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At least 397 records · Page 22Linked to original sources
PubMed1986

Elastase from polymorphonuclear leucocytes: a regulatory enzyme in immune complex disease.

In sputa of 21 cystic fibrosis patients suffering from chronic Pseudomonas aeruginosa lung infections, activities of lysosomal proteases released from polymorphonuclear leukocytes (PMN) and immune complexes were quantitatively determined. The results showed that low immune complex values correlated with high protease activities and vice versa. In a longitudinal study fluctuating, reciprocal changes of the parameters were observed. Therefore, the hypothesis was investigated as to whether PMN elastase cleaves immune complexes and regulates inflammation. It was shown that treatment of immune complex-positive sputa with PMN elastase decreased IgG and IgA immune complex values and lead to cleavage of the immunoglobulins in the hinge region. PMN elastase-treated samples were not able to stimulate the oxidative burst of PMN. Cleavage of in vitro built immune complexes did not lead to liberation of bound antigen. Western blot analysis of one sputum sample revealed split products of the IgG heavy chain. The results suggest that PMN elastase splits off the Fc portion of immunoglobulins in immune complexes and thus regulates inflammation by a feedback mechanism leading to cyclic inflammatory states.

Antigen-Antibody Complex↗
PubMed1978

Relation between component parts of fibrocystic disease complex and breast cancer.

Specimens of benign breast disease obtained from biopsies performed at Vanderbilt Hospital (Nashville, Tenn.) between 1952 and 1959 were histologically reviewed and characterized as to individual component types of fibrocystic disease. Follow-up for information regarding breast cancer development was 94% successful. Carcinoma developed more often when epithelial proliferative lesions were present. Atypical lobular hyperplasia had a greater predictive value than other epithelial lesions and was associated with an elevated risk six times that expected prior to the age of 45 years and a tripling of risk after the age of 45 years. Various ductal hyperplastic lesions are associated with approximately a doubly increased risk that is present only if the lesions are identified at biopsy after the age of 45 years. Women with cysts, sclerosing adenosis, fibrosis, and other nonhyperplastic changes were at no greater risk for subsequent carcinoma than women in the general population.

Adenofibroma↗
PubMed1999

A prospective randomized trial of four three-drug regimens in the treatment of disseminated Mycobacterium avium complex disease in AIDS patients: excess mortality associated with high-dose clarithromycin. Terry Beirn Community Programs for Clinical Research on AIDS.

The optimal regimen for treatment of Mycobacterium avium complex (MAC) disease has not been established. Eighty-five AIDS patients with disseminated MAC disease were randomized to receive a three-drug regimen of clarithromycin, rifabutin or clofazimine, and ethambutol. Two dosages of clarithromycin, 500 or 1,000 mg twice daily (b.i.d.), were compared. The Data and Safety Monitoring Board recommended discontinuation of the clarithromycin dosage comparison and continuation of the rifabutin vs. clofazimine comparison. After a mean follow-up of 4.5 months, 10 (22%) of 45 patients receiving clarithromycin at 500 mg b.i.d. had died (70 deaths per 100 person-years) compared with 17 (43%) of 40 patients receiving clarithromycin at 1,000 mg b.i.d. (158 deaths per 100 person-years) (relative risk, 2.43; 95% confidence interval, 1.11-5.34; P = .02). After 10.4 months, 20 (49%) of 41 patients receiving rifabutin had died (81 deaths per 100 person-years) compared with 23 (52%) of 44 patients receiving clofazimine (94 deaths per 100 person-years) (relative risk, 1.20; 95% confidence interval, 0.65-2.19; P = .56). Bacteriologic outcomes were similar among treatment groups. In treating MAC disease in AIDS patients, the maximum dose of clarithromycin should be 500 mg b.i.d.

AIDS-Related Opportunistic Infections↗
PubMed2005

Chronic necrotizing pulmonary aspergillosis complicated by a cavitary lesion caused by Pulmonary Mycobacterium-avium complex disease.

A 66-year-old woman who had undergone one year's treatment for pulmonary nontuberculous mycobacterial disease due to Mycobacterium avium (rifampicin, ethambutol, clarithromycin, streptomycin-->levofloxacin) five years earlier was admitted to our hospital because of continuous fever and a newly detected abnormal chest shadow, which was like a fungus ball in the right upper lobe on chest computed tomography in the giant cavitary lesion caused by pulmonary Mycobacterium-avium complex (MAC) disease. A diagnosis of chronic necrotizing pulmonary aspergillosis (CNPA) complicated by pulmonary MAC disease was made because Aspergillus niger was isolated from several sputum specimens, anti-aspergillus antibody was positive, and clinical symptoms such as fever, were disclosed with the radiological finding of a fungus ball-like shadow and an infiltration shadow around the cavity. The patient had received various forms of antifungal chemotherapy, but the clinical effect had been poor. Since then, she had been slowly worsening. Although mycetomas, with the typical appearance of a fungus ball on a chest radiograph, have been reported to easily form in cavitary lesions caused by previous pulmonary tuberculosis, we believe, as illustrated by the present case, that they could also form in such lesions caused by pulmonary MAC disease, since the frequency of pulmonary nontuberculous mycobacterial disease has recently been increasing in comparison with that of pulmonary tuberculosis.

Aged↗
PubMed1997

Optimal strategies for mapping complex diseases in the presence of multiple loci.

Recent advances in genome technology have led to mapping and subsequent isolation, by positional cloning, of a number of genes for common and/or complex human diseases. It therefore will be possible to utilize information about a known locus in the search for additional, perhaps less penetrant, genes for a particular disease. It is also unclear, under these situations, what the optimal sampling strategy should be. To address these questions, we have calculated the expected LOD score for localizing one locus in a variety of two-locus models of disease, for four different pedigree structures, and under three different scenarios regarding knowledge/testing of one of the two loci. These design considerations are evaluated by use of a cost function that incorporates the costs of ascertaining different family structures, the relative costs of genotyping and mutation testing family members, and the amount of information provided by each family structure and testing scenario. The results indicate that, in most cases, affected sib pairs are a particularly poor strategy, especially when linkage or mutation data are available at the known locus. We also demonstrate that prescreening the sample of families for mutations at known susceptibility loci is, in general, a cost-effective strategy.

Chromosome Mapping↗