Topological antiferromagnetism at Cr surfaces and interfaces.
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Biomedical subjects
Publications and source records attributed to A Vega.
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This paper presents results of experiments designed to further purify the membrane system involved in mitochondrial calcium transport. A partially purified extract, which transported calcium with a specific activity of 1194 nmol 45Ca2+/mg protein/5 min, was used to obtain mouse hyperimmune serum. This serum inhibited calcium uptake both in mitoplasts and in vesicles reconstituted with mitochondrial proteins containing cytochrome oxidase. Western blot analysis of the semipurified fraction showed that the serum recognized specifically two antigens of 75 and 20 kDa. Both antibodies were purified by elution from the nitrocellulose sheets and their inhibition capacity was analyzed. The antibody that recognized the 20-kDa protein produced a higher degree of inhibition than the other one.
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Rhesus monkeys immunized intramuscularly or orally with staphylococcal enterotoxin B (SEB) toxoid or SEB toxoid incorporated in microspheres made of poly(DL-lactide-co-glycolide) were challenged with a lethal dose of aerosolized SEB to study their immunity and cellular responses in the circulation. It was found that circulating antibodies play a critical role in preventing SEB from triggering toxicosis. Monkeys with high levels of antibodies survived, while those with low levels underwent 2 to 3 days of toxicosis and died. Intramuscular immunization induced high levels and oral immunization induced low levels of antibodies. The circulating antibodies in surviving monkeys decreased dramatically within 20 min and started to rebound at 90 min after SEB challenge. At 90 min, the dying monkeys showed in the circulation a dramatic increase of polymorphonuclear leukocytes and decreases of NK cells and monocytes (CD16 and CD56 markers) as well as of lymphocytes with HLA-DR, CD2, CD8, and IL2R alpha (CD25) markers. The number of polymorphonuclear leukocytes showed an inverse correlation with the numbers of monocytes and various lymphocyte subpopulations which, except for IL-2R, CD16, and CD56(+) cells, showed a direct correlation with one another. The changes in the populations of leukocytes, monocytes, NK cells, and lymphocytes seem to be an indication of initial toxicosis; however, the roles of these cells in toxicosis and death remain to be defined.
Clinical, mammographic, sonographic and pathologic examinations in 17 patients with nonpalpable stellate lesions showed radiographic findings suggestive of radial scars, with the exception of 2 cases which showed a dense central region. These findings were not sufficiently consistent to differentiate radial scar from carcinoma so that wire localization biopsy was necessary. Four patients had 7 radial scars associated with 6 tubular carcinomas, 2 of them having 3 and 2 radial scars with 2 tubular carcinomas, respectively. No characteristic radiographic findings were made in these cases. Four patients showed radial scar with punctate microcalcifications in the surrounding breast parenchyma as part of benign and premalignant conditions. Ultrasonography in 7 patients showed a hypoechoic area on 4 with acoustic shadow similar to that of carcinoma. Our study suggested that radial scar has a relationship with tubular carcinoma and surgical excision of these stellate lesions is, therefore, required.
Staphylococcal enterotoxin B (SEB) was tested in rodent mast cell cultures for the release of serotonin. Both rat RBL-2H3 mast cells and murine peritoneal cells released serotonin after SEB stimulation in culture. Release of serotonin in RBL-2H3 cells depended on the concentration of SEB; an appreciable release was seen at 50 micrograms/ml. The release of serotonin was not due to cell death. Serotonin release could be enhanced by bradykinin but not by vasoactive intestinal peptide, substance P, lipopolysaccharide from Salmonella typhimurium, the calcium ionophore A23187, acetylcholine, adenosine, 5-hydroxyeicosatetraenoic acid, indomethacin, or phorbol myristate acetate. SEB bound directly to the membrane of RBL-2H3 mast cells, and the SEB-binding site, the presumptive receptor, appeared to be a protein. The SEB receptor could not be capped under membrane-capping conditions, and serotonin release could not be enhanced by attempts to cross-link the receptor. These results suggest that mast cells may be an important cell type involved in SEB toxicosis and that release of serotonin may be enhanced by activation of the kinin-kallikrein system.
The purpose of this study was to determine the frequency of anomalies of the basichondrocranium in a series of 42 patients with Chiari type I malformation compared with a control group of 46 subjects. Sixteen patients also had syringomyelia. Linear, angular and posterior fossa surface area measurements were taken on conventional lateral skull x-rays. Posterior fossa volume was estimated by CT scanning. In patients there was shortening of clivus length, Twining-opisthion distance and Chamberlain's line. Basal and Boogard angles were enlarged. The size of the posterior fossa was smaller in patients than in controls. Only 10 (23.8%) patients had no evidence of occipital dysplasia. When discriminant analysis was applied to the data, the most discriminative variables were posterior fossa area and clivus length which allowed accurate identification of 76% of patients as belonging to the patient group and 79% of controls as belonging to the control group. These findings prove that under-development of the basichondrocranium with a small size of the posterior fossa is an outstanding feature in adult Chiari type I malformation, and support the hypothesis that tonsillar ectopia is secondary to the disproportion between the posterior fossa and the cerebellum, which is forced to grow into the cervical spinal canal.
The value of indium-111 labeled leukocyte scintigraphy for the diagnosis of infection in the general population is well documented; there is less information available on its role in the evaluation of the immunocompromised patient. In this study, leukocyte scintigraphy was performed on a 31-year-old immunocompromised woman who had a possible intra-abdominal abscess. No abscess was detected, but intense oral, esophageal, gastric, and vaginal uptake was observed. Candida infection was histologically confirmed at all four sites.
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Bacterial sepsis, a significant complication of chronic hemodialysis, is generally the result of infection at the vascular access site. We retrospectively reviewed the utility of indium-111-(111In) labeled autologous leukocyte scintigraphy in 26 patients (30 scans) with synthetic vascular grafts, on chronic hemodialysis, in whom hemodialysis access site infection was a diagnostic consideration. Leukocyte scintigraphy correctly identified all fifteen access-site infections; there was one false-positive study, for an overall sensitivity and specificity of 100% and 93%, respectively. Of particular significance is the fact that in nine (60%) of the fifteen access-site infections, physical examination was normal. Our data indicate that 111In-labeled leukocyte scintigraphy is a useful procedure for the diagnosis of hemodialysis access-site infection, and it is especially valuable when physical examination of the access site is normal.
Indium-111-labeled leukocyte scintigraphy was performed on a 66-yr-old male with polyarticular acute gouty arthritis. Images revealed intense labeled leukocyte accumulation in a pattern indistinguishable from septic arthritis, in both knees and ankles, and the metatarsophalangeal joint of both great toes, all of which were involved in the acute gouty attack. Joint aspirate as well as blood cultures were reported as no growth; the patient was treated with intravenous colchicine and ACTH for 10 days with dramatic improvement noted. Labeled leukocyte imaging, repeated 12 days after the initial study, revealed near total resolution of joint abnormalities, concordant with the patient's clinical improvement. This case demonstrates that while acute gouty arthritis is a potential pitfall in labeled leukocyte imaging, in the presence of known gout, it may provide a simple, objective, noninvasive method of evaluating patient response to therapy.
Fourteen patients (13 females, 1 male) with urinary incontinence from bladder instability were treated with intravaginal (intrarectal) electrical stimulation. Good results were achieved in 57.1% of the cases. The foregoing finding shows that intravaginal (intrarectal) electrical stimulation may constitute a therapeutic option in urinary incontinence from bladder instability.
Twenty-four patients with post-prostatectomy urinary incontinence were submitted to clinical and urodynamic evaluation. The clinical evaluation analyzed urinary symptoms and included rectal examination of the prostate lodge, neurourologic examination (perineal sensitivity, anal tone, bulbocavernous reflex, voluntary control of anal sphincter). The urodynamic study consisted of flowmetry, cystomanometry, detrusor pressure/micturition flow test and videocystography. An unstable bladder was demonstrated in 62.5% of the cases. Bladder dysfunction was recognized in 75% of the cases. Involvement of the striated periurethral sphincter was demonstrated in no patient. The clinical data did not provide orientation. No relation was observed between the urodynamic data, type of surgery, and amount of prostate removed. The urodynamic data appear to have a prognostic significance.