(HealthDay News) -- A newly discovered gene may help protect carriers against Crohn's disease and colitis, Inflammatory bowel disease (IBDs) that affect an estimated one million Americans, researchers say.
The gene produces a protein that's key to a cellular receptor for interleukin-23 (IL-23), a protein involved in the body's inflammatory processes, explains a report published in the Oct. 27 issue of Science.
"We're pleased about the finding because the IL-23 pathway is already known to be important in inflammatory conditions such as asthma," said lead researcher Dr. Richard H. Duerr, associate professor of medicine and human genetics at the University of Pittsburgh. "We were surprised because the most common variant of the gene provides protection. If we could understand what the protective variant is doing and how it affects downstream events, we could find ways to treat or prevent IBD."
The study was funded by the U.S. National Institutes of Health.
The finding is intriguing, said co-researcher Dr. Judy H. Cho, since most research into disease-linked genes find variants that boost the carrier's risk for the illness.
But in this case, "instead of looking at the genetics of disease we're looking at the genetics of health," said Cho, who is associate professor of medicine and genetics at Yale University School of Medicine
It is "a potentially important discovery" because it might be quickly translated into treatment, added Dr. John Braun, chairman of pathology and medicine at the University of California, Los Angeles. Braun is also chairman of the national scientific advisory committee of the Crohn's amp; Colitis Foundation of America.
There's an added plus to the finding: While other genes associated with IBD have been identified, "so far, none of those genes have drugs that are directly known to affect them," Braun said. But, "in this case, drugs are already available that act on the IL-23 system."
A number of drugs in various stages of development are being tested against IL-23-related conditions, including psoriasis, rheumatoid arthritis and multiple sclerosis, he said.
"The reason why this is such a nice finding is that the human genetics correspond with [the] immunology," Cho said. "This inflammatory pathway is typical of not only intestinal problems but also of others, like rheumatoid arthritis and psoriasis."
The IL-23 pathway is important in the body's infection defense system, Cho said. IBD appears to be caused by an abnormal reaction against the very high concentration of bacteria normally found in the intestines. Thus, it might be possible "to block IL-23 function in a way that markedly reduces disease," she said.
But it's also necessary to tread cautiously, Duerr said, because the IL-23 pathway also helps fight infection. "Acting on the variant that is protective in IBD might worsen other disorders," he warned. "We have to understand what the variant is doing in the IL-23 pathway."
The discovery was made by systematically scanning all of the 22,000 genes in the human genome, looking for variants present in persons with Crohn's disease but not in healthy individuals.
The scan detected two variants in one gene already associated with IBD, CARD15. The only other association was found in variants of the IL-23 gene. When the researchers looked closely at the gene, they found several variants associated with increased risk of IBD. But one appeared to confer very strong protection against IBD.
"One of every six or seven Caucasians are carriers of the protective allele [variant]," Cho said. "If you have one copy of the protective allele, you are two to four times less likely to develop Crohn's disease."
The low incidence of the protective variant is unusual, Duerr said. "Almost always, a good variant will have an increased frequency in the population," he said.
More information
For more on Crohn's disease and related conditions, consult the Crohn's amp; Colitis Foundation of America.
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Friday, October 27, 2006
Gene Screen Links Cancer Treatment to Tumor Type
(HealthDay News) -- U.S. scientists say they've developed new tests that analyze thousands of genes in a tumor to determine which kind of chemotherapy will be most effective against a particular tumor type.In laboratory experiments with cells derived from cancer patient tumors, these genomic tests were 80 percent accurate in predicting which chemotherapy drugs would be most effective in killing the tumor.
A team from Duke University's Institute for Genome Sciences and Policy, in Durham, N.C., published their findings in the November issue of Nature Medicine.
A clinical trial of the genomic tests in about 120 breast cancer patients is planned to begin next year, the Duke scientists said.
These new genomic tests may help save lives and reduce cancer patients' exposure to the toxic side effects of chemotherapy drugs, lead investigator Dr. Anil Potti, an assistant professor of medicine at the institute, said in a prepared statement.
Using the tests, doctors would be able to correctly determine the most effective form of chemotherapy for a patient's tumor, instead of trying various chemotherapy drugs until the correct one is found, Potti said.
"Over 400,000 patients in the United States are treated with chemotherapy each year, without a firm basis for which drug they receive," senior investigator Joseph Nevins, a professor of genetics at the institute, said in a prepared statement. "We believe these genomic tests have the potential to revolutionize cancer care by identifying the right drug for each individual patient."
More information
The American Cancer Society has more about chemotherapy.
Studies Link Gene Variant to Macular Degeneration
(HealthDay News) -- Two international research teams say they've found a genetic variation that greatly increases the risk of age-related macular degeneration, the leading cause of vision loss in older people.
But several vision experts aren't convinced that the studies prove their point.
The studies, from the United States and Hong Kong, link what is called a single nucleotide polymorphism (SNP) in a gene designated HTRA1 with age-related macular degeneration (AMD). The Hong Kong study compared the incidence of SNP in 96 people with AMD and 130 people with normal vision. The U.S. study included 581 people with AMD and 309 with normal vision.
"This gene confers about 50 percent of the risk of AMD," said Dr. Kang Zhang, associate professor of ophthalmology and visual sciences at the University of Utah School of Medicine, and lead author of the U.S. report. The presence of SNP, together with a previously identified gene for a protein called complement factor H, can explain up to 80 percent of AMD cases, Zhang added.
There are two forms of the eye disease. "Wet" AMD is caused by an overgrowth of blood vessels that creates a dead spot in the macula, the center of the retina. A different version, "dry" AMD, which accounts for 90 percent of all AMD cases, causes less sight loss.
The discovery of SNP could make possible screening programs to detect persons at high risk of AMD and might lead to treatments directed at the overproduction of a protein called serine protease that causes the damage of wet AMD, Zhang said.
The study findings are published in the Oct. 20 issue of the journal Science.
Several experts expressed doubt about the findings, however.
"They claim that they have found the real functional gene," said Rando Allikmets, associate professor of ophthalmology, pathology and cell biology at Columbia University in New York City. "Well, they may be correct but they don't prove it in this paper."
The region of chromosome 10 on which the studies focused was described a year ago by American and German researchers as being associated with AMD, Allikmets said. There are three closely related genes at that location, and it's unclear whether the specific SNP in the specific gene the new studies describe is responsible for AMD, he said.
"They might have found a causal link, but they don't prove it here," he said.
Similar caution was expressed by Anand Swaroop, professor of ophthalmology and visual sciences at the University of Michigan Kellogg Eye Center.
"Whether it is causal, that needs to be verified," he said of SNP. "There are many variations in this region that could have the same effect."
Previous reports have identified other SNPs in the region of chromosome 10 as associated with AMD, Swaroop said. "It is hard to say which is the causal one. The genetic data is fine, but it is not convincing and needs more work. Causality requires further verification."
Josephine Hoh, associate professor of epidemiology and public health at Yale University, and co-author of the Hong Kong paper, said the studies provide "preliminary proof. It would take several years to provide complete proof. The preliminary data already shows very interesting results, a connection between the function of this particular SNP and wet AMD."
Zhang added: "There is no question in my mind that this is a major gene for macular degeneration. The work from now on is to look at why this gene is responsible for macular degeneration. We can also go on to real drugs for AMD."
More information
For more on AMD, visit the U.S.National Eye Institute.
But several vision experts aren't convinced that the studies prove their point.
The studies, from the United States and Hong Kong, link what is called a single nucleotide polymorphism (SNP) in a gene designated HTRA1 with age-related macular degeneration (AMD). The Hong Kong study compared the incidence of SNP in 96 people with AMD and 130 people with normal vision. The U.S. study included 581 people with AMD and 309 with normal vision.
"This gene confers about 50 percent of the risk of AMD," said Dr. Kang Zhang, associate professor of ophthalmology and visual sciences at the University of Utah School of Medicine, and lead author of the U.S. report. The presence of SNP, together with a previously identified gene for a protein called complement factor H, can explain up to 80 percent of AMD cases, Zhang added.
There are two forms of the eye disease. "Wet" AMD is caused by an overgrowth of blood vessels that creates a dead spot in the macula, the center of the retina. A different version, "dry" AMD, which accounts for 90 percent of all AMD cases, causes less sight loss.
The discovery of SNP could make possible screening programs to detect persons at high risk of AMD and might lead to treatments directed at the overproduction of a protein called serine protease that causes the damage of wet AMD, Zhang said.
The study findings are published in the Oct. 20 issue of the journal Science.
Several experts expressed doubt about the findings, however.
"They claim that they have found the real functional gene," said Rando Allikmets, associate professor of ophthalmology, pathology and cell biology at Columbia University in New York City. "Well, they may be correct but they don't prove it in this paper."
The region of chromosome 10 on which the studies focused was described a year ago by American and German researchers as being associated with AMD, Allikmets said. There are three closely related genes at that location, and it's unclear whether the specific SNP in the specific gene the new studies describe is responsible for AMD, he said.
"They might have found a causal link, but they don't prove it here," he said.
Similar caution was expressed by Anand Swaroop, professor of ophthalmology and visual sciences at the University of Michigan Kellogg Eye Center.
"Whether it is causal, that needs to be verified," he said of SNP. "There are many variations in this region that could have the same effect."
Previous reports have identified other SNPs in the region of chromosome 10 as associated with AMD, Swaroop said. "It is hard to say which is the causal one. The genetic data is fine, but it is not convincing and needs more work. Causality requires further verification."
Josephine Hoh, associate professor of epidemiology and public health at Yale University, and co-author of the Hong Kong paper, said the studies provide "preliminary proof. It would take several years to provide complete proof. The preliminary data already shows very interesting results, a connection between the function of this particular SNP and wet AMD."
Zhang added: "There is no question in my mind that this is a major gene for macular degeneration. The work from now on is to look at why this gene is responsible for macular degeneration. We can also go on to real drugs for AMD."
More information
For more on AMD, visit the U.S.National Eye Institute.
Hockey Goalies' Eyes Keep Slapshots at Bay
(HealthDay News) -- He shoots -- he doesn't score! And a new study finds eagle-eyed goalies are often the reason why.
The very best ice hockey goalies are able to make big saves by always keeping their eyes on the puck, concludes a study from the University of Calgary in Canada.
"Looking at the puck seems fairly obvious, until you look at the eye movement of novice goaltenders, who scatter their gaze all over the place and have a much lower save percentage than the elite goalies," researcher Derek Panchuk, a graduate student, said in a prepared statement.
His on-ice study used wireless headgear with cameras that recorded the movements and object-of-interest of an athlete's eyes. The goalies wore the headgear while players shot pucks at them from a short distance.
The distance of the shot didn't seem to matter, as long as the goalies kept their gaze on the puck and on the shooter's stick in the critical seconds before the puck left the stick. Goalies who were able to do that made the save more than 75 percent of the time.
"Goalies often focus on physical things like improving technique, but they overlook the decision-making -- the cognitive side of things," Panchuk said. "I think this study shows that you also need to focus on your decision-making and your thinking processes. Having optimal focus is just as important as being in optimal physical shape."
The findings are expected to be published in the journal Human Movement.
More information
There's more on the science of hockey at the Exploratorium.
The very best ice hockey goalies are able to make big saves by always keeping their eyes on the puck, concludes a study from the University of Calgary in Canada.
"Looking at the puck seems fairly obvious, until you look at the eye movement of novice goaltenders, who scatter their gaze all over the place and have a much lower save percentage than the elite goalies," researcher Derek Panchuk, a graduate student, said in a prepared statement.
His on-ice study used wireless headgear with cameras that recorded the movements and object-of-interest of an athlete's eyes. The goalies wore the headgear while players shot pucks at them from a short distance.
The distance of the shot didn't seem to matter, as long as the goalies kept their gaze on the puck and on the shooter's stick in the critical seconds before the puck left the stick. Goalies who were able to do that made the save more than 75 percent of the time.
"Goalies often focus on physical things like improving technique, but they overlook the decision-making -- the cognitive side of things," Panchuk said. "I think this study shows that you also need to focus on your decision-making and your thinking processes. Having optimal focus is just as important as being in optimal physical shape."
The findings are expected to be published in the journal Human Movement.
More information
There's more on the science of hockey at the Exploratorium.
Saturday, October 21, 2006
Wednesday, October 11, 2006
Aspergillosis
Definition
Aspergillosis is a large spectrum of diseases caused by members of the genus Aspergillus(see Table below). The three principal entities are: allergic bronchopulmonary aspergillosis, pulmonary aspergilloma and invasive aspergillosis. Colonization of the respiratory tract is also common. The clinical manifestation and severity of the disease depends upon the immunologic state of the patient. Lowered host resistance due to such factors as underlying debilitating disease, neutropenia chemotherapy, disruption of normal flora, and an inflammatory response due to the use of antimicrobial agents and steroids can predispose the patient to colonization, invasive disease, or both. Aspergillus spp. are frequently secondary opportunistic pathogens in patients with bronchiectasis, carcinoma, other mycoses, sarcoid, and tuberculosis.
Forms of the disease
1This is the most common site of primary invasive aspergillosis.
Prognosis and therapy
Special resources: You may also want to refer to the Infectious Disease Society of America-Mycoses Study Group (IDSA-MSG) Practice Guidelines for this disease. It is available at the IDSA website. In addition, The Aspergillus web site offers an in-depth look into all aspects of invasive aspergillosis.
Prognosis depends upon the type and severity of disease as well as the immunological status of the patient. Allergic aspergillosis is typically a chronic entity, but evolves from episodes of acute corticosteroid-responsive asthma to fibrotic end-stage lung disease. Allergic aspergillosis has been successfully treated with corticosteroids, and intraconazole. The prolonged use of steroids in cases of chronic aspergillosis should be approached with caution.
Aspergillomas may be treated by surgical resection. However, this approach may cause significant morbidity and mortality, therefore it should be reserved for patients at high risk to develop severe hemoptysis.
Invasive aspergillosis may be treated with voriconazole, amphotericin B (deoxycholate and lipid preparations), and itraconazole [574, 2171]. The ability of voriconazole to effectively treat invasive aspergillosis and to reduce associated mortality was recently demonstrated by a large well-conducted randomized trial and is particulary noteworthy. A large number of new investigational drugs (posaconazole, ravuconazole, caspofungin, FK463, and anidulafungin (LY303366)) have activity against Aspergillus spp. and are being extensively evaluated. Caspofungin was also recently licensed in the United States for treatment of invasive aspergillosis in patients who are refractory to, or intolerant of other therapies (i.e., amphotericin B, lipid formulations of amphotericin B, and/or itraconazole). However, despite these advances in therapy, the invasive forms of aspergillosis are often associated with significant morbidity and mortality.
Selection of therapy also needs to consider the certainty of the diagnosis. Voriconazole, itraconazole, the investigational azoles with anti-mould activity, and amphotericin B all possess a reasonably broad-spectrum of activity against Aspergillus and the related hyaline moulds. Their activity does, however, vary for the agents of zygomycosis, with posaconazole being the azole with the most reliable activity against this class of fungi. The echinocandin glucan synthesis inhibitors (caspofungin, FK463, and anidulafungin) possess a narrower spectrum of activity and should only be used if the infection is known to be due to Aspergillus spp.
Histopathology
The tissue reaction in aspergillosis is acute suppurative inflammation with areas of ischemic necrosis. The fungus proliferates as septate hyphae 2.5-4.5 µm in diameter . The hyphae can be characterized as branching dichotomously (approximately 45°C angle) with the overall appearance of an army on the march. The hyphae may branch irregularly and appear similar to hyphae found in zygomycosis. Blood vessel invasion, thrombosis, infarction, and dissemination are extremely common.
Laboratory
Direct examination
Clinical material, such as fluids, sputa, or tissue, is mounted in 10% KOH. Long, branching, hyaline, septate hyphae approximately 3.0 µm in diameter typify aspergillosis. The demonstration of hyphae in the clinical specimen and the repeated recovery of the same species of Aspergillus in culture is critical in supporting the diagnosis of aspergillosis. It must always be remembered that a number of other fungi can be morphologically identical to Aspergillus in tissue. On rare occasions, the hyphae of an Aspergillus sp. may have lateral conidia in tissue.
Isolation
Inoculate the clinical material onto Sabouraud glucose agar, Inhibitory Mould Agar (IMA) or other proper medium with antibiotics (gentamicin or chlorampenicol) and incubate at 30°C. The aspergilli are sensitive to cycloheximide, hence they will not grow on media containing this antimicrobial agent. Discard negative cultures after 4 weeks.
Mycology (principal fungi)
- Aspergillus flavus
- Aspergillus fumigatus
- Aspergillus glaucus group
- Aspergillus nidulans
- Aspergillus niger
- Aspergillus terreus group
Detection of galactomannan antigen in serum
The mortality rate of invasive aspergillosis is as high as 50-100% and definitive diagnosis by culture may take as long as 4 weeks. Thus, early diagnosis is of remarkable significance for earlier initiation of antifungal therapy and reduction of mortality rates. Detection of galactomannan antigen, an exoantigen of Aspergillus, has recently been shown to be a useful screening test for early diagnosis of invasive aspergillosis. Platelia Aspergillus EIA (Bio-Rad Laboratories) is a commercially available kit used to detect galactomannan antigen in body fluids. This method can detect as little as 1 ng/ml of galactomannan in the tested sample. Serum is the most frequently tested specimen and appears to provide highest sensitivity. Use of other samples such as bronchoalveolar lavage and cerebrospinal fluid also appears to provide promising results.
Galactomannan antigen positivity is among the microbiological diagnostic criteria proposed by European Organization for Research and Treatment of Cancer (EUORTC) and Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group (MSG) for diagnosis of invasive aspergillosis. This tool continues to gain acceptance: the US Food & Drug Administration approved the marketing of Platelia Aspergillus EIA kit in USA on 16 May 2003.
Galactomannan antigen positivity can be detected 5-8 days (average) before clinical signs develop (in 65.2% of patients), findings on chest X-ray are visible (in 71.5% of patients) and culture results become positive (in 100% of patients). The test should be used as a screening test for patients at high risk of developing invasive aspergillosis. Detection of positive results particularly in two consecutive serum samples provides strong support for the diagnosis of invasive aspergillosis. Platelia Aspergillus EIA can also be used for follow-up of clinical response to antifungal therapy. The titer of the antigen tends to decrease in case of clinical response, except for patients who are treated with an echinocandin compound.
The overall sensitivity and specificity of the method were 80.7% and 89.2%, respectively, in the dataset submitted to the US FDA. False positive reactions have been observed in 1-18% of the tested samples and may be due to cross reactivity or false positive antigenemia. Cross reactivity may be due to the existence of other fungi, such as Penicillium chrysogenum, Penicillium digitatum, Rhodotorula rubra, and Paecilomyces variotii in the tested sample [2216]. The mechanism of false positive antigenemia, on the other hand, has not been fully clarified. It appears to be more frequent in children and may develop after translocation of galactomannan antigen found in various food stuff (bread, pasta, corn flakes, rice, cake, turkey, sausage, etc.) through the damaged intestinal mucosa. In addition to these, very recent data have shown that the serum samples of patients receiving piperacillin/tazobactam (Zosyn®), an injectable antibacterial combination product from Wyeth Pharmaceuticals, may also yield false positive galactomannan antigen test results. Detection of galactomannan antigen in certain batches of Zosyn® strengthened this finding. Thus, Bio-Rad, the manufacturer of the Platelia Aspergillus EIA kit, now states that positive galactomannan antigen test results in patients treated with Zosyn® should be interpreted cautiously. Since the existence of invasive aspergillosis cannot be ruled out in these patients, other methods should be used for confirmation of the diagnosis. You may refer to the practice caution document (released on November 20, 2003) concerning Zosyn® and the Platelia Aspergillus EIA test kit for more detailed information.
You may also want to review our subpage for more detailed information on the key data regarding the use of the galactomannan antigen test in the diagnosis of invasive aspergillosis.
Natural habitat
Aspergillus spp. are ubiquitous in the environment. They are especially common in the soil and decaying vegetation.
Susceptibility Testing
Susceptibility testing is not routinely used to guide therapy of aspergillosis. We offer both a general discussion of susceptibility testing and a searchable database from which you can retrieve specific results from a variety of published articles.
Related Sites and Therapy Information
- The Aspergillus web site is an excellent and comprehensive resource on all aspects of diagnosis and management of invasive aspergillosis.
- The Infectious Disease Society of America-Mycoses Study Group (IDSA-MSG) Practice Guideline for treating aspergillosis is available at the IDSA website.
References
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