Epidemics of non-A, non-B hepatitis in Pakistan.
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Biomedical subjects
Publications and source records attributed to M Ahmad.
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We examined the financial impact of diagnosis-related groups (DRGs) payment for Medicare patients receiving medical intensive care and looked for any change in the type of patients admitted to the medical intensive care unit (MICU) after one year's experience with DRGs. During 1984, payment for 267 Medicare patients receiving medical intensive care at a large, multispecialty referral hospital was calculated to be $2.6 million below cost, representing an average loss per discharge of $9,794. For those who died (42 percent), the average payment per case was $11,418 below the average per discharge cost. In 1985, 241 Medicare patients treated in the MICU showed an average loss per discharge of $14,113, which rose to $20,271 for those who expired (39.4 percent). There was no significant difference in mortality between the two groups and in type of patients per DRG assignment (p = 0.56 and p = 0.88, respectively) by Chi-squared test. Despite the 1984 DRG experience, there was no change in admission practices or utilization of MICU beds during 1985. Appropriate management responses are needed from both the Federal government and the medical profession for better utilization of MICU resources.
We followed the course of 47 consecutive patients with inoperable primary bronchogenic carcinoma who underwent palliative neodymium-yttrium-aluminum-garnet laser photoresection (YPR) between September 1983 and September 1986. Of these 47, 35 (74.5 percent) underwent both radiation therapy (XRT) and YPR. The survival of these 35 patients (median survival, 304 days) was compared with that of 58 who underwent only palliative palliative XRT (median survival, 253 days) from 1981 to 1983, when YPR was not yet available at our institution. There was no significant difference in overall survival (p = 0.17). A significant increase in survival (p = 0.04) was seen in 15 patients who underwent emergency palliative YPR as the initial therapeutic intervention compared with 11 patients who received emergency palliative XRT but would have received YPR had it been available at that time. A trend toward increased survival was also shown in patients who underwent endobronchial radiation therapy in addition to YPR and XRT.
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In previous reports, we have shown that purified human C-reactive protein (CRP) enhances tumoricidal activity of murine macrophages and human blood monocytes. In the present study, we wished to determine whether CRP induced similar activity in human macrophages. We evaluated the effect of CRP on the generation of in vitro tumoricidal activity in alveolar macrophages from 24 normal volunteers, among whom 10 were smokers and 14 were nonsmokers. CRP, in concentrations comparable with those found in blood during acute inflammation, induced dose-dependent cytotoxicity in nonsmoker alveolar macrophages against tritiated thymidine-labeled human tumor cells. Tumoricidal responses of smoker and nonsmoker macrophages did not significantly differ after exposure to lipopolysaccharide although smoker responses tended to be lower. Responses to CRP, however, were significantly (p less than 0.01) depressed in smokers. These findings suggest that during acute inflammation, CRP may enhance the tumoricidal properties of human alveolar macrophages. Macrophage responsiveness to CRP, however, appears to be detrimentally affected by smoking.
A Pakistani kindred comprising seven generations and 36 members with the split-hand/split-foot anomaly is described. The full expression of the trait, monodactylous or split hand and split foot, mainly of the lobster-claw type, was present in 33 males and 3 females. Other females showed a distinctly milder expression of the trait, usually in the form of partial syndactyly, metacarpal and phalangeal hypoplasia, and malformation. The distribution of the affected members in the pedigree is compatible with X-chromosomal inheritance. Hemizygous males and presumably homozygous females exhibit the typical split-hand/split-foot anomaly, whereas only a part of the obligatory heterozygous females show the milder expression. There were no associated anomalies, such as ectodermal dysplasia, cleft lip/palate, macular degeneration, malformations of the long bones or internal organs, and overt mental retardation.
Angiotensin-converting enzyme (ACE) was measured in tissue homogenates from the African lungfish and six species of air-breathing teleosts (Heteropneustes fossilis, Clarias batrachus, Channa gachua, Anabas testudineus, Notopterus chitala, and Monopterus cuchia) using a standard spectrophotometric assay. In most species, the highest levels of ACE activity were found in the respiratory organs (gills and/or accessory respiratory organs). ACE was also found in heart and kidney tissues from most species and occasionally in liver. Converting enzyme was not found in skin or skeletal muscle from any species and only in blood from H. fossilis and brain from C. batrachus. Captopril, a potent inhibitor of mammalian ACE, inhibited enzymatic activity from all tissues except C. gachua heart and liver and A. testudineus heart. As fish make the transition from aquatic to aerial respiration the gill microcirculation is usually reduced in size and the accessory respiratory organs become elaborated and occupy a more central position in the vascular tree. The presence of ACE in accessory respiratory organs of air-breathing fish appears to greatly enhance the metabolic efficiency of this enzyme on circulating substrates.
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Peripheral blood T lymphocytes from patients with idiopathic pulmonary fibrosis and matched normal controls were examined for their helper function in an in vitro antibody synthesis assay. This assay measures the dose-related T-cell regulation of antibody production by B cells in the presence of pokeweed mitogen. Eight patients of 14 expressed significantly increased helper T-cell activity, three exhibited no change, and three had depressed helper T-cell function. All of the patients with excessive helper T-cell function had an active neutrophilic alveolitis as determined by bronchoalveolar lavage on the day of study. Five of the 14 patients studied were determined to have a low percentage of neutrophils (less than 10%) in their BAL fluid. None of these were found to express excessive helper T-cell function; in fact three of the five had depressed helper T-cell function. No correlation between steroid therapy or smoking history and the expression of excessive helper function was observed. None of the peripheral blood T-cells from IPF patients were actively producing IL-2 in vitro without further stimulation, providing evidence against constitutive production in vivo. T cells were also examined for their ability to produce lymphokines promoting fibroblast proliferation. Enhanced stimulation of fibroblast proliferation was shown to positively correlate with disease activity as determined by the degree of neutrophilic alveolitis (r = 0.68). The significant correlation between neutrophilic alveolitis and excessive helper T-cell function observed here suggests that altered systemic immunoregulation accompanies local inflammation. The further participation of patient T cells in promoting fibroblast proliferation may contribute to the development of fibrosis, or to the contrary may be an attempt to limit the fibrotic process.
Short axis magnetic resonance images of a left ventricular aneurysm were compared to similar views obtained by echocardiography and by thallium-201 single photon emission computed tomography. Images of the dyskinetic left ventricular apex and the contractile left ventricular base were analyzed and compared. Unlike the previously reported orthogonal plane magnetic resonance images, short axis imaging provided representative and quantitative information in views comparable to those obtained by standard noninvasive imaging techniques. These data indicate that short axis magnetic resonance imaging is capable of identifying and sizing the aneurysmal and the residual segments of the left ventricle. The findings may be of prognostic value in patients with left ventricular aneurysm.
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Mebendazole (3.3 mumol), causes in vitro glycogen depletion and inhibits glucose uptake in Avitellina lahorea. Inhibition of non-specific phosphomonoesterases and adenosine triphosphatase by mebendazole discussed in the light of the role of phosphatases in uptake mechanisms. Mebendazole has no effect on hexokinase which has broad substrate specificity but influences the activities of some glycolytic enzymes such as phosphorylase, phosphoglucomutase and glucose-6-phosphatase. Thus, it appears that mebendazole also acts to disrupt certain enzymes of carbohydrate metabolism which may ultimately cause death of the parasite.
In a 5 1/2-year retrospective study of hospitalized children with osteomyelitis who had technetium bone scans, we found that 32 of 38 (84%) had increased radionuclide uptake, 4 (11%) had normal uptake and 2 (5%) had decreased uptake. The two patients with decreased uptake had a stormy course with extensive bone destruction and pathologic fractures in spite of prolonged courses of antibiotic therapy. Decreased uptake on bone scan in patients with clinical evidence of osteomyelitis could indicate a poor prognosis and early surgical drainage is indicated in order to decrease morbidity.
Although the adult form of acid maltase deficiency is characterized by weakness of the limb girdle muscles, weakness of the respiratory muscles out of proportion to that of the limb muscles may make the diagnosis less obvious. We present four patients aged 35 to 57 with respiratory muscle weakness associated with signs of cor pulmonale and symptoms of alveolar hypoventilation. Each had symptoms of fatigue, hypersomnolence, morning headache, and orthopnea, the cause of which was misdiagnosed. The key to diagnosis was paradoxic abdominal motion on inspiration. This finding, consistent with diaphragmatic paralysis, led to neurologic evaluation, electromyographic examination, and muscle biopsy to confirm the diagnosis. The symptoms of alveolar hypoventilation were reversed with chronic nocturnal ventilation, which assisted in rehabilitating some patients.
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Attempts to enrich and characterize human marrow T-cell precursors have been performed using discontinuous Percoll gradient centrifugation, phenotypic analysis of cells with monoclonal antibodies (Mabs), and T-cell colony-forming capacity. Marrow cells were extensively depleted of T cells and separated into seven fractions. The depletion was performed with the following Mabs: CD6 (MBG6 or RFT12) + CD8 (RFT8), CD2 (D66) + CD8 (RFT8), and CD6 (RFT12) + CD8 (RFT8) + CD7 (RFT2). A peak of cells with the capacity to differentiate into mature CD2+CD4+ T-cell agar colonies (TL-CFU) was obtained in a fraction with a density 1.063 less than d less than 1.069 g/ml. This peak was associated with the presence of cells expressing RFB1 and OKT10, two markers shared by hemopoietic precursors. Cells in this fraction were negative for CD3, CD4, CD1, CD8, and CD2 antigens. Their treatment by complement-dependent cytotoxicity with the CD7 Mab resulted in a loss of T-cell colony-forming capacity together with a reduction of T10-, RFB1-, and My10-positive cells.