Biomedical subjects
Publications and source records attributed to S A Wright.
Adult T-cell leukemia/lymphoma (ATLL) is characterized by cutaneous disease, hypercalcemia, associated HTLV-I infection, and a fulminant course refractory to therapy. A patient with acute ATLL is described, and the natural history of ATLL is reviewed.
The urease (EC 3.5.1.5) inhibitor, phenylphosphoryldiamidate (PPDA), was given by continuous infusion into the rumen of two sheep nourished by intragastric infusion and into either the rumen or abomasum of four sheep given a pelleted diet containing 119 g crude protein (nitrogen x 6.25)/kg dry matter. PPDA was given at 1 g/d in infusion sheep and 1.5 g/d in the normally-fed sheep. Measurements of urea kinetics were made using single injections of [14C]urea. Urease inhibition was complete within 24 h of starting PPDA infusions to the rumen; in this time-period, urea concentration in rumen contents reached equilibrium with that in plasma and this situation persisted until infusions were terminated. Relative to the control periods, plasma urea and rumen ammonia concentrations were unchanged but urea irreversible loss rate decreased by 26% in infusion sheep and 33% in fed sheep when PPDA was given. Urinary urea excretion was not affected, hence urea degradation, measured by difference, decreased by 77 and 58% respectively in response to urease inhibition. Administration of PPDA to the abomasum resulted in a reduction in rumen urease activity to about 40% of control values but had no effect on urea metabolism. Differences between treatments in daily nitrogen retention were not significant, indicating that under the dietary conditions imposed in these experiments, even substantial changes in urea recycling had only minor effects on the overall N economy of the animal.
1. Rat hepatic cytochrome P450IIE1 is an ethanol-inducible enzyme which catalyses ethanol oxidation and activation of the procarcinogen, N-nitrosodimethylamine (NDMA) to its carcinogenic metabolite. 2. Initial studies in adult rat indicated that the regulation of cytochrome P450IIE1 is complex, therefore we strove to identify a central regulatory mechanism, using primary monolayer hepatocyte culture. These studies examined the effect of a range of agents (i.e. inducers, hormones, sodium butyrate and 5-aminolaevulinic acid) on amounts of cytochrome P450IIE1 protein and mRNA expression in rat hepatocytes maintained in serum-free medium on both Vitrogen and Matrigel, a laminin-rich basement membrane. 3. At time 0, immunoreactive cytochrome P450IIE1 protein was easily detectable in control cultures, yet decreased rapidly with time in culture to nearly undetectable levels at 120 h. Addition of inducers (notably, pyrazole) to the culture medium increased cytochrome P450IIE1 above that of untreated cultures at similar time points, yet did not elevate cytochrome P450IIE1 or NDMA demethylation above their levels at time 0. 4. Cytochrome P450IIE1 hybridizable mRNA also rapidly declined in culture. The decline in mRNA was not significantly altered in cultures exposed to pyrazole or any other agent. Thus, post-transcriptional factors appear to play an important role in the regulation of hepatic cytochrome P450IIE1, with protein stabilization being the most probable mechanism.
The ability of membrane-associated peptidases from the brains of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats to metabolize iodinated angiotensin (125I-Ang II) and 125I-Ang III was compared. 125I-Ang II was metabolized to 125I-Ang III and other fragments exclusively by membrane-associated peptidases. In contrast to 125I-Ang III which was effectively degraded by both membrane-associated and residual cytosolic peptidases, 125I-Ang II was unaltered by contaminating cytosolic enzymes. The ability of SHR-derived membranes to metabolize 125I-Ang II and produce 125I-Ang III was enhanced when compared to membranes from WKY rats. No difference was observed in the ability of membrane or cytosolic enzymes from SHR and WKY rats to degrade 125I-Ang III. These data are consistent with an increased availability of Ang III in the brains of SHRs.
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Receptors for C3 degradation fragments (CR1, CR2, and CR3) are present on many human cells including phagocytes and lymphoid cells and may be critical in the attachment of invading microorganisms. In these studies Candida were found to mimic the human CR by binding erythrocytes coated with specific human C3 fragments. Yeast forms of Candida species were adhered to glass slides and were allowed to germinate. Sheep erythrocytes (E) were coated with IgM (EA) and human complement components to prepare EA, EAC14, EAC3b, EAC3bi, and EAC3d. These test cells were then examined for adherence to the organism. Antibodies to human CR1, CR2, and CR3 were used to evaluate their potential for blocking adherence of the test erythrocytes to Candida. Fluorescein-labeled antibodies to human complement receptors were also used to characterize the binding sites. EAC3bi and EAC3d, but not E, EA, or EAC14, bound extensively to the germ tubes and pseudohyphae of Candida albicans and C. stellatoidea. EAC3b bound infrequently. Other Candida species, generally considered less pathogenic, bound significantly fewer specific test erythrocytes than C. albicans. Monoclonal antibodies to human CR1 and CR3 (3D9, 1B4, C511, 2B6, anti-B2, Mo1, and anti-Mac-1), in general, did not block adherence of test erythrocytes. Blocking of adherence of EAC3bi and EAC3d test erythrocytes coated with small quantities of C3 fragments occurred with high concentrations of monoclonal (anti-CR2) HB-5 and polyclonal (anti-CR2) anti-GP 140. Immunofluorescence studies demonstrated binding of Mo-1 to the germinated forms of the organism, whereas binding of the other antibodies was not seen. These studies suggest a surface constituent on the organism similar to CR on human cells. Additional studies are necessary to further define the molecular nature of the binding site. The ability of organisms to mimic human CR may be more generalized than previously known and may serve as a mechanism for modification of the inflammatory and immune response.
Leu-M1, or MMA, originally was proposed as a differentiation antigen on myelomonocytic cells and was said to be useful as an aid in distinguishing lymphoid from myeloid leukemias. Subsequently, it was proposed by Hsu and Jaffe as a useful marker of Reed-Sternberg cells and their variants in paraffin-embedded sections in Hodgkin's disease and as an aid in the differential diagnosis among Hodgkin's disease, non-Hodgkin's lymphomas, and reactive lymphoid proliferations. In order to test the usefulness of this antibody in classifying acute leukemias and to investigate the spectrum of its positivity on B5 and/or formalin-fixed, paraffin-embedded tissue sections, a variety of benign and neoplastic hematopoietic and lymphoid disorders were studied, using Leu-M1 and the ABC immunoperoxidase technic. Definite positivity in neoplastic cells was present in 4 of 16 patients with acute nonlymphocytic leukemias, 0 of 9 patients with acute lymphocytic leukemias/lymphoblastic lymphoma, 11 of 13 patients with Hodgkin's disease, and 0 of 18 patients with non-Hodgkin's lymphomas. Granulocyte staining could be identified in many cases. Although not identified in tonsillar sections from three patients, variable numbers of sometimes large mononuclear and rare binucleate cells were identified in some of the 14 reactive lymph nodes studied as well. These data, together with other data recently reported, suggest that in routinely processed tissue sections, Leu-M1 is a relatively sensitive marker for Hodgkin's disease, but it does not appear to be specific for that diagnosis. Although marking some acute nonlymphocytic leukemias in tissue sections, its lack of sensitivity and possible lack of specificity severely limits its usefulness in classifying the acute leukemias.
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Partial-thickness tearing of the rotator cuff is common; however, relatively little is written on the subject. We reviewed 39 patients with partial-thickness rotator cuff tears who underwent acromioplasty, debridement of the abnormal tissue, and tendon suturing. Follow-up averaged 55 months (range 13 to 132 months). Twenty-three (59%) patients had an excellent result, 10 (26%) patients had a satisfactory result, and 6 (15%) patients had an unsatisfactory result. Four of the six patients with unsatisfactory results had also had unsuccessful previous surgery. Thirty-five (90%) patients rated their response to surgery as either much improved or improved. No complications occurred, and to date no reoperations have been required. Diagnosis of partial-thickness rotator cuff tears can be challenging. Magnetic resonance imaging supplies the most complete information about tendon structure. Conservative treatment is reasonable for most partial-thickness tears. When surgical treatment is indicated, acromioplasty, debridement, and tendon repair are effective.
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A nosocomial viral infection is defined as a viral infection the onset of which occurs when the patient has been hospitalized longer than the incubation period of the virus. Viruses account for about 5% of all nosocomial infections. Viral cross-infection is most common in infants and children but also occurs in other groups, including the elderly, institutionalized persons of all ages, immunocompromised hosts, and patients with underlying chronic pulmonary, renal, or cardiac disease. These infections are associated with extended length of hospital stay and considerable morbidity and mortality. The spectrum of nosocomial viruses is wide and includes blood-borne, respiratory tract, and enteric pathogens, among others. This review will discuss the clinical characteristics, transmission, and control of the common nosocomial respiratory viruses: respiratory syncytial virus, varicella zoster virus, influenza virus, adenovirus, parainfluenza, and rubeola.