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Biomedical subjects

E M Smith

Publications and source records attributed to E M Smith.

At least 217 records · Page 12Linked to original sources
PubMed1983

A national survey of hospital ethics committees.

A telephone survey of 602 randomly selected hospitals was conducted to identify existing ethics committees, i.e., those with the potential to become involved in the decision-making process in specific cases. Using the number of acute care beds as the criterion, hospitals were divided into 2 groups: (1) over 200 beds; n = 400; (2) 200 or fewer beds; n = 202. Chairpersons of identified committees completed detailed questionnaires. Seventeen committees were found--approximately 1% of all U.S. hospitals. A typical committee included physicians, clergymen, and other professionals. Almost all committees were advisory, not decision-making bodies, and considered very effective by their chairpersons. Ethics committees have not, however, solved current medical ethical problems; nor have they allayed the concerns of patients' rights advocates about patient representation and control. Further study is warranted.

Ethical Review↗
PubMed1983

Predictors of mortality in alcoholic women: prospective follow-up study.

An 11-year follow-up of 100 alcoholic women who were systematically interviewed and diagnosed during hospitalization found 31% dead, the majority as a result of alcohol-related causes. There were over 4 times as many deaths in alcoholic women as expected in the general population. The life span of alcoholic women was shortened by over 15 years. Only those women who had abstained during the interval following hospitalization had fewer than expected deaths. Five variables correctly predicted survival status for 79% of the subjects (80% of survivors and 77% of those who died): older age at index, onset of alcoholism before age 30, history of frequent benders, primary diagnosis of antisocial personality, and short-term drinking status.

Adolescent↗
PubMed1983

Transformed and normal cell surface glycoproteins that induce interferon production by nonsensitized lymphocytes.

Nonsensitized human and mouse lymphocytes produce interferon (IFN)-alpha and IFN-alpha/beta, respectively, in response to most transformed cells, as well as normal xenogeneic cells. The treatment of transformed human (WISH) and mouse (L) or normal mouse embryo (ME) cells with trypsin, pepsin, or neuraminidase resulted in a loss of the cell's ability to induce IFN-alpha or alpha/beta. These findings suggested that a cell surface glycoprotein is responsible for the induction of IFN-alpha and alpha/beta. The sonication of WISH, L, and ME cells released glycoproteins which retained IFN-inducing activity in the soluble form. The inducing molecules from WISH, L, and ME cells had molecular weights of 130,000, 90,000, and 68,000, respectively. Further purification, plus a confirmation of the glycoprotein nature of the inducer molecule, was shown by specifically binding and eluting L cell inducer bioactivity from a concanavalin A-Sepharose affinity column.

Animals↗
PubMed1983

Action of an opiate receptor blocker on ovine cardiopulmonary responses to endotoxin.

The involvement of endorphins in the ovine cardiopulmonary response to endotoxin was evaluated by measuring blood levels of opiate receptor binding substances and administering the opiate receptor blocking agent naloxone prior to and after the administration of lipopolysaccharide. The animals were prepared for chronic study by placement of cardiovascular catheters and cannulation of the lung lymphatic at least 1 wk prior to study. The sheep were given endotoxin (0.75 micrograms/kg) and studied for 6 h. This was accomplished twice in the same animal. Naloxone (2 mg/kg bolus + 2 mg X kg-1 X h-1) was given with one of the two doses of the lipopolysaccharide. The response to endotoxin could be divided into two phases. In phase 1, there was an increase in protein-poor lung lymph and a marked increase in pulmonary artery pressure. In phase 2, the pulmonary lymph flow was elevated but the lymph protein level was higher than in phase 1. The pulmonary artery pressure, however, was near normal. During both phases leukocytes and cardiac output were reduced and the hematocrit was elevated. There was an increase in opiatelike materials in the plasma of these animals, and the response to endotoxin was partially blocked by naloxone. This suggested that endorphin-like materials were involved in the response to endotoxin.

Animals↗
PubMed1983

Staphylococcus aureus protein A induces the production of interferon-alpha in human lymphocytes and interferon-alpha/beta in mouse spleen cells.

Human and mouse lymphocytes produced IFN-alpha and IFN-alpha/beta, respectively, when incubated with highly purified Staphylococcus aureus protein A (SPA). Maximum IFN induction occurred when lymphocytes were incubated with SPA at 250 to 500 micrograms/ml for 24 hr. The SPA induced-IFN were identified by neutralization of antiviral activity with specific antisera. A commercial preparation of SPA was found to induce both HuIFN-alpha and HuIFN-gamma, with the latter comprising over 90% of the antiviral activity. The SPA preparation that induced IFN-gamma was shown by SDS-polyacrylamide gel electrophoresis and an enzyme-linked immunosorbent assay to be contaminated with 5% S. aureus enterotoxin A (SEA), a potent T lymphocyte mitogen and IFN-gamma inducer. Preincubation of the commercial SPA with a specific antiserum to SEA blocked the induction of IFN-gamma and had no effect on IFN-alpha production. SEA is a very potent IFN-gamma inducer, effective at concentrations of 1 ng/ml or less. Thus, very minor contamination of SPA by SEA or other IFN-gamma inducers could be responsible for previous reports that SPA induces IFN-gamma in lymphocytes or that SPA behaves as a T cell mitogen.

Animals↗
PubMed1982

Virus-induced corticosterone in hypophysectomized mice: a possible lymphoid adrenal axis.

Infection of hypophysectomized mice with Newcastle disease virus caused a time-dependent increase in corticosterone and interferon production. Prior treatment with dexamethasone completely inhibited the virus-induced elevation in corticosterone concentration, but did not significantly alter the interferon response. Lymphocytes appear to be the most likely source of an adrenocorticotropin-like substance that is responsible for the increased corticosterone, since spleen cells from the virus-infected, but not from control or dexamethasone-treated, hypophysectomized mice showed positive immunofluorescence with antibody to adrenocorticotropin-(1-13 amide). Thus the adrenocorticotropin-like material and interferon appear to be coordinately induced the differentially controlled products of different genes. These findings strongly suggest the existence of a lymphoid-adrenal axis.

Adrenal Glands↗
PubMed1982

Regulation of the in vitro antibody response by neuroendocrine hormones.

Treatment of lymphocytes with inducers of interferon alpha (IFN-alpha) results in the production of corticotropin (ACTH) and endorphin-like activities. The pro-opiomelanocortin-derived hormones ACTH and alpha-, beta-, and gamma-endorphin and the structurally related hormones [Leu]- and [Met]enkephalin were therefore tested for their effects on the in vitro antibody response of mouse spleen cells. ACTH and alpha-endorphin were potent inhibitors (>/=80% suppression) of the antibody response to the T-cell-dependent antigen sheep erythrocytes at a concentration of 0.5 muM. [Met]- and [Leu]enkephalin were moderate inhibitors (approximately 60% suppression) at 0.2-2 muM, and beta- and gamma-endorphin were minimal inhibitors (approximately 20% suppression) at 5-6 muM. At higher concentrations ACTH also inhibited the antibody response to the T-cell-independent antigen dinitrophenyl-Ficoll, suggesting that T-cell function was more sensitive to blockage by these hormones than was B-cell function. ACTH and IFN had similar suppression properties; thus, the hormone-like activities associated with IFN-alpha may play a role in IFN-induced immunosuppression. alpha-Endorphin immunosuppression was blocked by naloxone, which suggested that alpha-endorphin exerted its effects through binding to opiate-like receptors on the spleen cells. The failure of beta-endorphin to suppress the immune response significantly was not due to its failure to bind to the opiate-like receptors because it blocked alpha-endorphin-induced suppression. Direct evidence for both opiate and ACTH receptors on the spleen cells was obtained in binding studies with labeled enkephalin and ACTH. Such studies revealed the presence of both high- and low-affinity receptors. The data show that neuroendocrine polypeptide hormones can regulate the immune response.

Adrenocorticotropic Hormone↗
PubMed1982

An analysis of cohort mortality from tongue cancer in Japan, England and Wales and the United States.

Alcohol and tobacco consumption were compared to rates of tongue cancer mortality among birth cohorts in Japan, England and Wales, and the United States for the years 1846-1975. During 1931-75 Japan had low and the US had high, stable sex, and age-specific and adjusted mortality. Rates in England and Wales, highest among the three nations, dropped dramatically, showing a classic cohort effect, which coincided with a continual rise in tobacco and a sharp decline in alcohol use since 1900. The US had a similar upsurge in smoking, but comparatively little change in drinking habits. In all countries, the alcohol but not the tobacco patterns were consistent with cohort deaths for not only tongue cancer but also other alcohol-related diseases when a dose-response time lapse was taken into account. In contrast to other studies this research suggests that alcohol may be a carcinogen even in the absence of tobacco.

Adult↗
PubMed1982

Drug recognition by nurses and anaesthetists.

A survey of nurses and anaesthetists in a 500-bed teaching hospital set out to discover how they located a drug container in order to read its label and verify its contents. Members of each group assessed the value of seven factors thought to help in this location and answered questions on personal errors in drug administration. The nurses found the expected position of the drug container in the trolley or cupboard to be the most important factor, followed by the size of the container. The anaesthetists placed the colour of the container as most important, followed by the manufacturer's distinctive container as their second best guide to drug location. This preference for colour and a distinctive container can be used to reduce the chance of confusing drugs locally. A scheme for colour-coding ampoules in broad groups to reduce gross mistakes in the future is presented.

Anesthesiology↗
PubMed1982

Development of a method for detection of human rotavirus in water and sewage.

The simian rotavirus SA11 was used to develop a simple, reliable, and efficient method to concentrate rotavirus from tap water, treated sewage, and raw sewage by absorption to and elution from Filterite fiberglass-epoxy filters. SA11 adsorbed optimally to Filterite filters from water containing 0.5 mM AlCl3 at pH 3.5. Filter-bound virus was eluted with 0.05 M glycine-NaOH supplemented with 10% tryptose phosphate broth at pH 10. SA11 was quantitated by plaque assay, whereas human rotavirus was detected by immunofluorescence. The method was applied to detect rotavirus in raw and treated sewage at two Houston, Tex., sewage treatment plants. The sewage isolates were identified as rotavirus, probably a human strain, based on several criteria. The sewage isolates were detectable by an immunofluorescence test, using anti-SA11 serum which would detect the simian, human bovine, and porcine rotaviruses. No reaction was noted by immunofluorescence with the reoviruses or several common enteroviruses. The sewage isolates were neutralized by convalescent sera from a human adult and infant who had been infected by rotavirus as well as by a hyperimmune serum prepared in guinea pigs against purified human rotavirus. Preimmune or preillness sera did not react with the isolates by neutralization or immunofluorescence. The natural isolates were sensitive to pH 11 and other inactivating agents, similar to SA11. The buoyant density of the sewage isolates in CsCl gradients was 1.36 g/cm3, which is the value usually reported for complete, infectious rotavirus particles. The double-shelled particle diameter was 67.1 +/- 2.4 nm. Finally, electron micrographs of cell lysates inoculated with the sewage isolate showed particles displaying characteristic rotavirus morphology.

Absorption↗
PubMed1981

Perforant path lesion depletes glutamate content of fascia dentata synaptosomes.

Destruction of the hippocampal perforant path fibers reduces the glutamate content of a crude synaptosomal fraction of the rat fascia dentata by about 40%, but does not reduce the aspartate content. This result supports the hypothesis that the perforant path fibers use glutamate as their transmitter. Since a perforant path lesion reduces the glutamate content of dentate homogenates to a much lesser degree, the reduction in synaptosomal glutamate may be offset by an increase in extraterminal glutamate stores. Thus, when evaluating the possible transmitter role of glutamate or aspartate, one can probably gain more definitive information by measuring the glutamate and aspartate content of a synaptosomal preparation than of the target region as a whole.

Animals↗
PubMed1981

Evidence from lesion studies for epileptogenic and non-epileptogenic neurotoxic interactions between kainic acid and excitatory innervation.

The toxicity of kainic acid toward rat hippocampal neurons depends on the presence of specific excitatory afferents. Acute destruction of the critical pathway essentially abolishes the neurotoxicity of intraventricular kainic acid, but some or all hippocampal neurons continue to be destroyed by locally-injected kainic acid until the critical pathway(s) degenerates. These results support the view that kainic acid destroys hippocampal neurons in two ways: (1) by initiating a lethal status epilepticus; and (2) by interacting with certain pathways independently of on-going electrical activity within those pathways.

Afferent Pathways↗