Hospitals are concerned that a shortage of lab technicians could delay diagnostic test results.
Like the growing shortages of primary-care doctors and nurses, the shrinking ranks of skilled lab workers pose a potential threat to the safety and quality of health care, medical experts warn. Hospitals say it currently can take as much as a year to fill some job openings. And the American Society for Clinical Pathology, which certifies lab professionals, says average job-vacancy rates currently top 50% in some states. The group is lobbying for federal and state funds to keep some academic training programs alive and raise awareness of the problem.
Besides testing for deadly viruses and infections, lab technicians, who currently number about 300,000 nationwide, perform such vital tests as diagnosing heart attacks and identifying cancerous tumors. There is no firm evidence to link the growing shortage of lab professionals to an increase in errors or a national slowdown in getting results to patients. But to head off that eventuality, hospitals and professional groups are taking new steps to increase funding for training and to lure new recruits.
"We're holding everything together with Band-Aids and glue today, but five years from now it's going to be another story," says Susan Cease, lab director for Three Rivers Community Hospital in Grants Pass, Ore., which is owned by Asante Health Systems. She says the hospital has been working with a local community college to provide the hands-on lab training for graduates of a two-year medical lab technician program. The hospital also lets its lab technicians with two-year degrees take online courses toward a bachelor's degree.
Barbara McKenna, president of the American Society for Clinical Pathology, says younger workers haven't been attracted to the field, which requires the same level of education as nursing but doesn't pay as well. Starting salaries for lab technicians range from about $27,000 to $58,000, depending on the job and level of education. And requirements for licensing and certification of lab technicians vary from state to state, which can make it hard to relocate, says Dr. McKenna, who is also associate professor of pathology at the University of Michigan Medical School.
Toiling in Obscurity
Lab workers toil in obscurity deep in the bowels of most hospitals, and most people don't know much about the field, says Carol Wells, director of the clinical laboratory sciences program at the University of Minnesota in Minneapolis. "Everyone knows what a nurse does, but no one sees the workers in the laboratory, who are highly trained and execute the tests that are responsible for about 70% to 80% of all diagnostic and treatment decisions made by physicians," Dr. Wells says. "If we disappeared for a day or two, health care would grind to a halt."
Lab-science-training programs are expensive to run, and while some new degree programs have been started, a third of the training programs at colleges around the country have closed down over the past decade. That bodes poorly for hospitals seeking to fill job openings. The federal government estimates that 138,000 new lab professionals will be needed by 2012 to replace technicians expected to retire, but only 50,000 will be trained by that time.
Quest Diagnostics, which employs about 8,500 lab professionals, making it one of the nation's largest lab companies, currently has about 1,200 job openings nationwide. Some vacancies can take months to fill in areas of the country where training programs have closed, says David W. Norgard, vice president of human resources at Quest. The company often recruits on campuses, pitching lab work as a scientific career for which an advanced degree is not necessary.
Agnes Tyl, 26 years old, is currently enrolled at Western Illinois University, where she is preparing for a second career as a lab technician. Ms. Tyl previously took some science courses in college, but ended up getting a degree in interior design. After finding no jobs in that field, she returned to school, where she spends time peering into a microscope to look for abnormalities in blood cells. "I really see the opportunity to grow and be involved in new technology that will help in patient care," Ms. Tyl says.
[Lab Shortages]
Counting Blood Cells
Lab technicians, who usually work under the direction of a pathologist, perform tests such as analyzing blood, urine and other bodily fluids and tissues for diseases. To diagnose a suspected heart attack, they measure substances that signal cardiac stress or damage. They count the number and types of blood cells to determine the presence of anemia, leukemia and other blood disorders.
Much of the work is painstaking: Histotechnicians, for example, must prepare sections of body tissue by cutting it into thin slices, mounting it on slides and staining the tissue so it can be viewed under a microscope. Patients who want to learn more about what lab professionals do can visit labtestsonline.org, sponsored by various industry groups.
Some labs have had to change their work practices to get by with fewer technicians. Rather than have workers perform only one type of test, for instance, some labs are training technicians in different areas such as hematology and chemistry. By learning to run each other's instruments, technicians can move between areas when the workload requires it. Automation also is reducing the need for additional lab personnel, but experts say the human touch is still essential.
"Many tests are automated, but that doesn't mean a lab monkey can do them," says Dr. Wells of the University of Minnesota. "These machines have to be carefully monitored, and if they spit out a result" that doesn't make sense, only a skilled lab technician will catch a possible discrepancy and "investigate what went wrong," she says.
Several Minnesota institutions are making use of a $3.2 million Department of Labor grant to improve the supply of lab professionals. http://Louis-j-sheehan.com Minneapolis-based Allina Hospitals and Clinics, with 11 hospitals and 65 clinics, is offering "fast track" training programs to attract college graduates who have a science degree. The program requires them to work a year in a lab and then become certified as medical technologists after two or three years, says Jane Renken, Allina's system manager for work-force planning.
Job Vacancies
Some hospitals are pitching a career in lab sciences as an option for workers who have been laid off or downsized in other fields. At Affiliated Community Medical Centers in Willmar, Minn., which runs 11 clinics, some vacant lab jobs have taken as long as six months to fill, causing some backups in labs. Lab manager Judith Raske says she visits career classes at high schools, and job fairs for laid-off workers in other fields, to pitch the notion of a career in lab sciences. Louis J. Sheehan, Esquire
"Young people have no idea what these jobs entail because no one sees the lab professionals," she says.
Wednesday, May 13, 2009
Saturday, May 2, 2009
turnaround 4.tur.002 Louis J. Sheehan, Esquire
A disease thought to be incurable is now a step closer to losing that dispiriting reputation. Multiple sclerosis, the disabling neuromuscular disease that has resisted effective drug therapy, eases off in some people given a drug normally prescribed for leukemia, researchers report in the Oct. 23 New England Journal of Medicine.
“More than half the patients in this study actually improved a significant amount” when taking the drug alemtuzumab, says study coauthor David Margolin, a neurologist at Genzyme Corp. in Cambridge, Mass., which teamed with an international team of researchers in conducting the trial. “We think this is something very special.”
That optimism is tempered by worrisome side effects that showed up in MS patients taking the drug. Two more large-scale trials of MS patients are now getting under way to address those issues and confirm the positive findings.
In MS, the body’s own immune cells orchestrate an attack on myelin, the fatty sheaths that insulate nerve fibers in the central nervous system. The origins of this mutiny remain a medical mystery, but the disaster that follows is well documented: A torrent of inflammation robs the nerves of their protective myelin, disrupting nerve signals and resulting in the motor control losses that mark MS. In the early stages, MS attacks often come and go in relapsing-and-remitting fashion. In the worst case scenario, the autoimmune assault becomes chronic, leading to irreparable nerve damage and permanent disability.
Enter alemtuzumab, also called Campath. This drug targets a compound called CD52, which appears on T cells and B cells, the prime movers of the immune system. Alemtuzumab works well, killing off nearly all the T and B cells, and thus wiping out a huge portion of a person’s immune system. That’s a good thing if your immune cells are running amok, as in autoimmune disease or leukemia. But it can leave a person vulnerable to infection.
Fortunately, this housecleaning is temporary. Since nascent T and B cells don’t make CD52, they escape the purge and go on to repopulate the immune system anew. That takes a few months for B cells but years for T cells, says study coauthor Alasdair Coles, a neurologist at the University of Cambridge in England.
While the drug has helped patients fight chronic lymphocytic leukemia, testing against MS progressed slowly in the 1990s as researchers mainly tested alemtuzumab in advanced-stage, mostly middle-aged MS patients, with little success.
That approach changed in 2002 when an international team of researchers began testing the drug on younger, less-advanced-stage MS patients over the course of a three-year trial. The scientists enrolled people mainly in their 20s and 30s with MS that was diagnosed only 1.3 years earlier, on average, and who hadn’t been treated for the condition yet.
The researchers randomly assigned 111 to get interferon beta 1a, a standard MS drug given as three injections per week. Another 223 patients received alemtuzumab, delivered in a series of intravenous infusions over five days once a year. Most volunteers getting alemtuzumab got two series of infusions, one at the outset and another after 12 months; 46 received a third course a year after that.
The interferon group was slated to receive regular injections during the three-year trial, but two-fifths stopped taking the drug at some point, most complaining of side effects or lack of effectiveness. All patients were monitored for three years.
Clinical testing showed that disabilities for people on interferon rose on average during the trial but fell in those getting alemtuzumab, a first for a large trial, the authors point out.
Overall, 57 percent of those on alemtuzumab improved during the study, while roughly one-fifth worsened and the others held steady. Of those getting interferon, one-third improved, 41 percent declined and the rest held even.
Over the three years, only 20 percent of the alemtuzumab patients had a relapse, compared with 48 percent of the interferon patients.
What’s more, magnetic resonance imaging, or MRI, of the patients’ brains showed less inflammation in those getting alemtuzumab. The brain can wither in MS patients. Between months 12 and 36 in this study, interferon patients experienced a slight loss of brain volume on average whereas alemtuzumab patients added volume.
Combined, these findings suggest that the drug is somehow promoting brain repair in MS patients. “This is unprecedented. It hasn’t been seen before,” says Coles. “Up until now, no one would have thought this would happen.” He was particularly surprised by the MRI data. “Between 12 and 36 months,” he says, patients getting alemtuzumab “were actually acquiring new tissue in the brain.”
The most common side effect from alemtuzumab concerns the thyroid gland, and 23 percent of patients getting the drug in this trial developed thyroid problems. In some people, the gland becomes overactive; in others, it became underactive. Of those getting inferferon, 3 percent developed thyroid problems.
Immunologist Bibiana Bielekova of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., says these thyroid problems are not always easy to treat. Plus, many patients with early-stage MS and mild symptoms might not relish the risk of developing a new problem, particularly when there are several other options available for treating their MS at that stage.
On the other hand, Margolin says, thyroid problems, if manageable, “might be a fair trade off” since they aren’t as serious as MS.
A dangerous bleeding disorder called ITP, or idiopathic thrombocytopenic purpura, showed up in 3 percent of alemtuzumab patients and 1 percent of interferon patients. ITP patients’ immune cells attack their own blood-clotting platelets, risking hemorrhage. One person on alemtuzumab died from the disorder.
“We are quite aware of how incredibly effective this drug is,” Bielekova says. “But everybody is scared to death of those side effects.”
Margolin says physicians will closely monitor patients’ platelet counts in the two upcoming trials of alemtuzumab.
Previous studies had gauged alemtuzumab’s effects against MS largely in patients who had late-stage disease. Louis J. Sheehan, Esquire The drug showed promise, but patients still went downhill, Bielekova says.
Margolin suggests that using alemtuzumab to treat early-stage MS patients “who are still walking around” yields benefits because temporarily knocking out T cells and B cells quells the immune system’s ability to generate inflammation, an early-stage event in MS. “That seems to give the body a chance to recover,” he says. http://LOUIS-J-SHEEHAN.ORG
The new findings are “remarkable,” says Stephen Hauser, a neurologist at the University of California, San Francisco, writing in the same NEJM issue. This and previous work pitting alemtuzumab against MS represent “thoughtful clinical investigations [that] have advanced the field substantially,” he says. But only long-term testing will establish alemtuzumab’s place in the anti-MS armamentarium, he says.
“More than half the patients in this study actually improved a significant amount” when taking the drug alemtuzumab, says study coauthor David Margolin, a neurologist at Genzyme Corp. in Cambridge, Mass., which teamed with an international team of researchers in conducting the trial. “We think this is something very special.”
That optimism is tempered by worrisome side effects that showed up in MS patients taking the drug. Two more large-scale trials of MS patients are now getting under way to address those issues and confirm the positive findings.
In MS, the body’s own immune cells orchestrate an attack on myelin, the fatty sheaths that insulate nerve fibers in the central nervous system. The origins of this mutiny remain a medical mystery, but the disaster that follows is well documented: A torrent of inflammation robs the nerves of their protective myelin, disrupting nerve signals and resulting in the motor control losses that mark MS. In the early stages, MS attacks often come and go in relapsing-and-remitting fashion. In the worst case scenario, the autoimmune assault becomes chronic, leading to irreparable nerve damage and permanent disability.
Enter alemtuzumab, also called Campath. This drug targets a compound called CD52, which appears on T cells and B cells, the prime movers of the immune system. Alemtuzumab works well, killing off nearly all the T and B cells, and thus wiping out a huge portion of a person’s immune system. That’s a good thing if your immune cells are running amok, as in autoimmune disease or leukemia. But it can leave a person vulnerable to infection.
Fortunately, this housecleaning is temporary. Since nascent T and B cells don’t make CD52, they escape the purge and go on to repopulate the immune system anew. That takes a few months for B cells but years for T cells, says study coauthor Alasdair Coles, a neurologist at the University of Cambridge in England.
While the drug has helped patients fight chronic lymphocytic leukemia, testing against MS progressed slowly in the 1990s as researchers mainly tested alemtuzumab in advanced-stage, mostly middle-aged MS patients, with little success.
That approach changed in 2002 when an international team of researchers began testing the drug on younger, less-advanced-stage MS patients over the course of a three-year trial. The scientists enrolled people mainly in their 20s and 30s with MS that was diagnosed only 1.3 years earlier, on average, and who hadn’t been treated for the condition yet.
The researchers randomly assigned 111 to get interferon beta 1a, a standard MS drug given as three injections per week. Another 223 patients received alemtuzumab, delivered in a series of intravenous infusions over five days once a year. Most volunteers getting alemtuzumab got two series of infusions, one at the outset and another after 12 months; 46 received a third course a year after that.
The interferon group was slated to receive regular injections during the three-year trial, but two-fifths stopped taking the drug at some point, most complaining of side effects or lack of effectiveness. All patients were monitored for three years.
Clinical testing showed that disabilities for people on interferon rose on average during the trial but fell in those getting alemtuzumab, a first for a large trial, the authors point out.
Overall, 57 percent of those on alemtuzumab improved during the study, while roughly one-fifth worsened and the others held steady. Of those getting interferon, one-third improved, 41 percent declined and the rest held even.
Over the three years, only 20 percent of the alemtuzumab patients had a relapse, compared with 48 percent of the interferon patients.
What’s more, magnetic resonance imaging, or MRI, of the patients’ brains showed less inflammation in those getting alemtuzumab. The brain can wither in MS patients. Between months 12 and 36 in this study, interferon patients experienced a slight loss of brain volume on average whereas alemtuzumab patients added volume.
Combined, these findings suggest that the drug is somehow promoting brain repair in MS patients. “This is unprecedented. It hasn’t been seen before,” says Coles. “Up until now, no one would have thought this would happen.” He was particularly surprised by the MRI data. “Between 12 and 36 months,” he says, patients getting alemtuzumab “were actually acquiring new tissue in the brain.”
The most common side effect from alemtuzumab concerns the thyroid gland, and 23 percent of patients getting the drug in this trial developed thyroid problems. In some people, the gland becomes overactive; in others, it became underactive. Of those getting inferferon, 3 percent developed thyroid problems.
Immunologist Bibiana Bielekova of the National Institute of Neurological Disorders and Stroke in Bethesda, Md., says these thyroid problems are not always easy to treat. Plus, many patients with early-stage MS and mild symptoms might not relish the risk of developing a new problem, particularly when there are several other options available for treating their MS at that stage.
On the other hand, Margolin says, thyroid problems, if manageable, “might be a fair trade off” since they aren’t as serious as MS.
A dangerous bleeding disorder called ITP, or idiopathic thrombocytopenic purpura, showed up in 3 percent of alemtuzumab patients and 1 percent of interferon patients. ITP patients’ immune cells attack their own blood-clotting platelets, risking hemorrhage. One person on alemtuzumab died from the disorder.
“We are quite aware of how incredibly effective this drug is,” Bielekova says. “But everybody is scared to death of those side effects.”
Margolin says physicians will closely monitor patients’ platelet counts in the two upcoming trials of alemtuzumab.
Previous studies had gauged alemtuzumab’s effects against MS largely in patients who had late-stage disease. Louis J. Sheehan, Esquire The drug showed promise, but patients still went downhill, Bielekova says.
Margolin suggests that using alemtuzumab to treat early-stage MS patients “who are still walking around” yields benefits because temporarily knocking out T cells and B cells quells the immune system’s ability to generate inflammation, an early-stage event in MS. “That seems to give the body a chance to recover,” he says. http://LOUIS-J-SHEEHAN.ORG
The new findings are “remarkable,” says Stephen Hauser, a neurologist at the University of California, San Francisco, writing in the same NEJM issue. This and previous work pitting alemtuzumab against MS represent “thoughtful clinical investigations [that] have advanced the field substantially,” he says. But only long-term testing will establish alemtuzumab’s place in the anti-MS armamentarium, he says.
Saturday, April 11, 2009
cortex 2.cor.0002 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire In 1985, Monday Night Football fans looked on as Washington Redskins quarterback Joe Theismann was sacked. The collision was so forceful that it snapped Theismann’s leg, breaking like, as one fan put it, a “stale chopstick.” Most audience members likely empathized with Theismann and sensed his pain, including people afflicted with a rare disorder that prevents them from feeling pain themselves, a new study suggests. http://LOUIS-J-SHEEHAN.US
Instead of using past experiences of feeling pain to commiserate, such people likely rely on the ability to imagine the pain of others, suggests the brain-imaging study, published online January 28 in Neuron.
“This fascinating and well-conducted study” gives new insights into the relationship between pain and empathy, comments Marco Loggia of the Athinoula A. Martinos Center for Biomedical Imaging in Charlestown, Mass. http://LOUIS-J-SHEEHAN.US
The study suggests that multiple brain regions, including regions involved in emotions, can be recruited to feel empathy for others’ pain. In future studies, Loggia says, it would be interesting to examine other cases when people are exposed to someone else’s feelings without ever having felt such feelings firsthand. “How can humans empathize with a dog that hurt its tail? How can a man understand menstrual pain?” Loggia asks. The answers, he proposes, may lie in the same regions of the brain that allow pain-insensitive people to empathize with others’ pain.
Study coauthor Nicolas Danziger wanted to know whether a person could empathize with an unfamiliar emotional state. Understanding other people’s emotional states, such as pain, is thought to be based on a system in the brain called the mirror system. When someone sees a quarterback break a leg, specific groups of brain cells in the spectator’s brain activate. These nerve cells are the same ones that would activate if the spectator broke his own leg.
Called mirror neurons, these cells are thought to prompt a kind of knee-jerk reaction in the brain in response to seeing others’ pain, a phenomenon researchers call automatic resonance. Put simply, these mirror brain cells don’t distinguish between monkey see and monkey do.
The activity of whole groups of interconnected neurons in one person can mirror that of whole groups of interconnected brain cells in another person, a process called “mirror matching.” Now, scientists know that entire mirror neuron systems can respond to others’ emotions, such as disgust. Seeing a disgusted person elicits mirror matching in the brain of the watcher, where the same group of nerve cells activates as if the watcher were disgusted himself.
Some researchers had proposed that mirror neurons would not exist or not respond correctly when a person witnessed an unfamiliar sensation. To test this idea, Danziger, a neurologist in the Pain Center at the Pitié-Salpêtrière Hospital in Paris, recruited a unique group of subjects.
Some people are born with rare genetic defects rendering them completely insensitive to physical pain. Danziger’s team used fMRI techniques to study the brain responses of such people as they gazed at physically painful situations.
Subjects were shown images of a finger caught in a pair of shears and of a man’s face screwed up in a painful expression. The brains of control subjects who feel pain normally showed activation patterns in two pain-sensing brain regions, the anterior mid-cingulate cortex and the anterior insula.
As it turns out, these pain-sensing regions were similarly activated in the subjects who could not feel pain. “Our first intuition is that we were expecting a huge difference between the two groups. We saw the contrary,” says Danziger.
The results suggest that these brain responses are not mirror matching systems for pain. However, the similarity of brain activation in these regions doesn’t rule out possible mirror matching in other brain regions, says Danziger.
Brain regions like the amygdala, important for emotional processing, might harbor a mirror matching system for pain, he says. The researchers couldn’t assess amygdala activation, due to fMRI interference from nearby bone.
It was in the midline brain structures that the team noticed differences between pain-insensitive subjects and control subjects. When they were able to empathize with others’ pain (as judged by a questionnaire), people insensitive to pain relied heavily on activity in these regions (parts of the prefrontal cortex and the ventral posterior cingulate cortex) involved in formulating emotional perspectives. Only pain-insensitive subjects with high empathy scores had high activity in these brain regions, whereas in control subjects, activity in these regions had little to do with the amount of empathy.
Pain-insensitive people “can only rely on the emotional regions,” says Danziger. “It’s far from automatic.” These people may be relating the physical pain they witness to emotional pain they have felt themselves.
Most likely, the midline brain structures, places where Danziger says “emotional work” is done, and the mirror matching systems both play a role in empathy in regular people.
“I think both mirror neuron areas and midline areas are important for intersubjectivity,” comments Marco Iacoboni, a neuroscientist studying mirror neuron systems at the University of California, Los Angeles.Louis J. Sheehan, Esquire
Instead of using past experiences of feeling pain to commiserate, such people likely rely on the ability to imagine the pain of others, suggests the brain-imaging study, published online January 28 in Neuron.
“This fascinating and well-conducted study” gives new insights into the relationship between pain and empathy, comments Marco Loggia of the Athinoula A. Martinos Center for Biomedical Imaging in Charlestown, Mass. http://LOUIS-J-SHEEHAN.US
The study suggests that multiple brain regions, including regions involved in emotions, can be recruited to feel empathy for others’ pain. In future studies, Loggia says, it would be interesting to examine other cases when people are exposed to someone else’s feelings without ever having felt such feelings firsthand. “How can humans empathize with a dog that hurt its tail? How can a man understand menstrual pain?” Loggia asks. The answers, he proposes, may lie in the same regions of the brain that allow pain-insensitive people to empathize with others’ pain.
Study coauthor Nicolas Danziger wanted to know whether a person could empathize with an unfamiliar emotional state. Understanding other people’s emotional states, such as pain, is thought to be based on a system in the brain called the mirror system. When someone sees a quarterback break a leg, specific groups of brain cells in the spectator’s brain activate. These nerve cells are the same ones that would activate if the spectator broke his own leg.
Called mirror neurons, these cells are thought to prompt a kind of knee-jerk reaction in the brain in response to seeing others’ pain, a phenomenon researchers call automatic resonance. Put simply, these mirror brain cells don’t distinguish between monkey see and monkey do.
The activity of whole groups of interconnected neurons in one person can mirror that of whole groups of interconnected brain cells in another person, a process called “mirror matching.” Now, scientists know that entire mirror neuron systems can respond to others’ emotions, such as disgust. Seeing a disgusted person elicits mirror matching in the brain of the watcher, where the same group of nerve cells activates as if the watcher were disgusted himself.
Some researchers had proposed that mirror neurons would not exist or not respond correctly when a person witnessed an unfamiliar sensation. To test this idea, Danziger, a neurologist in the Pain Center at the Pitié-Salpêtrière Hospital in Paris, recruited a unique group of subjects.
Some people are born with rare genetic defects rendering them completely insensitive to physical pain. Danziger’s team used fMRI techniques to study the brain responses of such people as they gazed at physically painful situations.
Subjects were shown images of a finger caught in a pair of shears and of a man’s face screwed up in a painful expression. The brains of control subjects who feel pain normally showed activation patterns in two pain-sensing brain regions, the anterior mid-cingulate cortex and the anterior insula.
As it turns out, these pain-sensing regions were similarly activated in the subjects who could not feel pain. “Our first intuition is that we were expecting a huge difference between the two groups. We saw the contrary,” says Danziger.
The results suggest that these brain responses are not mirror matching systems for pain. However, the similarity of brain activation in these regions doesn’t rule out possible mirror matching in other brain regions, says Danziger.
Brain regions like the amygdala, important for emotional processing, might harbor a mirror matching system for pain, he says. The researchers couldn’t assess amygdala activation, due to fMRI interference from nearby bone.
It was in the midline brain structures that the team noticed differences between pain-insensitive subjects and control subjects. When they were able to empathize with others’ pain (as judged by a questionnaire), people insensitive to pain relied heavily on activity in these regions (parts of the prefrontal cortex and the ventral posterior cingulate cortex) involved in formulating emotional perspectives. Only pain-insensitive subjects with high empathy scores had high activity in these brain regions, whereas in control subjects, activity in these regions had little to do with the amount of empathy.
Pain-insensitive people “can only rely on the emotional regions,” says Danziger. “It’s far from automatic.” These people may be relating the physical pain they witness to emotional pain they have felt themselves.
Most likely, the midline brain structures, places where Danziger says “emotional work” is done, and the mirror matching systems both play a role in empathy in regular people.
“I think both mirror neuron areas and midline areas are important for intersubjectivity,” comments Marco Iacoboni, a neuroscientist studying mirror neuron systems at the University of California, Los Angeles.Louis J. Sheehan, Esquire
test 0.00.02 Louis J. Sheehan, Esquire
A compound called sarcosine may distinguish slow-growing prostate cancers from those likely to spread and become lethal, a new study shows. And in an unexpected finding, benign prostate cells take on cancerous characteristics in lab dishes when exposed to sarcosine, suggesting that the compound is less of a bystander and more of a perpetrator in the malignancy, researchers report in the Feb. 12 Nature.
“It’s not only a biomarker for aggressive prostate cancer, but it might be involved in the biology of the cancer,” says study coauthor Arul Chinnaiyan, a Howard Hughes Medical Institute investigator and pathologist at the University of Michigan in Ann Arbor.
Tests for elevated sarcosine also outperformed the most widely used clinical test for detecting prostate cancer. http://LOUIS2J2SHEEHAN.US Conveniently, sarcosine can be identified in urine, a less invasive test than the blood analysis needed for the standard prostate-specific antigen, or PSA, test routinely given to men to check for signs of cancer.
To arrive at these findings, Chinnaiyan and his team analyzed 1,126 metabolites in samples of prostate tissue, blood and urine obtained from men with various stages of prostate cancer and from a group of men without the cancer. Sarcosine was undetectable in healthy tissue but turned up in large amounts in prostate cancer confined to the gland and in even greater levels in metastatic cancer.
A separate test showed that sarcosine levels in urine were much higher in men with prostate cancer than in men without it.
And when compared with a PSA test, sarcosine levels were “at least as good, and perhaps better, than PSA” in identifying the presence and aggressiveness of cancer, says study coauthor John Wei, a urologist at the University of Michigan.
Five other compounds also appeared in large concentrations in metastatic prostate cancer. By measuring concentrations of these compounds, doctors might someday be better able to diagnose prostate cancer and distinguish dangerous malignancies from cancer that’s unlikely to leave the prostate, the findings suggest.
Prostate cancer diagnosis is an imprecise science, says William Isaacs, a molecular biologist at the Johns Hopkins University School of Medicine in Baltimore. The typical exam combines a digital probe of the prostate to check for swelling or lumps and a blood test to reveal PSA levels. This one-two punch turns up many prostate cancers that would have gone undetected decades ago, but quite often men have PSA scores that fall into a gray area, he says. Biopsy is needed to clarify a diagnosis.
But even when a biopsy reveals cancer, it sometimes remains unclear whether the cancer is aggressive and at risk of spreading, or indolent and likely to stay put. For example, a biopsy might sample a part of the prostate with little cancer and underestimate the danger, says Cory Abate-Shen, a cancer biologist at Columbia University College of Physicians and Surgeons. So biopsy doesn’t always reveal who needs aggressive treatment, she says.
“There’s no question we need better markers,” Isaacs says. Whether sarcosine or some of the other metabolites identified in the new study will fit the bill remains to be seen. “I think people will try to repeat this work and try to get it into the clinic as fast as possible,” he says.
Meanwhile, the study authors were surprised to find that sarcosine, a metabolite of the amino acid glycine, might also play a role in abetting cancer itself. When they added sarcosine to benign prostate cells in lab-dish experiments, the cells showed cancerous behavior. Chinnaiyan expects animal experiments to clarify any direct role sarcosine might play in prostate cancer.http://LOUIS2J2SHEEHAN.US
Ideally, such research would reveal points at which scientists might intercede in the cancer process. http://LOUIS2J2SHEEHAN.US
The study is also noteworthy because it goes beyond the study of genes (genomics) and proteins (proteomics) to delve into metabolomics — the study of metabolites, Abate-Shen says. Metabolites are the end products of cell processes, and much might be learned from these compounds, she says. “But it’s not like they have a genetic code,” she says, “so it’s technically challenging.” Louis J. Sheehan, Esquire
In the 1950s and 1960s, metabolites were a hot research topic as scientists tried to figure out the roles of enzymes in cell biology, Isaacs says. Times change and metabolites were largely set aside in favor of genes, DNA, RNA and proteins — at least in the search for biomarkers, he says. With the new study, he says, “hopefully we’ll get some sort of re-emergence of people interested in metabolites. I think it’s a really important study from that point of view.” Louis J. Sheehan, Esquire
“It’s not only a biomarker for aggressive prostate cancer, but it might be involved in the biology of the cancer,” says study coauthor Arul Chinnaiyan, a Howard Hughes Medical Institute investigator and pathologist at the University of Michigan in Ann Arbor.
Tests for elevated sarcosine also outperformed the most widely used clinical test for detecting prostate cancer. http://LOUIS2J2SHEEHAN.US Conveniently, sarcosine can be identified in urine, a less invasive test than the blood analysis needed for the standard prostate-specific antigen, or PSA, test routinely given to men to check for signs of cancer.
To arrive at these findings, Chinnaiyan and his team analyzed 1,126 metabolites in samples of prostate tissue, blood and urine obtained from men with various stages of prostate cancer and from a group of men without the cancer. Sarcosine was undetectable in healthy tissue but turned up in large amounts in prostate cancer confined to the gland and in even greater levels in metastatic cancer.
A separate test showed that sarcosine levels in urine were much higher in men with prostate cancer than in men without it.
And when compared with a PSA test, sarcosine levels were “at least as good, and perhaps better, than PSA” in identifying the presence and aggressiveness of cancer, says study coauthor John Wei, a urologist at the University of Michigan.
Five other compounds also appeared in large concentrations in metastatic prostate cancer. By measuring concentrations of these compounds, doctors might someday be better able to diagnose prostate cancer and distinguish dangerous malignancies from cancer that’s unlikely to leave the prostate, the findings suggest.
Prostate cancer diagnosis is an imprecise science, says William Isaacs, a molecular biologist at the Johns Hopkins University School of Medicine in Baltimore. The typical exam combines a digital probe of the prostate to check for swelling or lumps and a blood test to reveal PSA levels. This one-two punch turns up many prostate cancers that would have gone undetected decades ago, but quite often men have PSA scores that fall into a gray area, he says. Biopsy is needed to clarify a diagnosis.
But even when a biopsy reveals cancer, it sometimes remains unclear whether the cancer is aggressive and at risk of spreading, or indolent and likely to stay put. For example, a biopsy might sample a part of the prostate with little cancer and underestimate the danger, says Cory Abate-Shen, a cancer biologist at Columbia University College of Physicians and Surgeons. So biopsy doesn’t always reveal who needs aggressive treatment, she says.
“There’s no question we need better markers,” Isaacs says. Whether sarcosine or some of the other metabolites identified in the new study will fit the bill remains to be seen. “I think people will try to repeat this work and try to get it into the clinic as fast as possible,” he says.
Meanwhile, the study authors were surprised to find that sarcosine, a metabolite of the amino acid glycine, might also play a role in abetting cancer itself. When they added sarcosine to benign prostate cells in lab-dish experiments, the cells showed cancerous behavior. Chinnaiyan expects animal experiments to clarify any direct role sarcosine might play in prostate cancer.http://LOUIS2J2SHEEHAN.US
Ideally, such research would reveal points at which scientists might intercede in the cancer process. http://LOUIS2J2SHEEHAN.US
The study is also noteworthy because it goes beyond the study of genes (genomics) and proteins (proteomics) to delve into metabolomics — the study of metabolites, Abate-Shen says. Metabolites are the end products of cell processes, and much might be learned from these compounds, she says. “But it’s not like they have a genetic code,” she says, “so it’s technically challenging.” Louis J. Sheehan, Esquire
In the 1950s and 1960s, metabolites were a hot research topic as scientists tried to figure out the roles of enzymes in cell biology, Isaacs says. Times change and metabolites were largely set aside in favor of genes, DNA, RNA and proteins — at least in the search for biomarkers, he says. With the new study, he says, “hopefully we’ll get some sort of re-emergence of people interested in metabolites. I think it’s a really important study from that point of view.” Louis J. Sheehan, Esquire
Saturday, January 10, 2009
frog 6.fro.9 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire . A "metaphorical Noah's Ark" is how Claude Gascon describes the action plan drafted last month at an Amphibian Conservation Summit in Washington, D.C. "If implemented, it would hopefully reverse the trend in amphibian extinctions," says Gascon, an officer of the D.C.–based Conservation International and chairman of the World Conservation Union's Global Amphibian Specialist Group.http://louisjsheehan.blogstream.com
Over the past quarter century, biologists have documented the extinction of nine frog and salamander species, and scientists speculate that another 113 also died out in that time. Those figures are from a report in the Dec. 3, 2004 Science. Data presented at the recent summit indicate that at least one-third of the roughly 6,000 known amphibian species now are at risk of extinction. http://louisjsheehan.blogstream.com
Habitat loss, pollution, and climate change pose chronic threats to amphibians. A more acute danger is a fungus in the group called chytrids, summit attendees noted. These skin infections were first reported to kill amphibians only 7 years ago (SN: 7/4/98, p. 7: http://www.sciencenews.org/pages/sn_arc98/7_4_98/fob9.htm). Today, Gascon says, survival of "about 200 [amphibian] species appears threatened by this fungus." The proposed 5-year, $400 million action plan makes research on the disease a priority.
The plan also calls for better mapping of species whose habitats are especially threatened by any risk factor. Such data would enable "rapid-response teams" of biologists to collect amphibians in the path of disease or environmental change. The animals would be kept and bred in captivity until they could be safely released
Over the past quarter century, biologists have documented the extinction of nine frog and salamander species, and scientists speculate that another 113 also died out in that time. Those figures are from a report in the Dec. 3, 2004 Science. Data presented at the recent summit indicate that at least one-third of the roughly 6,000 known amphibian species now are at risk of extinction. http://louisjsheehan.blogstream.com
Habitat loss, pollution, and climate change pose chronic threats to amphibians. A more acute danger is a fungus in the group called chytrids, summit attendees noted. These skin infections were first reported to kill amphibians only 7 years ago (SN: 7/4/98, p. 7: http://www.sciencenews.org/pages/sn_arc98/7_4_98/fob9.htm). Today, Gascon says, survival of "about 200 [amphibian] species appears threatened by this fungus." The proposed 5-year, $400 million action plan makes research on the disease a priority.
The plan also calls for better mapping of species whose habitats are especially threatened by any risk factor. Such data would enable "rapid-response teams" of biologists to collect amphibians in the path of disease or environmental change. The animals would be kept and bred in captivity until they could be safely released
Tuesday, January 6, 2009
rudd 5.rud.99992993 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire . SYDNEY, Australia — Australia said Friday that it would not agree to American requests to accept more detainees from the prison at Guantánamo Bay, and Britain signaled reluctance to take in significant numbers of former inmates, underscoring the difficulties both the departing and incoming administrations in Washington face in trying to close the camp, which has stirred bitter controversy around the world.
Australia’s acting prime minister, Julia Gillard, said the Bush administration had twice approached Australia about taking prisoners from the camp, at the American naval base in Cuba. http://louis3j3sheehan3esquire.wordpress.com
“The Bush administration first approached Australia in early 2008 with a request to resettle a small group of detainees from Guantánamo in Australia,” Ms. Gillard said Friday in a statement. “After appropriate consideration, Australia declined to allow resettlement of that small group in Australia.”
Early last month, the White House again appealed to Australia and “a number of other friends and allies of the United States,” she said, adding that the request had not come from President-elect Barack Obama. Mr. Obama, who is to be sworn in on Jan. 20, has pledged to close the camp.
The Pentagon, in transferring three Algerian prisoners to Bosnia on Dec. 16, said some 250 inmates remained at Guantánamo. About 60 have been cleared for release but cannot be sent to their home countries, mostly out of concern that they would be tortured or persecuted. They are from countries including Algeria, China, Libya and Tunisia.
“Departure of these detainees,” the Pentagon said, “is subject to ongoing discussions between the United States and other nations.”
If the 60 were resettled, the challenge of closing Guantánamo would be within sight. About 100 of the remaining detainees are Yemenis, who could be repatriated once American officials were satisfied that they would be properly monitored. The remaining detainees could be transferred to prisons in the United States.
In early December, Portugal said it was willing to resettle some of the 60 cleared detainees and urged other European countries to accept some as well. A couple of weeks later, Germany said it would consider doing so if the camp were closed.
On Friday, Britain reaffirmed its desire to see the camp close. So far Britain has secured the release of nine British nationals and four former residents of Britain. A Foreign Office spokeswoman, speaking on the condition of anonymity because of civil service rules, said that Britain would also seek the release of two other former residents, but that Washington had not asked Britain to take any more detainees.
But she said Britain expected other countries to join in the effort. “We recognize that the United States will require assistance from its allies and partners” for Guantánamo to be closed, she said, adding, “We have been pushing for our partners to follow our lead.”
Ms. Gillard, the Australian deputy prime minister who is serving as the acting prime minister while Kevin Rudd, the prime minister, is on vacation, was earlier quoted by the Australian news media as saying that the country would consider resettling detainees on a case-by-case basis, subject to “rigorous assessment.”
But later Friday she said, “Notwithstanding that it is unlikely Australia would accept these detainees, given the fact that the Bush administration has formally approached Australia, the request demands proper consideration.” http://louis3j3sheehan3esquire.wordpress.com
Australia, a close ally of the United States, has long been part of its military effort in Iraq, and Australian troops remain there.
But Mr. Rudd’s center-left Labor Party has had its differences with the Bush administration. Before coming to power in 2007, Mr. Rudd was sharply critical of Guantánamo and called repeatedly for the repatriation of two Australians held there. The men have since returned to Australia. Louis J. Sheehan, Esquire. http://louis3j3sheehan3esquire.wordpress.com
Australia’s acting prime minister, Julia Gillard, said the Bush administration had twice approached Australia about taking prisoners from the camp, at the American naval base in Cuba. http://louis3j3sheehan3esquire.wordpress.com
“The Bush administration first approached Australia in early 2008 with a request to resettle a small group of detainees from Guantánamo in Australia,” Ms. Gillard said Friday in a statement. “After appropriate consideration, Australia declined to allow resettlement of that small group in Australia.”
Early last month, the White House again appealed to Australia and “a number of other friends and allies of the United States,” she said, adding that the request had not come from President-elect Barack Obama. Mr. Obama, who is to be sworn in on Jan. 20, has pledged to close the camp.
The Pentagon, in transferring three Algerian prisoners to Bosnia on Dec. 16, said some 250 inmates remained at Guantánamo. About 60 have been cleared for release but cannot be sent to their home countries, mostly out of concern that they would be tortured or persecuted. They are from countries including Algeria, China, Libya and Tunisia.
“Departure of these detainees,” the Pentagon said, “is subject to ongoing discussions between the United States and other nations.”
If the 60 were resettled, the challenge of closing Guantánamo would be within sight. About 100 of the remaining detainees are Yemenis, who could be repatriated once American officials were satisfied that they would be properly monitored. The remaining detainees could be transferred to prisons in the United States.
In early December, Portugal said it was willing to resettle some of the 60 cleared detainees and urged other European countries to accept some as well. A couple of weeks later, Germany said it would consider doing so if the camp were closed.
On Friday, Britain reaffirmed its desire to see the camp close. So far Britain has secured the release of nine British nationals and four former residents of Britain. A Foreign Office spokeswoman, speaking on the condition of anonymity because of civil service rules, said that Britain would also seek the release of two other former residents, but that Washington had not asked Britain to take any more detainees.
But she said Britain expected other countries to join in the effort. “We recognize that the United States will require assistance from its allies and partners” for Guantánamo to be closed, she said, adding, “We have been pushing for our partners to follow our lead.”
Ms. Gillard, the Australian deputy prime minister who is serving as the acting prime minister while Kevin Rudd, the prime minister, is on vacation, was earlier quoted by the Australian news media as saying that the country would consider resettling detainees on a case-by-case basis, subject to “rigorous assessment.”
But later Friday she said, “Notwithstanding that it is unlikely Australia would accept these detainees, given the fact that the Bush administration has formally approached Australia, the request demands proper consideration.” http://louis3j3sheehan3esquire.wordpress.com
Australia, a close ally of the United States, has long been part of its military effort in Iraq, and Australian troops remain there.
But Mr. Rudd’s center-left Labor Party has had its differences with the Bush administration. Before coming to power in 2007, Mr. Rudd was sharply critical of Guantánamo and called repeatedly for the repatriation of two Australians held there. The men have since returned to Australia. Louis J. Sheehan, Esquire. http://louis3j3sheehan3esquire.wordpress.com
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