Wed Mar 2, 2011 1:06pm EST
* RVR rate 70 pct with telaprevir combination therapy
* RVR rate 5 pct on standard hepatitis C drugs alone
* Vertex expects final cure rate data in 2012
By Bill Berkrot
NEW YORK, March 2 (Reuters) - Vertex Pharmaceuticals Inc's (VRTX.O) hepatitis C drug telaprevir helped eliminate the virus in 70 percent of patients who were also infected with HIV, according to interim analysis from a small midstage clinical trial, the company said.
Telaprevir is awaiting a U.S. approval decision after demonstrating an ability to greatly improve hepatitis cure rates when combined with current standard of care medicines compared with those drugs alone.
Patients in the co-infection study, which was presented at a medical meeting on Wednesday, had not yet received other treatment for hepatitis. Telaprevir was tested in one group of patients who were not receiving antiretroviral therapy for HIV and another group who were.
The interim analysis looked for a rapid viral response (RVR), meaning the hepatitis C virus was undetectable in the blood after four weeks of treatment.
At four weeks, 70 percent of those in the 60-patient study who received combination therapy with telaprevir had achieved RVR compared with 5 percent who received only the standard drugs of pegylated interferon and ribavirin, according to data presented at the Conference on Retroviruses and Opportunistic Infections in Boston.
Undetectable virus must be maintained for a far longer period of time in order to achieve sustained viral response (SVR), which is tantamount to a cure. But RVR can be an early indicator of eventual success rates.
SVR rates from the study are expected to be available next year, Vertex said.
In patients who were not also receiving HIV antiretroviral therapy, 71 percent of those treated with telaprevir achieved RVR compared with none on the standard drugs.
For co-infected patients taking Gilead Sciences Inc's(GILD.O) Atripla for HIV, 75 percent on telaprevir combination therapy hit RVR versus one patient, or 13 percent, in the control arm.
For HIV patients being treated by Bristol-Myers Squibb's (BMY.N) Reyataz, 64 percent on telaprevir hit RVR versus no one in the eight-patient control arm.
Vertex shares were up $1.12, or 2.4 percent, at $47.17 in afternoon trade on Nasdaq. (Reporting by Bill Berkrot, editing by Dave Zimmerman)
http://www.reuters.com/article/2011/03/02/vertex-idUSN0224123520110302
Wednesday, March 2, 2011
Hepatitis C;IL28B Gene Predicts Treatment Outcome For Liver Transplantation
IL28B Gene Predicts Treatment Outcome For Liver Transplantation Patients
Posted on: Wednesday, 2 March 2011, 16:48 CST
Genetic variants determine severity of HCV-related graft disease and antiviral treatment response
German researchers have found a significant association of IL28B genotypes to interferon-based antiviral treatment outcome, and to graft inflammation caused by hepatitis C virus (HCV). The study determined that the presence of G-allele serves as a marker for severe HCV-induced graft inflammation, as well as a predictor for unsuccessful treatment. Study findings—the largest to report on the role IL28B variants in a transplant cohort with recurrent HCV—are published in the March issue of Liver Transplantation, a journal of the American Association for the Study of Liver Diseases.
The IL28B gene encodes interferons (IFNs), which are proteins made by lymphocytes to motivate the immune system in the presence of pathogens. IFN-α proteins are produced by leukocytes and are prevalent in the presence of a viral infection such as HCV. Researchers determined the prevalence of IL28B genotypes (GG, GT, TT) in 183 liver transplant patients, analyzing 605 protocol liver biopsies performed six months to ten or more years after transplantation
The authors determined that the presence of G-allele was a marker for more severe graft inflammation and was observed to have a strong association to antiviral treatment failure in 103 of 159 patients. T-allele was more frequent among patients with lower inflammation grades, concluding a definite association between IL28B G-allele and HCV-induced graft inflammation, and the G-allele as a predictor of unsuccessful antiviral treatment. The team also found that IL28B genotypes did not seem to affect median fibrosis.
"Successful liver transplantation creates a unique population of quasi-normal individuals relying on a harmonic interaction of two different genetic backgrounds," said Dennis Eurich, MD, from the Department of General, Visceral and Transplant Surgery at Charité, Campus Virchow in Berlin and lead author of the current study. "IL28B polymorphisms may help to identify patients at risk for developing more severe graft hepatitis. These genetic variants might help to individually predict potential response to antiviral therapy, enabling medical professionals to appropriately adapt treatment."
A related editorial also published in Liver Transplantation this month acknowledges the association between IL28B polymorphisms and HCV-induced graft inflammation, and the prediction of treatment outcomes. Geoffrey McCaughan from the Centenary Institute in Australia said, "The exact mechanisms of how this association results in higher sustained virologic response rates remain unclear, however the data has invigorated research into both prediction of treatment outcomes and the mechanisms of control of HCV replication and clearance."
Infection with HCV is the primary cause of cirrhosis of the liver and liver cancer worldwide. Up to 30% of liver transplants will develop graft cirrhosis within five years after liver transplantation due to recurrent HCV-infection. HCV-induced graft fibrosis is the main determinant of morbidity and mortality of liver transplant patients.
---
On the Net:
Wiley-Blackwell
Liver Transplantation
Posted on: Wednesday, 2 March 2011, 16:48 CST
Genetic variants determine severity of HCV-related graft disease and antiviral treatment response
German researchers have found a significant association of IL28B genotypes to interferon-based antiviral treatment outcome, and to graft inflammation caused by hepatitis C virus (HCV). The study determined that the presence of G-allele serves as a marker for severe HCV-induced graft inflammation, as well as a predictor for unsuccessful treatment. Study findings—the largest to report on the role IL28B variants in a transplant cohort with recurrent HCV—are published in the March issue of Liver Transplantation, a journal of the American Association for the Study of Liver Diseases.
The IL28B gene encodes interferons (IFNs), which are proteins made by lymphocytes to motivate the immune system in the presence of pathogens. IFN-α proteins are produced by leukocytes and are prevalent in the presence of a viral infection such as HCV. Researchers determined the prevalence of IL28B genotypes (GG, GT, TT) in 183 liver transplant patients, analyzing 605 protocol liver biopsies performed six months to ten or more years after transplantation
The authors determined that the presence of G-allele was a marker for more severe graft inflammation and was observed to have a strong association to antiviral treatment failure in 103 of 159 patients. T-allele was more frequent among patients with lower inflammation grades, concluding a definite association between IL28B G-allele and HCV-induced graft inflammation, and the G-allele as a predictor of unsuccessful antiviral treatment. The team also found that IL28B genotypes did not seem to affect median fibrosis.
"Successful liver transplantation creates a unique population of quasi-normal individuals relying on a harmonic interaction of two different genetic backgrounds," said Dennis Eurich, MD, from the Department of General, Visceral and Transplant Surgery at Charité, Campus Virchow in Berlin and lead author of the current study. "IL28B polymorphisms may help to identify patients at risk for developing more severe graft hepatitis. These genetic variants might help to individually predict potential response to antiviral therapy, enabling medical professionals to appropriately adapt treatment."
A related editorial also published in Liver Transplantation this month acknowledges the association between IL28B polymorphisms and HCV-induced graft inflammation, and the prediction of treatment outcomes. Geoffrey McCaughan from the Centenary Institute in Australia said, "The exact mechanisms of how this association results in higher sustained virologic response rates remain unclear, however the data has invigorated research into both prediction of treatment outcomes and the mechanisms of control of HCV replication and clearance."
Infection with HCV is the primary cause of cirrhosis of the liver and liver cancer worldwide. Up to 30% of liver transplants will develop graft cirrhosis within five years after liver transplantation due to recurrent HCV-infection. HCV-induced graft fibrosis is the main determinant of morbidity and mortality of liver transplant patients.
---
On the Net:
Wiley-Blackwell
Liver Transplantation
Gallstones Tied to Earlier Death: Published in the journal Gastroenterology.
Gallstones Tied to Earlier Death
Wednesday, March 2, 2011 7:37 AM
People who have gallstones are more likely to die within 20 years of diagnosis than people without the disease, a new study says.
Gallstones sufferers are also more likely to die from heart disease or cancer, said the study, published in the journal Gastroenterology.
The findings don't mean that one condition causes the other. Instead, gallstone disease and heart disease may have the same root cause, Dr. Philip Barie, professor of surgery and public health at Weill Cornell Medical College in New York, told Reuters Health.
"People with gallstones may have an abnormal balance of fats in their body, including cholesterol, although there's no clear relationship between gallstone disease per se and high cholesterol," said Barie, who was not involved in the study.
More than 25 million people in the United States have gallstone disease, and almost a million new cases are diagnosed every year, according to the American Gastroenterological Association.
Gallstones happen when material in the bile hardens and sticks in the ducts leading from the gall bladder, where bile is stored, to the small intestine. Because bile can still get from the liver, where it is made, to where it needs to go, the gallbladder isn't necessary and can be removed.
The researchers looked at the medical records of more than 14,000 people between 20 and 74 years old. About one in 14 had gallstones, and one in 20 had their gallbladders removed between 1988 and 1994.
About one in three people who had gallstones or their gallbladders removed died from any cause during the follow-up time, compared to about one in seven similarly aged people without the disease.
Heart disease claimed the lives of slightly less than one in five gallstone sufferers, compared to one in 20 people without. Death from cancer was also more likely, with one in 10 people with gallstones falling victim, compared to one in 25 people without the disease.
The researchers followed all patients until 2006, and recorded all causes of death from the patients' death certificates.
One of the authors on the paper, from Social and Scientific Systems Inc., did not respond to an inquiry from Reuters Health by deadline, and the other, at the National Institutes of Health, declined to comment.
Severe gallstones are usually treated by cutting out the gallbladder, said Barie, who does such operations. The risk of dying from an emergency gallbladder surgery is about one in 50, depending on the age of the patient. But if the gallbladder is removed before it becomes an emergency, the risk of dying is only about one in 500, he said.
Barie suggests that people with gallstones keep on a low-fat diet to reduce the risks of heart disease or stroke.
"Just a good healthy diet," he said.
© 2011 Reuters. All rights reserved. Republication or redistribution of Reuters content, including by caching, framing or similar means, is expressly prohibited without the prior written consent of Reuters.
Wednesday, March 2, 2011 7:37 AM
People who have gallstones are more likely to die within 20 years of diagnosis than people without the disease, a new study says.
Gallstones sufferers are also more likely to die from heart disease or cancer, said the study, published in the journal Gastroenterology.
The findings don't mean that one condition causes the other. Instead, gallstone disease and heart disease may have the same root cause, Dr. Philip Barie, professor of surgery and public health at Weill Cornell Medical College in New York, told Reuters Health.
"People with gallstones may have an abnormal balance of fats in their body, including cholesterol, although there's no clear relationship between gallstone disease per se and high cholesterol," said Barie, who was not involved in the study.
More than 25 million people in the United States have gallstone disease, and almost a million new cases are diagnosed every year, according to the American Gastroenterological Association.
Gallstones happen when material in the bile hardens and sticks in the ducts leading from the gall bladder, where bile is stored, to the small intestine. Because bile can still get from the liver, where it is made, to where it needs to go, the gallbladder isn't necessary and can be removed.
The researchers looked at the medical records of more than 14,000 people between 20 and 74 years old. About one in 14 had gallstones, and one in 20 had their gallbladders removed between 1988 and 1994.
About one in three people who had gallstones or their gallbladders removed died from any cause during the follow-up time, compared to about one in seven similarly aged people without the disease.
Heart disease claimed the lives of slightly less than one in five gallstone sufferers, compared to one in 20 people without. Death from cancer was also more likely, with one in 10 people with gallstones falling victim, compared to one in 25 people without the disease.
The researchers followed all patients until 2006, and recorded all causes of death from the patients' death certificates.
One of the authors on the paper, from Social and Scientific Systems Inc., did not respond to an inquiry from Reuters Health by deadline, and the other, at the National Institutes of Health, declined to comment.
Severe gallstones are usually treated by cutting out the gallbladder, said Barie, who does such operations. The risk of dying from an emergency gallbladder surgery is about one in 50, depending on the age of the patient. But if the gallbladder is removed before it becomes an emergency, the risk of dying is only about one in 500, he said.
Barie suggests that people with gallstones keep on a low-fat diet to reduce the risks of heart disease or stroke.
"Just a good healthy diet," he said.
© 2011 Reuters. All rights reserved. Republication or redistribution of Reuters content, including by caching, framing or similar means, is expressly prohibited without the prior written consent of Reuters.
Hepatitis C Morning News; Ohio VA hospital has resulted in 9 patients testing positive for hepatitis
Scope pointed out an article over at Time entitled "Healing the Hurt," by writer Alice Park covering chronic pain; an issue so many with HCV are all too familiar with. In other news, sadly the scandal at the Ohio VA hospital has resulted in 9 patients testing positive for hepatitis. Out of the 375 patients tested so far, seven tested positive for hepatitis C and two for hepatitis B. There were no patients that tested positive for HIV. The infections resulted because of a dentist who failed to change gloves and sterilize instruments properly between patients. Reuters reported on a study recently published in the journal Gastroenterology which found "people who have gallstones are more likely to die within 20 years of diagnosis than people without the disease."
Quoted from yesterdays blog post : "Scientists at the UCSF Cardiovascular Research Institute have discovered how a change in growth hormone activity in mice leads to fatty liver disease, a condition whose human counterpart is of rising concern worldwide."
New at Medcape comes a report from the German study which shows that teens and young adults who started using Marijuana early in life have an increased risk of having psychotic experiences in subsequent years. Also at medscape the blogger Cole Petrochko was inspired by an article in the New York Times about the newest breakfast menu at McDondalds. Check out his blog and read his take on breakfast at the golden arches. I am running late this morning for my lunch date with my momma, but before I go I thought you may enjoy this video I found while hanging out at Scope this morning;
A look at the many strange effects of placebos.
A look at the many strange effects of placebos.
Created by:Daniel Keogh -
Have a wonderful afternoon folks.
Tina
Tuesday, March 1, 2011
Harvard Scientists: Microchip Spots Cancerous Tumors Within an Hour
Scientists from Harvard have developed a hand-held scanner that is able to detect cancer at a patient’s bedside using only a small speck of tissue.
Video From ; Bloomberg
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When small meets speedy for cancer diagnosis
http://csb.mgh.harvard.edu/highlights/overview
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In today’s fast paced world, waiting for anything is often frustrating and stressful. But few delays can be worse than the wait following a diagnostic blood test or biopsy, where results can take days to come back. Recently, a new device developed by Massachusetts General Hospital (MGH) scientists at the Center for Systems Biology has been shown capable of on the spot cancer diagnosis.
The portable device, known as DMR—diagnostic magnetic resonance—can detect cellular markers for cancer from minute amounts of patient tissue in less than an hour. Not only that, but the data generated is more accurate than that of standard diagnostic procedures. The findings of a human clinical study comparing the DMR to standard pathological tests are published in the February issue of Science Translational Medicine.
The Challenge of Cancer Diagnosis
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A long held dream in medicine has been the capability for quick and accurate cancer diagnosis. Cancer being the complex disease that it is, however, achieving this goal has been far from trivial.
One problem with current diagnostic techniques is the large amounts of tissue required from patients (especially for protein analyses) and the inconsistency of specimens. “When you deal with real patients, samples are very variable,” explains Cesar Castro, a physician at MGH and joint first author of the paper. “Tumors are not ‘clean’—you get inflammatory cells and other non-tumorous cells intertwined. And you get different numbers of cells in each sample.” Hence the need for more tissue.
While it may be fine to remove tumor mass from a patient undergoing surgery, however, minimally invasive approaches that spare patients undue pain and suffering are obviously preferable.
The development and adoption of novel diagnostic technologies, promising faster and more accurate cancer detection, has not proved any easier. Often these devices require particular skills to operate or extra processing steps, and even the data generated can be subject to interpretation or may require costly specialized machinery.
The challenge, therefore, has been to create a portable, fast and accurate diagnostic device, one that is not only user friendly, but is also capable of quantifiably detecting cancer from small amounts of patient tissue.
Impossible?
It appears not. In a recent clinical trial at MGH, a DMR device created by Ralph Weissleder’s laboratory at the Center for Systems Biology was tested in a total of 70 patients with suspected abdominal malignancy. All patients in the study underwent a biopsy in addition to a minimally invasive procedure known as fine needle aspiration—essentially a mini biopsy that collects cells rather than tissue. Specimens acquired via biopsy were then sent to the lab for standard diagnostic testing, whereas the aspirates were run through the DMR system.
World’s smallest cancer diagnostic system
About the size of a coffee mug, the DMR is the world’s smallest cancer diagnostic system. It is based on the same magnetic principals as MRI and is essentially composed of two parts: one that holds antibodies targeted for specific cellular markers of cancer, and one that holds tiny signal-generating magnetic particles. When a patient sample is run through the device, these two systems mix together and via new innovative chemistry, the magnetic particles bind to the antibodies. Consequently, when the antibodies seek out and latch onto their target within the sample, the attached magnetic particles act essentially as flags, signaling the presence of a particular cancer marker. These signals are subsequently detected and quantified by the DMR.
The tricky part is detecting the signals, particularly if the amounts of cancer marker are extremely low. But it appears the researchers have got around that. “Using our novel labeling chemistry,” explains Hakho Lee, assistant professor at MGH, who spearheaded development of the system, “we could load more particles onto our antibodies to generate more signal. So even at low levels of marker-particle interaction, you can still detect a signal.”
According to Lee, the original DMR prototype was only capable of detecting one or two cancer markers. But they soon came to realize that it’s not the case that one cancer marker fits all.
“It’s more of a panel,” Castro explains. “Since there are often random differences, even within the general population, you can’t just rely on one cancer marker. Instead, we looked for a pattern of cancer marker expression.”
Through a process of trial and error involving a panel of 12 cancer markers, the researchers eventually discovered that analysis of a specific four-marker combination could detect cancerous cells in patient samples with an accuracy of 96 percent; a result which was then validated in a separate group of patients. Better yet, this information could be generated in under an hour compared to the several day turnaround time for routine pathology.
If that wasn’t convenient enough, the DMR can also interface with a smartphone or tablet. “Test results can be obtained on the spot and transferred to the doctor directly.” says Lee.
This rapid turnaround time for DMR results is not only a benefit to patients in terms of alleviating anxiety, but also serves to ensure minimal loss of specimen.
According to Castro, standard cytology can take 3 to 4 days because biopsy specimens are left to accumulate until they can be processed in batches. But delay in obtaining results is not the only problem. “We found that if you left the specimens over time, you see marked degradation in the protein markers,” explains Castro. “So either you have to do some sort of fixing to make sure that they are stabilized or run the sample as soon as possible.”
So it would seem, when compared to standard cancer diagnostics, the DMR wins on all accounts, not only in terms of accuracy and safety, but also because its speed ensures maximum specimen integrity.
The future
According to the researchers, the implications for patients are manifold. “As our knowledge advances and we become aware of more relevant markers, we could use different antibodies to improve diagnostics or detect [drug] resistance,” says Lee. ”We could then tailor the platform to specific subsets of cancer.”
Even beyond cancer, tuberculosis is another area of active research in the lab. And since the turnaround time for TB diagnosis is not 3 to 4 days but weeks or months, there is an urgent need for faster techniques. “By changing the antibodies you can detect many different things besides cancer cells,” explains Lee.
As for the device itself, “We are always striving to improve the chemistries; we are not going to end at this DMR version,” says Castro. “We are already working on the next generation.”
Yvonna Fisher-Jeffes
Haun JB*, Castro CM*, Wang R, Peterson VM, Marinelli BS, Lee H, Weissleder R. MicroNMR Enables Rapid and Multiplexed Molecular Analysis of Scant Human Cancer Cells. Science Transl Med, 3, 71ra16
Additional Resources
Science Podcast – Conversation with Ralph Weissleder, who talks about his miniature micro-NMR machine operated by smart phone technology that can detect cancer cells in tissue biopsies from patients in less than an hour. (6 minutes, 23 February 2011) (mp3)
10.1126/scitranslmed.3002048
Research Article Cancer Diagnostics
Micro-NMR for Rapid Molecular Analysis of Human Tumor Samples
Jered B. Haun1,*,
Cesar M. Castro1,2,*,
Rui Wang3,4,
Vanessa M. Peterson1,5,
Brett S. Marinelli1,
Hakho Lee1 and
Ralph Weissleder1,2,6,†
+ Author Affiliations
1Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
2Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA.
3MGH Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, USA.
4Department of Biostatistics, Harvard School of Public Health, Boston, MA 02115, USA.
5Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
6Department of Systems Biology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
†To whom correspondence should be addressed. E-mail: rweissleder@mgh.harvard.edu
/
Abstract
Although tumor cells obtained from human patients by image-guided intervention are a valuable source for diagnosing cancer, conventional means of analysis are limited. Here, we report the development of a quantitative micro-NMR (nuclear magnetic resonance) system for rapid, multiplexed analysis of human tumors. We implemented the technology in a clinical setting to analyze cells obtained by fine-needle aspirates from suspected lesions in 50 patients and validated the results in an independent cohort of another 20 patients. Single fine-needle aspirates yielded sufficient numbers of cells to enable quantification of multiple protein markers in all patients within 60 min. Moreover, using a four-protein signature, we report a 96% accuracy for establishing a cancer diagnosis, surpassing conventional clinical analyses by immunohistochemistry. Our results also show that protein expression patterns decay with time, underscoring the need for rapid sampling and diagnosis close to the patient bedside. We also observed a surprising degree of heterogeneity in protein expression both across the different patient samples and even within the same tumor, which has important implications for molecular diagnostics and therapeutic drug targeting. Our quantitative point-of-care micro-NMR technique shows potential for cancer diagnosis in the clinic.
Although tumor cells obtained from human patients by image-guided intervention are a valuable source for diagnosing cancer, conventional means of analysis are limited. Here, we report the development of a quantitative micro-NMR (nuclear magnetic resonance) system for rapid, multiplexed analysis of human tumors. We implemented the technology in a clinical setting to analyze cells obtained by fine-needle aspirates from suspected lesions in 50 patients and validated the results in an independent cohort of another 20 patients. Single fine-needle aspirates yielded sufficient numbers of cells to enable quantification of multiple protein markers in all patients within 60 min. Moreover, using a four-protein signature, we report a 96% accuracy for establishing a cancer diagnosis, surpassing conventional clinical analyses by immunohistochemistry. Our results also show that protein expression patterns decay with time, underscoring the need for rapid sampling and diagnosis close to the patient bedside. We also observed a surprising degree of heterogeneity in protein expression both across the different patient samples and even within the same tumor, which has important implications for molecular diagnostics and therapeutic drug targeting. Our quantitative point-of-care micro-NMR technique shows potential for cancer diagnosis in the clinic.
Footnotes
↵* These authors contributed equally to this work.
Citation: J. B. Haun, C. M. Castro, R. Wang, V. M. Peterson, B. S. Marinelli, H. Lee, R. Weissleder, Micro-NMR for Rapid Molecular Analysis of Human Tumor Samples. Sci. Transl. Med. 3, 71ra16 (2011).
Copyright © 2011, American Association for the Advancement of Science
Read the Full Text
Podcast: Cancer Diagnostics Science Translational Medicine Podcast: 23 February 2011
Ralph Weissleder and
Orla Smith Sci Transl Med 23 February 2011 3:71pc3
Abstract
Podcast
Press Coverage
ScienceNOW – Cancer Diagnosis by Smart Phone (pdf)
SmartPlanet – A SmartPhone diagnoses tumors at your bedside (pdf)
U.S. News & World Report – Microchip Spots Cancerous Tumors Within an Hour, Study Shows (pdf)
Bloomberg – Harvard Scientists Create Hand-Held Device to Detect Cancer at Bedside (pdf) (video)
Toronto Star’s healthzone.ca – Smartphone app helps diagnose cancers (pdf)
TechNewsDaily – Researchers Use Smartphones to Detect Cancers (pdf)
PhysOrg.com – Smartphone app for cancer diagnosis may be on the way (pdf)
ABC News Radio – Microchip Provides One-Hour Tumor Diagnosis at Patient’s Bedside (pdf)
Boston Globe – Device linked to smartphone helps diagnose cancer (pdf)
Gizmodo – $200 Handheld Scanner Detects Cancer in Just One Hour
Doctors Lounge – New System Detects Tumor Cells Quickly (pdf)
ThirdAge.com – Smartphone App Developed to Identify Cancer (pdf)
TG Daily – Smartphone app could help diagnose cancer (pdf)
USA Today – Study: Microchip spots cancerous tumors within an hour (pdf)
FierceMobile Healthcare – Cancer detection faster, more precise with new app (pdf)
Wall Street Journal – Researchers Create Better Ways to Spot Cancer Cells (pdf)
Health.com – Microchip Spots Cancerous Tumors Within an Hour, Study Shows (pdf)
Daily Mail – The mobile phone app that ‘spots cancer with 100% accuracy in ONE HOUR (pdf)
Fast Company – Detecting Cancer? There’s a Star Trek-Like App for That (pdf)
MIT Technology Review – A One-Hour Cancer Detector (pdf)
Discovery News – Portable Scanner Analyzes Cancer Cells In An Hour (pdf)
medGadget – MicroNMR Device Expedites Cancer Diagnosis Process (pdf)
UCSF; Uncovers hormone pathway to fatty liver disease
UCSF researchers uncover hormone pathway to fatty liver disease
Scientists at the UCSF Cardiovascular Research Institute have discovered how a change in growth hormone activity in mice leads to fatty liver disease, a condition whose human counterpart is of rising concern worldwide.
Disruption of a key protein in the pathway that responds to growth hormone could explain how fatty liver disease develops, the researchers said, but may also offer insights into how our bodies regulate fat in general.
The team's findings and the first reports of a mouse model to study the pathway will appear in the April issue of the Journal of Clinical Investigation and online March 1 at www.jci.org.
Until recently, the growth of fat deposits in the liver that characterizes fatty-liver disease was mainly considered a result of alcoholism. Over the last decade, though, scientists have been baffled by the rising incidence of the non-alcoholic version of the disease, which now affects as many as one in four people worldwide, according to UCSF cardiologist Ethan Weiss, MD, senior author of the paper.
Known risk factors for the condition include obesity, diabetes and malnutrition, among many others, but its precise mechanism had eluded researchers.
"Fatty liver disease is an increasingly prevalent condition that is poorly understood," Weiss said. "We knew that growth hormone had been linked to fatty liver, but previous reports showed that it both causes and cures the condition. We set out to figure out why that happens."
The team focused on a protein in the liver known as JAK2. While better known as being linked to cancers such as blood cancers, this protein is also a key player in an important chemical pathway in the liver.
Normally, the pituitary gland secretes growth hormone, which communicates with JAK2 and sets off a series of steps to produce insulin-like growth factor 1 (IGF-1), an important mediator of growth and other effects. It was common knowledge that disrupting this pathway would halt IGF-1 production, but in their analysis, Weiss and his team found that disrupting the pathway also caused fatty liver disease.
The team engineered a mouse model in which the gene producing JAK2 had been removed solely in the liver, disrupting the pathway that produces the insulin-like growth factor. As expected, the levels of growth factor in these mice were low or nonexistent and the mice developed early and severe fatty-liver disease. Further analysis showed that another protein, called CD36, was working in the liver to draw in the fat in the JAK2-deficient mice.
The amount of growth hormone secreted by the pituitary gland also was dramatically elevated. The team realized that low IGF-1 levels were sending the pituitary gland into overdrive, secreting more growth hormone in order to jumpstart the growth factor's production. But without JAK2, the signaling pathway was broken and IGF-1 production was at a standstill.
That explained the low growth factor levels, but not the fatty livers. The team then took advantage of a second set of mice with no capability of producing growth hormone, which is known to activate energy from fat stores. When crossing the JAK2-deficient mice with the growth hormone-deficient "little" mice, the researchers noticed a huge difference in the offspring.
"We saw a complete disappearance of the fatty liver in these offspring," he said. "It was just gone."
The team concluded that the growth hormone signaling pathway is not only essential in producing IGF-1 and mobilizing fat, but in regulating how fat is taken up by the liver.
This newfound understanding has huge implications for understanding and treating fatty liver disease in humans, Weiss said, such as the possibility of developing a therapeutic drug that works within this pathway.
###
Brandon C. Sos, from the UCSF Cardiovascular Research Institute, was lead author on the paper. Co-authors include Sarah M. Nordstrom and Jennifer L. Tran, also from the UCSF Cardiovascular Research Institute; Charles Harris, from the UCSF Division of Endocrinology and the UCSF-affiliated Gladstone Institute of Cardiovascular Diseases; Mercedesz Balázs and Patrick Caplazi, from Genentech, a subsidiary of Roche Group, South San Francisco, California; Maria Febbraio and Milana A.B. Applegate, of the Lerner Research Institute of the Cleveland Clinic, Cleveland, OH; and Kay-Uwe Wagner, of the Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska.
This research was funded in part by grants from the UCSF Liver Center and the National Institutes of Health (NIH). The authors declare no conflicts of interest.
UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.
For more information, visit www.ucsf.edu .
Scientists at the UCSF Cardiovascular Research Institute have discovered how a change in growth hormone activity in mice leads to fatty liver disease, a condition whose human counterpart is of rising concern worldwide.
Disruption of a key protein in the pathway that responds to growth hormone could explain how fatty liver disease develops, the researchers said, but may also offer insights into how our bodies regulate fat in general.
The team's findings and the first reports of a mouse model to study the pathway will appear in the April issue of the Journal of Clinical Investigation and online March 1 at www.jci.org.
Until recently, the growth of fat deposits in the liver that characterizes fatty-liver disease was mainly considered a result of alcoholism. Over the last decade, though, scientists have been baffled by the rising incidence of the non-alcoholic version of the disease, which now affects as many as one in four people worldwide, according to UCSF cardiologist Ethan Weiss, MD, senior author of the paper.
Known risk factors for the condition include obesity, diabetes and malnutrition, among many others, but its precise mechanism had eluded researchers.
"Fatty liver disease is an increasingly prevalent condition that is poorly understood," Weiss said. "We knew that growth hormone had been linked to fatty liver, but previous reports showed that it both causes and cures the condition. We set out to figure out why that happens."
The team focused on a protein in the liver known as JAK2. While better known as being linked to cancers such as blood cancers, this protein is also a key player in an important chemical pathway in the liver.
Normally, the pituitary gland secretes growth hormone, which communicates with JAK2 and sets off a series of steps to produce insulin-like growth factor 1 (IGF-1), an important mediator of growth and other effects. It was common knowledge that disrupting this pathway would halt IGF-1 production, but in their analysis, Weiss and his team found that disrupting the pathway also caused fatty liver disease.
The team engineered a mouse model in which the gene producing JAK2 had been removed solely in the liver, disrupting the pathway that produces the insulin-like growth factor. As expected, the levels of growth factor in these mice were low or nonexistent and the mice developed early and severe fatty-liver disease. Further analysis showed that another protein, called CD36, was working in the liver to draw in the fat in the JAK2-deficient mice.
The amount of growth hormone secreted by the pituitary gland also was dramatically elevated. The team realized that low IGF-1 levels were sending the pituitary gland into overdrive, secreting more growth hormone in order to jumpstart the growth factor's production. But without JAK2, the signaling pathway was broken and IGF-1 production was at a standstill.
That explained the low growth factor levels, but not the fatty livers. The team then took advantage of a second set of mice with no capability of producing growth hormone, which is known to activate energy from fat stores. When crossing the JAK2-deficient mice with the growth hormone-deficient "little" mice, the researchers noticed a huge difference in the offspring.
"We saw a complete disappearance of the fatty liver in these offspring," he said. "It was just gone."
The team concluded that the growth hormone signaling pathway is not only essential in producing IGF-1 and mobilizing fat, but in regulating how fat is taken up by the liver.
This newfound understanding has huge implications for understanding and treating fatty liver disease in humans, Weiss said, such as the possibility of developing a therapeutic drug that works within this pathway.
###
Brandon C. Sos, from the UCSF Cardiovascular Research Institute, was lead author on the paper. Co-authors include Sarah M. Nordstrom and Jennifer L. Tran, also from the UCSF Cardiovascular Research Institute; Charles Harris, from the UCSF Division of Endocrinology and the UCSF-affiliated Gladstone Institute of Cardiovascular Diseases; Mercedesz Balázs and Patrick Caplazi, from Genentech, a subsidiary of Roche Group, South San Francisco, California; Maria Febbraio and Milana A.B. Applegate, of the Lerner Research Institute of the Cleveland Clinic, Cleveland, OH; and Kay-Uwe Wagner, of the Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska.
This research was funded in part by grants from the UCSF Liver Center and the National Institutes of Health (NIH). The authors declare no conflicts of interest.
UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.
For more information, visit www.ucsf.edu .
Subset of HIV/HCV Co-infected at Risk for Hepatic Steatosis
By: MARY ANN MOON,
Internal Medicine News Digital Network
03/01/11
In patients co-infected with HIV and hepatitis C virus, alcohol use and a high body mass index are associated with progression of hepatic steatosis, whereas exposure to certain antiretrovirals and a high baseline CD4 count appear to be protective against steatosis, Dr. Tinsay A. Woreta and her colleagues reported in the March issue of Gastroenterology.
In their study of 222 patients who were co-infected with HIV and HCV, more than 90% showed no progression of steatosis during nearly 3 years of follow-up.
The findings indicate that efforts to diagnose and prevent hepatic steatosis "should be focused on persons with a high body mass index and excessive alcohol intake," said Dr. Woreta of Johns Hopkins University, Baltimore, and her associates (Gastroenterology 2011 March [doi:10.1053/j.gastro.2010.11.052]).
Hepatitis C virus is not uncommon in patients with HIV infection, and hepatic steatosis affects 30%-70% of those with both infections. The steatosis is associated with hepatic fibrosis and is thought to contribute to the more rapid progression of liver disease in co-infected patients than in those who don’t have concomitant HIV.
"The natural history of hepatic steatosis is incompletely understood" because most studies have been cross-sectional rather than longitudinal," wrote Dr. Woreta and her colleagues. They performed their longitudinal study to prospectively examine the natural history of steatosis, using data from HIV/HCV–co-infected patients who underwent serial liver biopsies while attending an urban HIV clinic.
There were 345 pairs of serial biopsies available for analysis. The study subjects had a median age of 44 years; 66% were men and 87% were black. Nearly half were overweight or obese. Almost all (94%) had HCV genotype 1.
Most patients (194, or 87%) had no or only trivial hepatic steatosis at baseline, and it did not progress during follow-up in 165 (74%) of them. The other 29 patients who had no or only trivial hepatic steatosis at baseline progressed to significant steatosis during follow-up.
In all, 28 patients had significant hepatic steatosis at baseline, and the steatosis actually regressed in 21 (75%) of them. The other seven patients who had significant hepatic steatosis at baseline maintained that steatosis.
Persistence or progression of steatosis was strongly associated with a history of alcohol abuse. Although few patients reported current alcohol abuse, the medical records showed chronic alcoholism or abuse in approximately half. Many study subjects were probably underreporting their current exposure, particularly because they were aware that they were participating in a study of liver outcomes. "Clinicians evaluating fatty liver disease in HIV-infected patients should remain cognizant about the likelihood of underreporting of alcohol consumption," the investigators noted.
Obesity also was strongly associated with persistent or progressive steatosis, which was not unexpected. Although HIV infection was, until a short time ago, "a progressively fatal disease characterized by severe wasting, the advent of HAART [highly active antiretroviral therapy] has transformed HIV into a chronic disease with an increase in the prevalence of obesity."
"These data underscore the importance of measures to prevent and treat obesity in HIV/HCV–co-infected patients, [given] the development or worsening of hepatic steatosis in these patients," the researchers said.
Longer exposure to antiretroviral therapy appeared to be protective against persistent or progressive steatosis. One possible mechanism for this finding is that HIV infection may promote steatosis by facilitating HCV replication in hepatocytes, so reducing the HIV load would ease steatosis.
"Another possibility is that HIV acts synergistically with HCV to disrupt lipid metabolism. Thus, direct inhibition of HIV viral replication could decrease steatosis, particularly if the antiretroviral agent [has] minimal impact on mitochondrial replication and function," Dr. Woreta and her colleagues said.
They emphasized that stavudine, which has been designated as a "nonpreferred" antiretroviral agent because it was thought to contribute to steatosis, was used by only 6% of patients in this study, so the authors were unable to assess its effects.
A higher CD4 cell count at baseline also appeared to be protective against steatosis. The investigators did not offer any possible explanations for this effect. No association was found between steatosis progression and patient age, sex, race, diabetes status, HCV genotype, fibrosis status, or HCV therapy, they noted.
This study was supported by the National Institute on Drug Abuse, the National Institute on Alcohol Abuse and Alcoholism, the National Center for Complementary and Alternative Medicine, the Agency for Healthcare Policy and Research, and the clinical research unit at the Johns Hopkins Medical Institutions. The investigators reported that they had no financial conflicts of interest.
Internal Medicine News Digital Network
03/01/11
In patients co-infected with HIV and hepatitis C virus, alcohol use and a high body mass index are associated with progression of hepatic steatosis, whereas exposure to certain antiretrovirals and a high baseline CD4 count appear to be protective against steatosis, Dr. Tinsay A. Woreta and her colleagues reported in the March issue of Gastroenterology.
In their study of 222 patients who were co-infected with HIV and HCV, more than 90% showed no progression of steatosis during nearly 3 years of follow-up.
The findings indicate that efforts to diagnose and prevent hepatic steatosis "should be focused on persons with a high body mass index and excessive alcohol intake," said Dr. Woreta of Johns Hopkins University, Baltimore, and her associates (Gastroenterology 2011 March [doi:10.1053/j.gastro.2010.11.052]).
Hepatitis C virus is not uncommon in patients with HIV infection, and hepatic steatosis affects 30%-70% of those with both infections. The steatosis is associated with hepatic fibrosis and is thought to contribute to the more rapid progression of liver disease in co-infected patients than in those who don’t have concomitant HIV.
"The natural history of hepatic steatosis is incompletely understood" because most studies have been cross-sectional rather than longitudinal," wrote Dr. Woreta and her colleagues. They performed their longitudinal study to prospectively examine the natural history of steatosis, using data from HIV/HCV–co-infected patients who underwent serial liver biopsies while attending an urban HIV clinic.
There were 345 pairs of serial biopsies available for analysis. The study subjects had a median age of 44 years; 66% were men and 87% were black. Nearly half were overweight or obese. Almost all (94%) had HCV genotype 1.
Most patients (194, or 87%) had no or only trivial hepatic steatosis at baseline, and it did not progress during follow-up in 165 (74%) of them. The other 29 patients who had no or only trivial hepatic steatosis at baseline progressed to significant steatosis during follow-up.
In all, 28 patients had significant hepatic steatosis at baseline, and the steatosis actually regressed in 21 (75%) of them. The other seven patients who had significant hepatic steatosis at baseline maintained that steatosis.
Persistence or progression of steatosis was strongly associated with a history of alcohol abuse. Although few patients reported current alcohol abuse, the medical records showed chronic alcoholism or abuse in approximately half. Many study subjects were probably underreporting their current exposure, particularly because they were aware that they were participating in a study of liver outcomes. "Clinicians evaluating fatty liver disease in HIV-infected patients should remain cognizant about the likelihood of underreporting of alcohol consumption," the investigators noted.
Obesity also was strongly associated with persistent or progressive steatosis, which was not unexpected. Although HIV infection was, until a short time ago, "a progressively fatal disease characterized by severe wasting, the advent of HAART [highly active antiretroviral therapy] has transformed HIV into a chronic disease with an increase in the prevalence of obesity."
"These data underscore the importance of measures to prevent and treat obesity in HIV/HCV–co-infected patients, [given] the development or worsening of hepatic steatosis in these patients," the researchers said.
Longer exposure to antiretroviral therapy appeared to be protective against persistent or progressive steatosis. One possible mechanism for this finding is that HIV infection may promote steatosis by facilitating HCV replication in hepatocytes, so reducing the HIV load would ease steatosis.
"Another possibility is that HIV acts synergistically with HCV to disrupt lipid metabolism. Thus, direct inhibition of HIV viral replication could decrease steatosis, particularly if the antiretroviral agent [has] minimal impact on mitochondrial replication and function," Dr. Woreta and her colleagues said.
They emphasized that stavudine, which has been designated as a "nonpreferred" antiretroviral agent because it was thought to contribute to steatosis, was used by only 6% of patients in this study, so the authors were unable to assess its effects.
A higher CD4 cell count at baseline also appeared to be protective against steatosis. The investigators did not offer any possible explanations for this effect. No association was found between steatosis progression and patient age, sex, race, diabetes status, HCV genotype, fibrosis status, or HCV therapy, they noted.
This study was supported by the National Institute on Drug Abuse, the National Institute on Alcohol Abuse and Alcoholism, the National Center for Complementary and Alternative Medicine, the Agency for Healthcare Policy and Research, and the clinical research unit at the Johns Hopkins Medical Institutions. The investigators reported that they had no financial conflicts of interest.
Hepatitis C News; The Race is On for New Hepatitis C Drugs
by Dr. Joe Galati on February 28, 2011
For those of us that are involved in the care of patients with chronic hepatitis C, the “never too soon” announcement that we will finally have new drugs to treat our hepatitis C patients with cannot come soon enough. There is a real possibility that one and possibly two new agents for hepatitis C will be granted approval by the FDA in the months to come. When that day will be is unknown to me, but I anticipate later this summer at the latest.
There is a frenzy of discussion in the press, as well as the blogosphere on the new drugs, namely Telaprevir, manufactured by Vertex, and Boceprevir, manufactured by Merck. I have had the opportunity to use both of these drugs in clinical studies over the past several years, and understand how they both work, and what patients can expect. Much to everyone’s surprise, patients will still need to take one of the pegylated interferons once weekly, and ribavirin twice daily. The new drugs are added to this backbone of therapy. Besides the expected interferon and ribavirin side effects, the protease inhibitors do add some additional problems, but for the most part, in experienced hands, they can be managed fine. Once these drugs are approved, I anticipate a mad-dash of patients, wanting to get their hands on these therapies.
My advise is to start requesting your old records now if you were previously treated. Knowing exactly how many weeks you were treated, what your response was, and what complications developed, will be important information prior to commencing any sort of new therapy, regardless of which protease inhibitor you are started on. It can take weeks to get these records, so start asking now.
There are hundreds of thousands of patients with hepatitis C that are either naive to therapy (never treated), or previously treated with a partial response (null responder, non-responder, or responder-relapser). All of these individuals should be considered for these new therapies, but you need to be sure you are being seen by a practice that can handle these patients. With the new protease inhibitor drugs, resistance can become an issue, and discontinuing the therapy in a timely fashion is important. The treatment protocols are different from prior therapies, with a lead-in phase with interferon. All of these steps requires careful monitoring and communication with the patient. An experienced staff of nurses will be needed. Prior to being evaluated for these new exciting drugs, you, as a consumer, need to ask these questions to see if your care provider has the necessary experience, as well as a dedicated team to support them once patients are started on therapy.
Besides the two contenders for FDA approval later this summer, the pipeline for additional drugs is incredibly long. We are conducting research studies on an additional 12 drugs, all of which look promising. Some of the protocols are free of the hated interferon. Imagine, HCV therapy without interferon? That day will be here, allbeit several more years. I am currently in Chicago with the HCV team from Abbott, who also has a number of exciting compounds we will start studying soon with our patients in Houston.
So, when will the new hepatitis C drugs be available? My best educated guess will be by Labor Day, but we may all be surprised sooner, based on the chatter in the press and FDA hallways.
I am eager to hear what you think? Comment on your prior experience with hepatitis C therapy.,
,
In The News APASL
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From NATAP
. ,
The 21st Conference of the Asian Pacific Association for the Study of the Liver
APASL Feb 17-20, 2011 Bangkok, Thailand
APASL: Associations between two SNPs (rs12979860, rs12980275) and complete early virological response for peginterferon alfa-2a (40KD) - based treatment in naive patients and previous non-responders - (02/28/11)
APASL: Retrospective pooled safety analysis of standard- versus high-dose peginterferon alfa-2a (40KD) (PEGASYS) in chronic hepatitis C genotype 1 or 4 patients - (02/28/11)
. ,
The 21st Conference of the Asian Pacific Association for the Study of the Liver
APASL Feb 17-20, 2011 Bangkok, Thailand
APASL: Associations between two SNPs (rs12979860, rs12980275) and complete early virological response for peginterferon alfa-2a (40KD) - based treatment in naive patients and previous non-responders - (02/28/11)
APASL: Retrospective pooled safety analysis of standard- versus high-dose peginterferon alfa-2a (40KD) (PEGASYS) in chronic hepatitis C genotype 1 or 4 patients - (02/28/11)
Hepatitis-associated aplastic anemia (HAAA) is an uncommon but distinct variant of aplastic anemia in which pancytopenia appears two to three months after an acute attack of hepatitis. HAAA occurs most frequently in young male children and is lethal if leave untreated.The etiology of this syndrome is proposed to be attributed to various hepatitis and non hepatitis viruses. Several hepatitis viruses such as HAV, HBV, HCV, HDV, HEV and HGV have been associated with this set of symptoms.Viruses other than the hepatitis viruses such as parvovirus B19, Cytomegalovirus, Epstein bar virus, Transfusion Transmitted virus (TTV) and non-A-E hepatitis virus (unknown viruses) has also been documented to develop the syndrome. Considerable evidences including the clinical features, severe imbalance of the T cell immune system and effective response to immunosuppressive therapy strongly present HAAA as an immune mediated mechanism.
However, no association of HAAA has been found with blood transfusions, drugs and toxins. Besides hepatitis and non hepatitis viruses and immunopathogenesis phenomenon as causative agents of the disorder, telomerase mutation, a genetic factor has also been predisposed for the development of aplastic anemia.Diagnosis includes clinical manifestations, blood profiling, viral serological markers testing, immune functioning and bone marrow hypocellularity examination. Patients presenting the features of HAAA have been mostly treated with bone marrow or hematopoietic cell transplantation from HLA matched donor, and if not available then by immunosuppressive therapy.New therapeutic approaches involve the administration of steroids especially the glucocorticoids to augment the immunosuppressive therapy response. Pancytopenia following an episode of acute hepatitis response better to hematopoietic cell transplantation than immunosuppressive therapy.Author: Bisma RauffMuhammad IdreesShahida ShahSadia ButtAzeem ButtLiaqat AliAbrar HussainIrshad RehmanMuhammad AliCredits/Source: Virology Journal 2011, 8:87
CROI: HIV-Resistant T Cells on Horizon
BOSTON -- Researchers are cautiously excited about preliminary data showing HIV-resistant T cells can be created in the lab and returned to patients, possibly offering a new approach to therapy.
However, no association of HAAA has been found with blood transfusions, drugs and toxins. Besides hepatitis and non hepatitis viruses and immunopathogenesis phenomenon as causative agents of the disorder, telomerase mutation, a genetic factor has also been predisposed for the development of aplastic anemia.Diagnosis includes clinical manifestations, blood profiling, viral serological markers testing, immune functioning and bone marrow hypocellularity examination. Patients presenting the features of HAAA have been mostly treated with bone marrow or hematopoietic cell transplantation from HLA matched donor, and if not available then by immunosuppressive therapy.New therapeutic approaches involve the administration of steroids especially the glucocorticoids to augment the immunosuppressive therapy response. Pancytopenia following an episode of acute hepatitis response better to hematopoietic cell transplantation than immunosuppressive therapy.Author: Bisma RauffMuhammad IdreesShahida ShahSadia ButtAzeem ButtLiaqat AliAbrar HussainIrshad RehmanMuhammad AliCredits/Source: Virology Journal 2011, 8:87
CROI: HIV-Resistant T Cells on Horizon
BOSTON -- Researchers are cautiously excited about preliminary data showing HIV-resistant T cells can be created in the lab and returned to patients, possibly offering a new approach to therapy.
Published: Mar 1, 2011 10:40 am
A new study of patients with both HIV and hepatitis C found they had a higher rate of osteoporosis than people in previous studies who had HIV but not hepatitis C. The researchers also found that controlled HIV replication, but not the severity of liver disease, was associated with increased risk of osteoporosis in people with both HIV and hepatitis C.
The study investigators noted that the primarily African-American study participants had a higher rate of osteoporosis than patients in a similar study of Caucasians in Italy. While factors other than race may be involved, the researchers suggested that African-Americans with HIV and hepatitis C virus (HCV) co-infection may be at higher risk of osteoporosis than expected.
A new study of patients with both HIV and hepatitis C found they had a higher rate of osteoporosis than people in previous studies who had HIV but not hepatitis C. The researchers also found that controlled HIV replication, but not the severity of liver disease, was associated with increased risk of osteoporosis in people with both HIV and hepatitis C.
The study investigators noted that the primarily African-American study participants had a higher rate of osteoporosis than patients in a similar study of Caucasians in Italy. While factors other than race may be involved, the researchers suggested that African-Americans with HIV and hepatitis C virus (HCV) co-infection may be at higher risk of osteoporosis than expected.
Hepatitis B Rates Drop Among Kids Due To Effective Vaccination Programs, More Efforts Needed For Adults
28 February 2011Approximately 5.1% of the American population had been exposed to HBV (Hepatitis B virus) between 1988 and 1994, researchers wrote in Annals of Internal Medicine. Since that date, extensive vaccination campaigns for...
28 February 2011Approximately 5.1% of the American population had been exposed to HBV (Hepatitis B virus) between 1988 and 1994, researchers wrote in Annals of Internal Medicine. Since that date, extensive vaccination campaigns for...
Breast Milk Ice Cream Confiscated Over Hepatitis Fears
Published March 01, 2011
FoxNews.com
Published March 01, 2011
FoxNews.com
LONDON -- A London borough council confiscated breast milk ice cream being sold in a shop in the city's tourist district over fears it could contain hepatitis viruses and sent it for testing.
"Following two complaints from members of the public and concerns from the Health Protection Agency and Food Standards Agency, our officers visited the premises and removed all ice cream being sold as containing breast milk," council officer Brian Connell told the London Evening Standard newspaper Tuesday. "Selling foodstuffs made from another person's bodily fluids can lead to viruses being passed on and in this case, potentially hepatitis."
"Following two complaints from members of the public and concerns from the Health Protection Agency and Food Standards Agency, our officers visited the premises and removed all ice cream being sold as containing breast milk," council officer Brian Connell told the London Evening Standard newspaper Tuesday. "Selling foodstuffs made from another person's bodily fluids can lead to viruses being passed on and in this case, potentially hepatitis."
Woman Gets New Liver From Church Parishioner
March 1, 2011 7:52 AM
CHICAGO (WBBM) – A 68-year-old local woman has received a liver donation from a member of her Northwest Side church.
Roberta Sturgill contracted hepatitis C from a blood transfusion in 1995. She was in need of a liver transplant, but thought all hope may be lost when her niece’s liver was rejected for being too small.
Wellness
Açaí Juice
In the nutraceutical or nutritional supplements market, there is never any shortage of bandwagons. One of the loudest and largest these days is the açaí bandwagon. Harvested from a Brazilian palm, açaí (ah-SAH-ee) berries are a dietary staple in Brazil and have also been used medicinally by Amazonian tribes. Açaí juice was introduced in the U.S. in 2001, and there are now more than 50 new food and drink products containing açaí. As a juice, pulp, powder, or capsule, it is marketed as a magic path to weight loss, a wrinkle remover, a way to cleanse the body of "toxins," and indeed just a plain old miracle cure. It is often combined with other ingredients, such as glucosamine, so that the claims for benefits multiply exponentially.
Offers for açaí have flooded the nation’s email boxes.
On the Internet you’ll find a bouquet of endorsements from such celebrities as Oprah, Nicholas Perricone (the TV "skin doctor"), and Rachael Ray (the TV chef), plus statements by these same celebrities denying any such endorsement, or at least any endorsement of a particular brand, except that Dr. Perricone sells a brand of his own. You will also find a war of words among makers of açaí products, each one claiming safety and effectiveness for its particular formulation, and warning of scams by others.
Since açaí came on the market there have been a few studies pointing to potential benefits. Like many other fruits, açaí berries are high in antioxidants (molecules that quell cell-damaging free radicals) and other interesting compounds. But these were lab studies, and the results may not apply to humans. There is no scientific basis for weight-loss claims or any other health claims for açaí. The term "antioxidant" has become a sales tool.
Consumer protection groups such as the Center for Science in the Public Interest (CSPI) and the Better Business Bureau (BBB) have now come out against açaí marketers. "If Bernard Madoff were in the food business," said a CSPI nutritionist, "he’d be offering ‘free’ trials of açaí-based weight-loss products." Online ads regularly promise a free trial, saying that all you have to pay is shipping and handling. The catch is that you must supply your credit card number, and you’ll automatically be signed up for $50 monthly shipments that will prove hard to cancel.
We urge you not to give your credit card number to anybody selling açaí products. Hundreds of complaints have been registered, and you may never get your money back. Beware of web-sites warning you of açaí scams—far from helping you get your money back, most turn out to be just sales pitches for more açaí.
There is no magic berry for weight loss or good health. Açaí berries are no doubt a good food, like other berries, but why pay a fortune for them or supplements containing them?
Liver Cancer
RICHMOND, Va., March 1, 2011 /PRNewswire/ -- Wako Diagnostics, a division of Wako Chemicals USA, has received 510(k) clearance from the U.S. Food and Drug Administration (FDA) to market the uTASWako i30 instrument with alpha-fetoprotein L3 (AFP-L3) and des-gamma-carboxy prothrombin (DCP) in vitro diagnostic (IVD) tests in the USA. The AFP-L3 and DCP assays are intended for use by healthcare professionals as an aid in the risk assessment of patients with chronic liver disease for development of hepatocellular carcinoma (HCC).
"Wako is very pleased to receive 510(k) clearance for these assays using microfluidic technology," said Peter Panfili Ph.D., General Manager, Wako Diagnostics. "We expect that the adoption of these biomarkers into HCC surveillance programs will complement the use of imaging technologies to bring about the desired earlier detection and treatment of liver cancer."
HCC, primary liver cancer, is currently the fastest growing cause of cancer-related death in the USA. It has been demonstrated that HCC surveillance programs for at-risk patients improves applicability of curative therapies. Incorporating these biomarkers as additional surveillance tools will improve the chance of detecting early stage HCC and improve patient outcomes.
Microfluidics has enabled miniaturization and integration of key analyzer processes for the uTASWako i30: sampling, mixing, separation, and detection on microfluidic chips. The system uses immunochemical and electrophoretic techniques to achieve rapid, accurate, precise and sensitive assay results.
As a bench top automated instrument, the uTASWako i30 is designed for efficiency and ease of use in a clinical chemistry setting. Up to six analytes may be selected per patient sample with the first result reported in nine minutes. With automated calibration and quality control, the uTASWako i30 requires minimal setup time. Reagent usage is tracked using radio frequency identification (RFID) tags.
The uTASWako i30 reports AFP-L3%, total AFP, and DCP values using Wako's unique reagents. This IVD test system is available to hospital laboratories, reference laboratories and tertiary care centers. Wako is the only company that offers 510(k)-cleared AFP-L3 and DCP assays for IVD use.
Microfluidics has enabled miniaturization and integration of key analyzer processes for the uTASWako i30: sampling, mixing, separation, and detection on microfluidic chips. The system uses immunochemical and electrophoretic techniques to achieve rapid, accurate, precise and sensitive assay results.
As a bench top automated instrument, the uTASWako i30 is designed for efficiency and ease of use in a clinical chemistry setting. Up to six analytes may be selected per patient sample with the first result reported in nine minutes. With automated calibration and quality control, the uTASWako i30 requires minimal setup time. Reagent usage is tracked using radio frequency identification (RFID) tags.
The uTASWako i30 reports AFP-L3%, total AFP, and DCP values using Wako's unique reagents. This IVD test system is available to hospital laboratories, reference laboratories and tertiary care centers. Wako is the only company that offers 510(k)-cleared AFP-L3 and DCP assays for IVD use.
Hepatitis Awareness: 10 Liver Cancer Risks
Liver cancer rates doubled in the United States between 1976 and 2002, and is one of the most deadly cancers worldwide. A recent review article reported on the risk factors:
1. Hepatitis B or C virus infection. Worldwide, viral liver infections are the most common cause of liver cancer. Rates of hepatitis C infection are on the rise in the United States, and this is one contributing factor to the rising rates of liver cancer.
2. Alcohol. Liver damage is the most familiar hazard of excessive alcohol consumption. Cirrhosis is a common step on the way to liver cancer..............
Pharmaceuticals
Pharma jobs outlook bleak as European sites axed
Tue Mar 1, 2011 5:50am EST
* Pfizer, Merck, AstraZeneca sites in Europe face closure
Drug industry moving to "fragmented" model of research
* 6,000 pharmaceutical jobs gone in UK in last 12 months
By Ben Hirschler
LONDON, March 1 (Reuters) - Drug companies are pulling down the shutters on major European research laboratories, posing a serious challenge to the region's ambitions for creating new high-tech jobs.
Nowhere is the problem more acute than in Britain, where Prime Minister David Cameron named pharmaceuticals as one of five "industries of the future" in early January -- only to have the rug pulled from under his feet two weeks later.
Pfizer's (PFE.N) new CEO Ian Read told Cameron on Jan. 24 the world's biggest drugmaker's was closing its Sandwich site in southern England with the loss of up to 2,400 jobs.
Company executives said on Monday they had been discussing the possibility of shutting Sandwich as early as last November, when site head Ruth McKernan started to wind down recruitment for the flagship research centre.
Pfizer, facing massive revenue losses from drugs whose patents are expiring, is exiting Sandwich as part of a drive to cut 2012 research and development (R&D) spending by as much as $2 billion from an originally planned $8.0-8.5 billion.
The group is talking to a number of companies interested in using part of Sandwich, and McKernan said it was encouraging staff hoping to form spin-outs or management buy-outs.
But she acknowledged finding a single occupier for the 3 million square feet available at Sandwich "would be a real challenge".
"This is really an evolution of the industry to a more fragmented model," McKernan told a parliamentary committee probing Pfizer's plans to quit Sandwich within 18-24 months.
NEW TENANTS?
Pfizer's site is the biggest casualty of the current round of drug industry retrenchment but it is not alone -- and the flood of specialist lab-equipped real estate now hitting the market makes it doubly tough to find new occupiers.
From Pharmalot
Abbott & Glaxo Go To Court Over AIDS Drug Price
By Ed Silverman // March 1st, 2011 /
8:39 am
Abbott sells a combo pill called Kaletra that includes Norvir and its own protease inhibitor. The lawsuit claims Abbott raised Norvir’s price - but not the Kaletra price - in order to boost Kaletra sales at the expense of other protease inhibitors that require Norvir as a booster. In other words, Abbott allegedly tried to use Norvir to create an illegal monopoly over the market for protease inhibitors. The stakes are high, though, because the damages can be tripled
Off The Cuff
Liver cancer rates doubled in the United States between 1976 and 2002, and is one of the most deadly cancers worldwide. A recent review article reported on the risk factors:
1. Hepatitis B or C virus infection. Worldwide, viral liver infections are the most common cause of liver cancer. Rates of hepatitis C infection are on the rise in the United States, and this is one contributing factor to the rising rates of liver cancer.
2. Alcohol. Liver damage is the most familiar hazard of excessive alcohol consumption. Cirrhosis is a common step on the way to liver cancer..............
Pharmaceuticals
Pharma jobs outlook bleak as European sites axed
Tue Mar 1, 2011 5:50am EST
* Pfizer, Merck, AstraZeneca sites in Europe face closure
Drug industry moving to "fragmented" model of research
* 6,000 pharmaceutical jobs gone in UK in last 12 months
By Ben Hirschler
LONDON, March 1 (Reuters) - Drug companies are pulling down the shutters on major European research laboratories, posing a serious challenge to the region's ambitions for creating new high-tech jobs.
Nowhere is the problem more acute than in Britain, where Prime Minister David Cameron named pharmaceuticals as one of five "industries of the future" in early January -- only to have the rug pulled from under his feet two weeks later.
Pfizer's (PFE.N) new CEO Ian Read told Cameron on Jan. 24 the world's biggest drugmaker's was closing its Sandwich site in southern England with the loss of up to 2,400 jobs.
Company executives said on Monday they had been discussing the possibility of shutting Sandwich as early as last November, when site head Ruth McKernan started to wind down recruitment for the flagship research centre.
Pfizer, facing massive revenue losses from drugs whose patents are expiring, is exiting Sandwich as part of a drive to cut 2012 research and development (R&D) spending by as much as $2 billion from an originally planned $8.0-8.5 billion.
The group is talking to a number of companies interested in using part of Sandwich, and McKernan said it was encouraging staff hoping to form spin-outs or management buy-outs.
But she acknowledged finding a single occupier for the 3 million square feet available at Sandwich "would be a real challenge".
"This is really an evolution of the industry to a more fragmented model," McKernan told a parliamentary committee probing Pfizer's plans to quit Sandwich within 18-24 months.
NEW TENANTS?
Pfizer's site is the biggest casualty of the current round of drug industry retrenchment but it is not alone -- and the flood of specialist lab-equipped real estate now hitting the market makes it doubly tough to find new occupiers.
From Pharmalot
Abbott & Glaxo Go To Court Over AIDS Drug Price
By Ed Silverman // March 1st, 2011 /
8:39 am
Abbott sells a combo pill called Kaletra that includes Norvir and its own protease inhibitor. The lawsuit claims Abbott raised Norvir’s price - but not the Kaletra price - in order to boost Kaletra sales at the expense of other protease inhibitors that require Norvir as a booster. In other words, Abbott allegedly tried to use Norvir to create an illegal monopoly over the market for protease inhibitors. The stakes are high, though, because the damages can be tripled
Off The Cuff
From Celebrity Dianosis;
Recently, radio/TV personality, internist and host of Celebrity Rehab Dr. Drew Pinsky was asked to comment on one of Charlie Sheen's recent public statements and said, "He's in an acute manic state now ... whether it's drug-induced or drug-withdrawal or he has bipolar disorder, I don't know but right now he's manic and that's an acute psychiatric emergency. Bipolar patients who are manic are more likely to kill themselves or hurt themselves than when they're depressed. So this is somebody ...........
21st Century Medicine, 19th Century Practices
8:19 AM Friday February 25, 2011
8:19 AM Friday February 25, 2011
Editor's note: This post is part of a three-week series examining innovation in health care, published in partnership with the Advanced Leadership Initiative at Harvard University.
By the time I saw Mr. Johnson (not his real name), he had received three CT scans in less than 24 hours — and we had done nothing to make him feel better or cure his clinical problem. The day prior, he had seen his primary care physician in rural Maine for fever and belly pain, and had a CT scan which showed an abscess in his abdomen. At the nearby emergency room, where he went next, another physician, unable to obtain the original films, reordered the CT scan. The ER physician was about to hospitalize the patient when Mr. Johnson reported being a veteran and was promptly transferred to the Boston VA. The films were misplaced during his transfer to Boston and after arriving, he had — you guessed it — yet another CT scan confirming the abscess. All that diagnosing and still no treatment! Although this true story is alarming, it's hardly atypical for our $2.5 trillion healthcare system.........
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