEM tomography approach. "This exciting new method, with its ability to provide nanoscale structural details over three dimensions, has the potential for broad application in cell biology," says NIBIB Director Roderic Pettigrew. "This should open new vistas in the understanding of the interplay between cellular structure and function, and is a great example of NIBIB-supported research that moves medical science forward through technological innovation."
This work was supported by the Intramural Research Programs of the NIBIB and the NICHD at the National Institutes of Health. In addition, Dr. Hohmann-Marriott received support through the Joint NIST/NIBIB Postdoctoral Associateship Program of the National Research Council, USA.
NIBIB, a component of NIH, is dedicated to improving health by bridging the physical and biological sciences to develop and apply new biomedical technologies. Additional information and publications are available at
The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
------------
REFERENCE: Nanoscale 3D cellular imaging by axial scanning transmission electron tomography. Martin F Hohmann-Marriott, Alioscka A Sousa, Afrouz A Azari, Svetlana Glushakova, Guofeng Zhang, Joshua Zimmerberg & Richard D Leapman. Published online: 30 August 2009 | doi:10.1038/nmeth.1367.
##
This NIH News Release is available online at:
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Biomedical Imaging and Bioengineering (NIBIB)
For Immediate Release: Thursday, September 3, 2009
CONTACT: Cheryl Fee, 301-451-6772,
Tuesday, September 1, 2009
MicroRNAS IN BLOOD MAY BE BIOMARKERS OF PANCREATIC CANCER
We desperately need this new test for pancreatic cancer and we need a cure ASAP. - BRH.
MicroRNAS IN BLOOD MAY BE BIOMARKERS OF PANCREATIC CANCER
Small molecules known as microRNAs, which can be detected in blood samples, have the potential to help identify patients with pancreatic cancer, a study finds. The study, by researchers at The University of Texas M.D. Anderson Cancer Center in Houston, was supported by the Early Detection Research Network (EDRN) of the National Cancer Institute (NCI), part of the National Institutes of Health. The paper appeared online Sept. 1, 2009, in Cancer Prevention Research.
Pancreatic cancer is a highly fatal disease that is difficult to detect at early stages. In most patients, symptoms do not appear until the cancer is locally advanced or has spread to other parts of the body. The absence of symptoms in early-stage disease and the current lack of effective, minimally invasive screening and diagnostic techniques limit the available treatment options. Both contribute to the high mortality rate observed for patients with pancreatic cancer.
"The development of a minimally invasive test for the early detection and diagnosis of pancreatic cancer is greatly needed," said Sudhir Srivastava, Ph.D., chief of the Cancer Biomarkers Research Group in NCI's Division of Cancer Prevention. "An important step is to identify biomarkers for pancreatic cancer, such as microRNAs, circulating in the bloodstream that can be used to distinguish individuals with pancreatic cancer from individuals without the disease."
MicroRNAs, or miRNAs, are short strands of RNA. The miRNAs regulate gene expression by controlling the translation of a specific type of RNA called messenger RNA which relays the genetic instructions for making proteins. Previous research has indicated that miRNAs play important roles in regulating normal cell proliferation and in cancer. Altered patterns of miRNA expression have been seen in pancreatic cancer as well as many other cancers. In addition, it has recently been reported that tumor-derived miRNAs can be detected in blood and that these molecules are stable in stored samples. Thus, miRNAs circulating in the blood may have the potential to serve as novel biomarkers for the detection and diagnosis of pancreatic cancer.
To evaluate the feasibility of using miRNAs in the blood as biomarkers for pancreatic cancer, the researchers selected a set of four miRNAs that have been associated with pancreatic cancer -- miR-21, miR-210, miR-155, and miR-196a. Among these, miR-155 has been identified as a candidate biomarker for early pancreatic cancer, and expression of miR196a has been shown to increase during disease progression. Levels of all four miRNAs were assessed in blood samples from 28 pancreatic cancer patients and 19 healthy volunteers. The study population consisted of patients with pathologically confirmed pancreatic cancer and healthy disease free individuals recruited at the M.D. Anderson Cancer Center between 2002 and 2008. The team found that sensitivity -- or ability to accurately detect pancreatic cancer -- using the panel of four miRNAs was 64 percent. The panel also showed an 89 percent specificity, which indicates the proportion of study participants who did not have pancreatic cancer and were correctly identified as being disease free.
"Our results demonstrate proof of principle in developing a blood test based on miRNA signatures for pancreatic cancer," said senior author Subrata Sen, Ph.D., of M.D. Anderson's Department of Molecular Pathology. "More work is needed to evaluate this strategy in different grades and stages of the disease. We are in the process of initiating such studies in collaboration with members of EDRN." For example, the researchers will test the ability of the miRNAs to detect pancreatic cancer in separate patient populations.
Pancreatic cancer, the fourth most common cause of cancer death in the United States, has a poor survival rate compared with that of other types of cancer. Less than five percent of the patients with pancreatic cancer survive five years past diagnosis.
For more information about the Department of Molecular Pathology at M.D. Anderson, please go to.
For more information on NCI's EDRN, please go to:.
NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit.
##
This NIH News Release is available online at:
.
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Tuesday, September 1, 2009, 1 p.m., EDT
CONTACT: NCI Office of Media Relations, 301-496-6641,![Reblog this post [with Zemanta]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_st9kI4hYeFOJWUMlCEYv-R0NI_FA23-D5KxTJVpeQqsjtTyohREi0wa6LIsHsWMjQ9MTRoIJQvqIxVVSbqJ2_l9tn1wFu8YEFpk0sNzTqYk-nincEhhchjGBUFJqTHxT5tb-4xY-wNktLR1sPGaA3L=s0-d)
MicroRNAS IN BLOOD MAY BE BIOMARKERS OF PANCREATIC CANCER
Small molecules known as microRNAs, which can be detected in blood samples, have the potential to help identify patients with pancreatic cancer, a study finds. The study, by researchers at The University of Texas M.D. Anderson Cancer Center in Houston, was supported by the Early Detection Research Network (EDRN) of the National Cancer Institute (NCI), part of the National Institutes of Health. The paper appeared online Sept. 1, 2009, in Cancer Prevention Research.
Pancreatic cancer is a highly fatal disease that is difficult to detect at early stages. In most patients, symptoms do not appear until the cancer is locally advanced or has spread to other parts of the body. The absence of symptoms in early-stage disease and the current lack of effective, minimally invasive screening and diagnostic techniques limit the available treatment options. Both contribute to the high mortality rate observed for patients with pancreatic cancer.
"The development of a minimally invasive test for the early detection and diagnosis of pancreatic cancer is greatly needed," said Sudhir Srivastava, Ph.D., chief of the Cancer Biomarkers Research Group in NCI's Division of Cancer Prevention. "An important step is to identify biomarkers for pancreatic cancer, such as microRNAs, circulating in the bloodstream that can be used to distinguish individuals with pancreatic cancer from individuals without the disease."
MicroRNAs, or miRNAs, are short strands of RNA. The miRNAs regulate gene expression by controlling the translation of a specific type of RNA called messenger RNA which relays the genetic instructions for making proteins. Previous research has indicated that miRNAs play important roles in regulating normal cell proliferation and in cancer. Altered patterns of miRNA expression have been seen in pancreatic cancer as well as many other cancers. In addition, it has recently been reported that tumor-derived miRNAs can be detected in blood and that these molecules are stable in stored samples. Thus, miRNAs circulating in the blood may have the potential to serve as novel biomarkers for the detection and diagnosis of pancreatic cancer.
To evaluate the feasibility of using miRNAs in the blood as biomarkers for pancreatic cancer, the researchers selected a set of four miRNAs that have been associated with pancreatic cancer -- miR-21, miR-210, miR-155, and miR-196a. Among these, miR-155 has been identified as a candidate biomarker for early pancreatic cancer, and expression of miR196a has been shown to increase during disease progression. Levels of all four miRNAs were assessed in blood samples from 28 pancreatic cancer patients and 19 healthy volunteers. The study population consisted of patients with pathologically confirmed pancreatic cancer and healthy disease free individuals recruited at the M.D. Anderson Cancer Center between 2002 and 2008. The team found that sensitivity -- or ability to accurately detect pancreatic cancer -- using the panel of four miRNAs was 64 percent. The panel also showed an 89 percent specificity, which indicates the proportion of study participants who did not have pancreatic cancer and were correctly identified as being disease free.
"Our results demonstrate proof of principle in developing a blood test based on miRNA signatures for pancreatic cancer," said senior author Subrata Sen, Ph.D., of M.D. Anderson's Department of Molecular Pathology. "More work is needed to evaluate this strategy in different grades and stages of the disease. We are in the process of initiating such studies in collaboration with members of EDRN." For example, the researchers will test the ability of the miRNAs to detect pancreatic cancer in separate patient populations.
Pancreatic cancer, the fourth most common cause of cancer death in the United States, has a poor survival rate compared with that of other types of cancer. Less than five percent of the patients with pancreatic cancer survive five years past diagnosis.
For more information about the Department of Molecular Pathology at M.D. Anderson, please go to
For more information on NCI's EDRN, please go to:
NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
##
This NIH News Release is available online at:
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Cancer Institute (NCI)
Embargoed for Release: Tuesday, September 1, 2009, 1 p.m., EDT
CONTACT: NCI Office of Media Relations, 301-496-6641,
STUDIES IN ANIMALS SUGGEST 2009 H1N1 VIRUS MAY HAVE BIOLOGICAL ADVANTAGE OVER SEASONAL INFLUENZA VIRUSES
Another study that suggests that the swine flu may be a huge problem this winter. - BRH
STUDIES IN ANIMALS SUGGEST 2009 H1N1 VIRUS MAY HAVE BIOLOGICAL ADVANTAGE OVER SEASONAL INFLUENZA VIRUSES
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Allergy and Infectious Diseases (NIAID)
For Immediate Release: Monday, August 31, 2008
CONTACT: Anne A. Oplinger, 301-402-1663,
Preliminary findings in ferrets suggest that the novel 2009 H1N1 influenza virus may outcompete human seasonal influenza viruses, researchers say. Tests in animals showed that levels of the 2009 H1N1 virus rose more quickly than levels of the seasonal virus strains, and the new virus caused more severe disease. In line with previous findings by other research groups, the University of Maryland researchers also observed that the novel H1N1 virus was transmitted more easily from infected to uninfected ferrets than either of the two seasonal influenza viruses.
The researchers found no evidence that the 2009 H1N1 virus combined with either of two seasonal flu viruses to form new, so-called reassortant viruses. These findings suggest that while 2009 H1N1 virus probably will predominate in the coming flu season, there may not be biological pressure for the new virus to re-combine with other circulating viruses, the researchers say.
The work was done by Daniel Perez, Ph.D., and colleagues from the University of Maryland. The researchers were supported by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
"This elegant study, conducted in a useful animal model of human influenza, provides important information about how the 2009 H1N1 influenza virus interacts with other flu virus strains," says NIAID Director Anthony S. Fauci, M.D. "The results suggest that 2009 H1N1 influenza may outcompete seasonal flu virus strains and may be more communicable as well. These new data, while preliminary, underscore the need for vaccinating against both seasonal influenza and the 2009 H1N1 influenza this fall and winter."
When the investigators inoculated ferrets with 2009 H1N1 virus plus either seasonal H1N1 virus or seasonal H3N2 virus, the animals became co-infected with both viruses. However, only the 2009 H1N1 virus was then transmitted from co-infected ferrets to uninfected ferrets; there was no evidence that either of the seasonal flu viruses were transmitted between co-infected and uninfected animals. "The H1N1 pandemic virus has a clear biological advantage over the two main seasonal flu strains and all the makings of a virus fully adapted to humans," says Dr. Perez.
Next, the team conducted experiments to learn whether 2009 H1N1 virus would combine with seasonal flu viruses in co-infected animals to create new reassortant viruses. Some scientists have speculated that reassortant viruses may be more virulent or transmissible than either 2009 H1N1 or seasonal flu viruses alone. The researchers collected virus-containing material from the ferrets' nasal cavities, but found no evidence of reassortment between the 2009 H1N1 and seasonal influenza strains, either in ferrets that were directly infected with both viruses or in ferrets that came in contact with the co-infected animals.
The investigators' findings are posted on PLoS Currents: Influenza, a Web site for rapid communication of new scientific data on influenza. Submissions to PLoS Currents: Influenza are screened by a panel of leading influenza experts prior to posting but do not undergo formal peer review. The new research may be submitted later for peer review and eventual publication in scientific journals.
This research was supported in part through the NIAID Centers of Excellence for Influenza Research and Surveillance (CEIRS) program.
For more information on influenza, visit for one-stop access to U.S. government information on avian and pandemic influenza. Also, visit NIAID's Flu Portal,
NIAID conducts and supports research-at NIH, throughout the United States, and worldwide-to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit.
---------------------------------
REFERENCE: Perez et al. Fitness of pandemic H1N1 and seasonal influenza A viruses during co-infection. PLoS Currents: Influenza. Posted Aug. 25, 2009. RRN1011. Available at:
Additional information about research in Dr. Perez's laboratory is at:
##
This NIH News Release is available online at:
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. ![Reblog this post [with Zemanta]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_szkoqj7Q59F8Uyq_cBGCY5wZwzQMsWpu5X4ZTrE1SwZi5DTqd_RC7EVrvsU1D6YsV5lPwUrya87ZY_ygKdsnuVs7v2EAohLDCtluf2GqktxozTF_2aTldcPf20VoyfM5cpHbgh5ay9V857xBGt9yjF=s0-d)
STUDIES IN ANIMALS SUGGEST 2009 H1N1 VIRUS MAY HAVE BIOLOGICAL ADVANTAGE OVER SEASONAL INFLUENZA VIRUSES
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Allergy and Infectious Diseases (NIAID)
For Immediate Release: Monday, August 31, 2008
CONTACT: Anne A. Oplinger, 301-402-1663,
Preliminary findings in ferrets suggest that the novel 2009 H1N1 influenza virus may outcompete human seasonal influenza viruses, researchers say. Tests in animals showed that levels of the 2009 H1N1 virus rose more quickly than levels of the seasonal virus strains, and the new virus caused more severe disease. In line with previous findings by other research groups, the University of Maryland researchers also observed that the novel H1N1 virus was transmitted more easily from infected to uninfected ferrets than either of the two seasonal influenza viruses.
The researchers found no evidence that the 2009 H1N1 virus combined with either of two seasonal flu viruses to form new, so-called reassortant viruses. These findings suggest that while 2009 H1N1 virus probably will predominate in the coming flu season, there may not be biological pressure for the new virus to re-combine with other circulating viruses, the researchers say.
The work was done by Daniel Perez, Ph.D., and colleagues from the University of Maryland. The researchers were supported by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
"This elegant study, conducted in a useful animal model of human influenza, provides important information about how the 2009 H1N1 influenza virus interacts with other flu virus strains," says NIAID Director Anthony S. Fauci, M.D. "The results suggest that 2009 H1N1 influenza may outcompete seasonal flu virus strains and may be more communicable as well. These new data, while preliminary, underscore the need for vaccinating against both seasonal influenza and the 2009 H1N1 influenza this fall and winter."
When the investigators inoculated ferrets with 2009 H1N1 virus plus either seasonal H1N1 virus or seasonal H3N2 virus, the animals became co-infected with both viruses. However, only the 2009 H1N1 virus was then transmitted from co-infected ferrets to uninfected ferrets; there was no evidence that either of the seasonal flu viruses were transmitted between co-infected and uninfected animals. "The H1N1 pandemic virus has a clear biological advantage over the two main seasonal flu strains and all the makings of a virus fully adapted to humans," says Dr. Perez.
Next, the team conducted experiments to learn whether 2009 H1N1 virus would combine with seasonal flu viruses in co-infected animals to create new reassortant viruses. Some scientists have speculated that reassortant viruses may be more virulent or transmissible than either 2009 H1N1 or seasonal flu viruses alone. The researchers collected virus-containing material from the ferrets' nasal cavities, but found no evidence of reassortment between the 2009 H1N1 and seasonal influenza strains, either in ferrets that were directly infected with both viruses or in ferrets that came in contact with the co-infected animals.
The investigators' findings are posted on PLoS Currents: Influenza, a Web site for rapid communication of new scientific data on influenza. Submissions to PLoS Currents: Influenza are screened by a panel of leading influenza experts prior to posting but do not undergo formal peer review. The new research may be submitted later for peer review and eventual publication in scientific journals.
This research was supported in part through the NIAID Centers of Excellence for Influenza Research and Surveillance (CEIRS) program.
For more information on influenza, visit
NIAID conducts and supports research-at NIH, throughout the United States, and worldwide-to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
---------------------------------
REFERENCE: Perez et al. Fitness of pandemic H1N1 and seasonal influenza A viruses during co-infection. PLoS Currents: Influenza. Posted Aug. 25, 2009. RRN1011. Available at:
Additional information about research in Dr. Perez's laboratory is at:
##
This NIH News Release is available online at:
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