Biomedical subjects
Publications and source records attributed to K Morris.
The authors describe the case history of a patient who suffered a subarachnoid haemorrhage originating from an ependymoma of the fourth ventricle. The unusual nature of this presentation is emphasised in their review of a series of 22 patients with ependymomas of the craniocervical junction.
Drugs possessing membrane stabilizing activity might act to diminish the augmented microvascular permeability resulting from acute lung injury. To test this rats were pretreated with quinidine, procainamide, or lidocaine and then given the lung injury-inducing agent thiourea. Vascular permeability, assessed as the extravascular accumulation of radiolabeled protein, was increased more than threefold by thiourea. This increase was diminished by 29, 34, and 43% after pretreatment with procainamide, quinidine, and lidocaine, respectively. Lidocaine also returned the thiourea-induced increase in lung wet weight-to-dry weight ratios to control levels. This protection was not likely due to hemodynamic effects of these agents, since no differences were noted in cardiac output between pretreated rats and those receiving thiourea alone and a small increase in mean pulmonary arterial pressure in the lidocaine-pretreatment group was the only difference noted. O2 metabolites have been implicated in the pathogenesis of thiourea-induced lung injury. None of these agents scavenged O2- or H2O2 directly, but quinidine and procainamide diminished in vitro neutrophil O2- and H2O2 production, and lidocaine inhibited neutrophil H2O2 production. However, neutropenia (PMN less than 100/ml) induced with either vinblastine or cyclophosphamide (Cytoxan) failed to prevent thiourea-induced increases in pulmonary vascular protein leak. In conclusion, procainamide, quinidine, and lidocaine diminished lung injury in rats after thiourea. Although these agents diminish PMN O2 metabolite production in vitro their salutary role in thiourea-induced lung injury appears to be through an unknown mechanism that is independent of their effects on neutrophil O2 metabolite-dependent toxicity.
Forty right-handed college subjects tapped with and without a verbal task under two instructional conditions (tap as quickly as possible vs. tap as consistently as possible) and two levels of verbal production (silent vs. aloud). The tapping task consisted of the alternate tapping of two keys with the index finger of the left vs. right hands, while the verbal task was anagram solution. Three rate and four variability measures of tapping performance were evaluated in the identification of lateralized interference. The results indicate that reliable lateralized interference, more right-hand than left-hand tapping disruption, was observed only for variability measures under instructions to tap as consistently as possible. Furthermore, only one of these variability measures was sensitive to an increase in lateralized interference produced by verbal production. Because of the limited demonstration of verbal laterality effects with the two-key tapping procedure in this study, conclusions suggest that the simpler manual task of repetitive tapping of one key should be viewed as the method of choice in future dual-task studies.
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We have used a single intensive chemotherapy regimen in the treatment of young patients with diffuse, aggressive, malignant lymphomas. There were two major histologic types of lymphoma in our series: lymphoblastic lymphomas, which presented most often with mediastinal tumor (64%), and undifferentiated lymphomas (mostly Burkitt's lymphomas), which occurred predominantly in the abdomen (86%). Our objective was to examine the determinants of prognosis in a uniformly treated patient group that included 31 children (2-16 yr) and 34 young adults 17-35 yr). Patients with extensive bone marrow involvement (greater than 50% replacement by tumor cells) were included in the study. Treatment consisted essentially of a 4-drug combination (cytoxan, adriamycin, vincristine, and prednisone) alternating with a 42-hr methotrexate infusion, followed by leukovorin rescue, and included intrathecal prophylactic therapy against central nervous system (CNS) disease. Patients with localized or resected undifferentiated lymphoma received 6 therapy cycles; all other patients received 15 cycles. Radiation therapy was used only in exceptional circumstances. Fifty-eight of 65 patients (89%) achieved complete remission: 97% of children and 82% of adults. The estimated 3-yr survival was 60% (SE 6.4%) with a median follow-up of 3 yr. Analysis of factors associated with remission duration and survival indicated that bone marrow involvement at referral and extensive disease were poor prognostic variables. Patients with lymphoblastic lymphomas and patients with completely resected undifferentiated lymphomas had the best prognosis (81% +/- 12% and 94% +/- 6% estimated 3-yr survival, respectively). Patients with extensive intraabdominal undifferentiated lymphoma (stage D) had the worst prognosis (33% +/- 11% estimated 3 yr survival), but even in this subgroup, bone marrow involvement was an adverse factor (estimated survival in stage D patients with and without bone marrow involvement was 14% +/- 13% and 43% +/- 15%, respectively). Elevated uric acid and/or lactic dehydrogenase (LDH) were also of prognostic significance, but predominantly reflected state, i.e., extent of disease. Age did not significantly influence prognosis. In the undifferentiated lymphoma subgroup, histology (i.e., Burkitt's lymphoma versus non-Burkitt's lymphoma) was not of prognostic significance. Total white count was below 1,000/cu mm in 39% of cycles, and fever associated with granulocytopenia occurred in 17% of cycles. Stomatitis of moderate to severe extent occurred in 50% of cycles.(ABSTRACT TRUNCATED AT 400 WORDS)
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One mechanism by which glucocorticoids could exert their anti-inflammatory action is via rapidly saturable, stereo-specific cytoplasmic protein receptors. This report is of an investigation into such a possibility in synovial cells. Synovium, obtained from knee joints of rheumatoid patients undergoing surgery, was incubated with clostridiopeptidase A and trypsin-EDTA to obtain cell suspensions. These, together with cells obtained from synovial fluid aspirated from patients with rheumatoid arthritis, were identified by electron microscopy. Duplicate samples of these cell suspensions were incubated with increasing concentrations of H3Dexamethasone (1 x 10(-10)M-1 x 10(-9)M) for 30 minutes at 37 degrees C. Analysis of the proportion of steroid bound to whole cells showed evidence for specific, rapidly saturable, receptors in the cells obtained from synovial tissue, but this was not found in synovial fluid cells. Electron micrographs showed that cells obtained from synovial tissue consisted of synovial fibroblast - and macrophage-types, lymphocytes, monocytes and macrophages. Polymorphonuclear leucocytes appeared to be absent. However, in synovial fluid cell type polymorphonuclear leucocytes were the predominant cell type. We concluded from this, that one or more of the cell types present in synovial tissue contain a specific steroid receptor, but that this is lacking in synovial fluid polymorphonuclear leucocytes.
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The response of endogenous angiotensin II levels to positional change, lateral to supine recumbency, was investigated in a prospective study of 55 primigravid patients during the last half of pregnancy. Blood samples were obtained in the lateral and supine recumbent positions. The mean supine angiotensin II level was significantly higher between 29 and 34 weeks' gestation in those patients destined to develop pregnancy-induced hypertension than in those who remained normotensive (P less than 0.05). As gestation advanced, the mean per cent relative change of angiotensin II from the lateral to the supine position altered from negative to positive in those patients destined to develop pregnancy-induced hypertension, whereas it remained negative in those patients who remained normotensive. These findings are discussed in relation to pathophysiologic alterations in the development of pregnancy-induced hypertension.