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Biomedical subjects

S Hill

Publications and source records attributed to S Hill.

At least 253 records · Page 14Linked to original sources
PubMed1982

Monocyte function in cirrhosis.

Monocyte function has been studied in a total of 51 patients with biopsy-proven cirrhosis and 35 controls. There was significantly reduced monocyte spreading (p less than 0.05), chemotaxis (p less than 0.02), bacterial phagocytosis (p less than 0.05) and bacterial killing (p less than 0.02) in the cirrhotics compared to the controls. Monocytes from patients with cirrhosis produced significantly less of the lysosomal enzymes N-acetyl beta-glucosaminidase and beta-glucuronidase than those obtained from the controls (p less than 0.02). There was no significant difference in the number of monocytes obtained, the number of macrophage precursors, and the nitro-blue tetrazoline (NBT) reduction between the cirrhotic and the controls. The reduced function appeared to be mainly due to a circulating inhibitory factor and could be corrected by incubation of the cirrhotic cells in serum from control subjects. The response of monocytes from patients with cirrhosis did not differ from the controls in their response to added endotoxin or latex particles suggesting that they are capable of a normal response in the absence of the inhibitory factor. Paired specimens of portal and systemic serum were collected from patients with no evidence of liver disease undergoing vascular surgery. When added to normal human monocytes the portal serum caused a significant reduction in bacterial killing (p less than 0.02) and chemotaxis (p less than 0.05) compared to results obtained in the paired systemic serum. Mixing experiments suggests the presence of an active inhibitor in the portal serum. The results suggest that monocyte function is reduced in cirrhosis apparently due to a serum inhibitor which may have originated from the portal vein. The abnormalities may account in part for the increased susceptibility of these patients to infection.

Acetylglucosaminidase↗
PubMed1982

Immunopathology of B-cell lymphomas induced in C57BL/6 mice by dualtropic murine leukemia virus (MuLV).

Combined clinicopathologic and immunomorphologic evidence is presented that would indicate that a murine leukemia virus (MuLV) with the dualtropic host range is capable of producing a clinically malignant lesion composed of immunoblasts and associated plasma cells in C57BL/6 mice. This process, morphologically diagnosed as an immunoblastic lymphoma of B cells using standard histopathologic criteria, was found to be distinctly polyclonal with regard to immunoglobulin (Ig) isotype when analyzed for both surface and cytoplasmic Ig. Further studies demonstrated that this clinicopathologically malignant, dualtropic MuLV-induced, polyclonal immunoblastic lymphoma of B cells in C57BL/6 mice was normal diploid and unable to be successfully transplanted to nonimmunosuppressed syngeneic recipients. Although all serum heavy and light chain components were found to be progressively elevated as the tumor load increased, the polyclonal increase in serum immunoglobulins was most pronounced for mu heavy and kappa light chains (ie, mu greater than gamma 2A greater than alpha greater than gamma 2B greater than gamma 1; kappa greater than lamba). The dissociation of clinicopathologic and biologic criteria for malignancy in the presently described dualtropic (RadLV) MuLV-induced B-cell lesion is sharply contrasted with the thymotropic (RadLV), MuLV-induced T-cell lymphoblastic lymphoma in C57BL/6 mice. This process is also a clinicopathologically malignant lesion but, when one uses biologic criteria, is found to be distinctly monoclonal, aneuploid, and easily transplanted to nonimmunosuppressed syngeneic recipients. The close clinicopathologic and biologic similarities of the dualtropic MuLV-induced animal model to corresponding human B-cell lymphoproliferative diseases are stressed.

Animals↗
PubMed1981

Nitrogen fixation gene (nifL) involved in oxygen regulation of nitrogenase synthesis in K. pneumoniae.

The enzyme complex nitrogenase, which reduces N2 to NH+4, involves two redox proteins, both irreversibly damaged by O2 (ref. 1). Enzyme activity therefore requires anaerobic conditions, a source of reductant and a large amount of ATP (approximately 16 ATPs per N2). In both aerobic and facultative anaerobic N2-fixing bacteria, nitrogenase synthesis is regulated by O2 and NH+4, but in the aerobes there are also processes to protect the enzyme from O2 damage. The mechanisms of repression by O2 and NH+4 seem to be independent in the organisms so far examined. In the facultative anaerobe, Klebsiella pneumoniae, O2 was shown to repress nitrogenase synthesis in an NH+4-constitutive strain. The fusion of the Escherichia coli lacZ gene into each transcriptional unit of the nitrogen fixation (nif) gene cluster in K. pneumoniae has facilitated studies with O2, because expression from the various nif promoters results in an O2-stable product (beta-galactosidase). Notably, the nifHDK operon (the nitrogenase structural genes) was more sensitive to O2 repression than the nifLA operon (regulatory genes). The characterization of mutants, reported here, indicates the involvement of a nif-regulatory gene product in the mechanism of O2 control of nitrogenase synthesis.

Aerobiosis↗
PubMed1980

Management: carrying their own cans.

The NHS is being urged to collaborate with the private health sector. In spite of the presence of many ex-NHS administrators, the approach to management is rather different, as Stanley Hill found when he talked to the people concerned with the embryonic Cromwell Hospital in London. This brings to a close this first series of three articles, but in a few months' time Stanley Hill will be looking at three more organizations outside the NHS, and how they are managed.

Hospital Administration↗
PubMed1980

Analysis of regulation of Klebsiella pneumoniae nitrogen fixation (nif) gene cluster with gene fusions.

Gene fusions in which the lac genes are under the control of each promoter in the Klebsiella pneumoniae, nitrogen fixation (nif) gene cluster have been constructed. These fusions have been used to examine positive control of the cluster and the response of individual genes to repression by ammonia and oxygen. De-repression of nif transcriptional units is coordinate and molybdate is required for maximal expression of the structural gene operon, which is autogenously regulated.

Ammonia↗
PubMed1980

Roles of nifF and nifJ gene products in electron transport to nitrogenase in Klebsiella pneumoniae.

Crude extracts of the wild-type Klebsiella pneumoniae reduced C2H2 with either pyruvate or formate as reductant (specific activity, 3 nmol min-1 mg of protein-1), whereas crude extracts of nifF mutant were almost inactive (specific activity, 0.05). However, activity in the latter extracts was stimulated by adding Azotobacter chroococcum flavodoxin (specific activity, 10). Thus, nifF mutants may lack an electron transport factor. Crude extracts of nifJ mutants had about 20% of the wild-type level of active MoFe protein, and thus nifJ has a presumptive role in maintaining active MoFe protein. Studies on pyruvate or formate as reductants for nitrogenase in extracts of the nifJ mutants suggest in addition a role in electron input to nitrogenase for the following reasons. (i) Nitrogenase activity with these reductants was very low (specific activity, 0.06) and was not stimulated by extra MoFe protein or the flavodoxin. (ii) Activity was increased by adding a crude extract of a mutant lacking the structural nif genes (specific activity, 1) or a crude extract of the nifF mutant (specific activity, 4).

Acetylene↗
PubMed1980

Use of enhanced computerized tomography to evaluate osmotic blood-brain barrier disruption.

Enhanced computerized tomography (CT) is a noninvasive means of monitoring blood-brain barrier (BBB) disruption. In the present study this technique was used to monitor the degree, distribution, extent, and reversibility of osmotic BBB disruption. With a canine model, the timing of administration of iodinated contrast agent was shown to be crucial to optimize enhancement by CT of the disrupted BBB. Meglumine iothalamate given intravenously resulted in excellent enhancement on CT scan. Intracarotid infusion of this contrast agent was less satisfactory. Under similar conditions, enhancement due to metrizamide was less marked and more transient than that observed with meglumine iothalamate. Systemically administered methotrexate after osmotic BBB disruption resulted in increased brain levels in areas that closely correlated with CT scan enhancement. These results suggest that the CT scan provides an excellent noninvasive monitor of both BBB disruption and the delivery of chemotherapeutic agents to the brain. (Neurosurgery 6: 49--56, 1980)

Animals↗
PubMed1980

Reversible osmotic blood-brain barrier disruption in humans: implications for the chemotherapy of malignant brain tumors.

The blood-brain barrier seems to be an important factor in drug access to malignant brain tumors. Successful experimental reversible disruption of the blood-brain barrier in animals provided the basis for a clinical evaluation of osmotic disruption in five patients with primary and metastatic malignant brain tumors. Good to excellent blood-brain barrier disruption was achieved in four patients with a single nontransient complication, a superficial wound infection at the burr hole site in the first patient. Reversible, transient osmotic barrier disruption was achieved 15 times in five patients without additional toxicity. Computed tomography and radionuclide brain imaging were shown to be useful noninvasive monitors of the adequacy and extent of barrier disruption. These studies also provide further evidence that the barrier is at least partially intact in human tumors because in one patient a metastsis was seen only after barrier disruption.

Adenocarcinoma↗
PubMed1980

Carcinoembryonic antigen in cerebrospinal fluid of adult brain-tumor patients.

Carcinoembryonic antigen (CEA) was measured in plasma and cerebrospinal fluid (CSF) in patients with neoplasms and non-neoplastic neurologic conditions of the central nervous system (CNS). Seventy-two control patients had a mean CEAcsf of 0.04 ng/cu cm, 31 patients with benign tumors had a mean CEAcsf of 0.03 ng/cu cm, and 21 patients with malignant CNS tumors had mean CEAcsf of 21.7 ng/cu cm. In the absence of intradural metastasis, the existence of non-CNS malignancies did not cause CEA to appear in the CSF. There was no relationship between the plasma and CSF levels of CEA. The CSF is normally free of CEA, and its detection is strongly suggestive of either primary or secondary intradural malignancy. The titres of CEA decline with effective therapy, and may be of use in monitoring treated patients for recurrence.

Adolescent↗
PubMed1980

Outcome of very low birth weight (VLBW) infants. I. Neonatal behavior of 188 infants.

Behavioral characteristics of very low birth weight infants (less than 1,501 gm) were determined with the term Brazelton Neonatal Behavioral Assessment Scale and selected items from a preliminary form of the scale for premature and at-risk infants. The behavior of 188 infants was assessed at a time as optimal as possible for social interaction. Our very low birth weight infants were upset less easily, had several reflexes with below average scores, and were less responsive to visual stimuli than term infants of other studies. Improved description of interactive abilities and tolerance of the testing procedure was made possible with some items from the preliminary premature scale. Orienting responses in 6 infants tested after 44 weeks because of prolonged illness were less than optimal with a single exception. This suggests that behavioral capacity, not age, should define where the Brazelton scale is not applicable. Perinatal factors including birth weight, gestational age, and age that weight gain began, predicted some motoric and state control responses. Whether this predictive capacity will persist or change with time awaits results of follow-up of these infants.

Adult↗
PubMed1979

Multidisciplinary terms.

Explore the source record for details and available documents.

Commitment of Persons with Psychiatric Disorders↗
PubMed1979

Glucocorticoid induction of pulmonary maturation in the rabbit fetus. The effect of maternal injection of betamethasone on the activity of enzymes in fetal lung.

1. Maternal administration of betamethasone (0.2 mg/kg) on day 25 or 26 of gestation produced a significant decrease in the lung/body weight ratio of the rabbit fetuses within 24 h. 2. The incorporation of [14C]choline but not [14C]ethanolamine into the lipids of fetal lung slices was significantly increased, indicating that there was a specific effect on phosphatidylcholine synthesis. 3. The activities of a number of marker enzymes for subcellular organelles were elevated, especially in the lungs of fetuses delivered on day 26. The increases in monoamine oxidase (mitochondrial outer membrane), beta-glycerophosphatase and aqueously dispersed phosphatidic acid-dependent phosphatidic acid phosphohydrolase (lysosomal) activities were significant. 4. Although the activity of cholinephosphotransferase was not affected by glucocorticoid treatment, the activities of glycerol-3-phosphate phosphatidyltransferase and the activities of two enzymes in the auxiliary pathways for the production of disaturated phosphatidylcholine (lysophosphatidylcholine:lysophosphatidylcholine transacylase and lysophosphatidylcholine:acyl-CoA acyl-transferase) were significantly increased. 5. Membrane-bound phosphatidic acid-dependent phosphatidic acid phosphohydrolase activity was elevated to a lesser extent than the aqueously dispersed phosphatidate-dependent activity and this increase was not significant. 6. The incorporation of E135S]methionine into protein by slices of fetal lung was significantly reduced after maternal treatment with betamethosone. 7. These results are consistent with the general view that glucocorticoids can induce pulmonary maturation and surfactant production in the rabbit fetus but indicate that some of the former hypotheses regarding the mechanism by which lipid synthesis is accelerated must be reevaluated.

Animals↗