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Biomedical subjects

E Hines

Publications and source records attributed to E Hines.

15 recordsLinked to original sources
PubMed2004

[Raman scattering study of water up to 600 MPa at 290 K].

Raman scattering studies of the stretching band from liquid water have been conducted up to 600 MPa at 290 K. It is shown that (r1)(max) decreases with increasing pressure initially and reaches the minimum at about 200 MPa, and increases at higher pressure up to about 400 MPa, then decreases with increasing pressure up to 600 MPa. And this is also in accordance with the behavior of r(oo) under pressure. The authors conclude that, just like ice phase transition ice ( I h) --> ice(II) --> ice (V), there also probably exists water phase transition water ( I h) --> water (III) --> water (V).

Crystallization↗
PubMed2001

Intrinsic AHR in IL-5 transgenic mice is dependent on CD4(+) cells and CD49d-mediated signaling.

Overexpression of interleukin (IL)-5 by the airway epithelium in mice using the rat CC10 promoter (NJ.1726 line) leads to several histopathologies characteristic of human asthma, including airway hyperreactivity (AHR). We investigated the contribution of B and T cells, as well as CD4 expression, to the development of AHR in IL-5 transgenic mice. NJ.1726 mice on a T cell or CD4 knockout background, but not on a B cell knockout background, lost intrinsic AHR. These effects occurred without decreases in IL-5 or eosinophils. We further investigated the contribution of alpha(4)-integrin signaling to the development of AHR in IL-5 transgenic mice through the administration of anti-CD49d (alpha(4)-integrin) antibody (PS/2). Administration of PS/2 resulted in immediate (16-h) inhibition of AHR. The inhibition of AHR was not associated with a decrease in airway eosinophils. These studies demonstrate that, despite the presence of increased levels of IL-5 and eosinophils in the lungs of NJ.1726 mice, CD4(+) cells and alpha(4)-integrin signaling are necessary for the intrinsic AHR that develops in IL-5 transgenic mice.

Animals↗
PubMed1998

The use of a neural network for studying the relationship between air pollution and asthma-related emergency room visits.

To establish the relationship between air pollution levels and bronchial asthma-associated emergency room (ER) visits, we adapted artificial network technology to conduct this study which focused on three different pollutants, sulphur dioxide, nitrogen oxide and ozone. The study population was comprised of adults presenting to the emergency room of a large metropolitan hospital in Israel during a 3-month period with acute exacerbation of bronchial asthma and who had a past history of intermittent airway disease compatible with bronchial asthma. The range of mean daily pollutants levels for the whole period were: O3 = 15-26 micrograms m-3, NOx = 36-108 micrograms m-3, NO = 16-70 micrograms m-3, and SO2 = 11-32 micrograms m-3. The data sets were composed of input air pollution levels and output ER visits. The first 126 data sets used for the training phase showed that maximal ER visits were mainly associated with the highest cumulative values of air pollution and mostly with nitrogen oxide. In phase two, an attempt was made to predict ER visits based on air pollution level in 49 data sets. The study findings demonstrated that ordinary network technology can be used for learning the effect of air pollution ER visits and, although limited in accuracy, to also predict future ER visits.

Adolescent↗
PubMed1995

The sulfakinins of the blowfly Calliphora vomitoria. Peptide isolation, gene cloning and expression studies.

The nonapeptide, Phe-Asp-Asp-Tyr(SO3)-Gly-His-Met-Arg-Phe-NH2 was isolated from heads of the blowfly Calliphora vomitoria. Designated callisulfakinin I, the peptide is identical to the earlier known drosulfakinin I of Drosophila melanogaster and to neosulfakinin I of Neobellieria bullata. It belongs to the sulfakinin family, all known members of which (from flies, cockroaches and locusts) have the C-terminal heptapeptide sequence Asp-Tyr(SO3)-Gly-His-Met-Arg-Phe-NH2. The callisulfakinin gene of C. vomitoria was cloned and sequenced. In addition to callisulfakinin I, the DNA revealed a coding sequence for the putative tetradecapeptide. Gly-Gly-Glu-Glu-Gln-Phe-Asp-Asp-Tyr-Gly-His- Met-Arg-Phe-NH2, callisulfakinin II. However, this peptide was not identified in the fly head extracts. Confocal laser scanning immunocytochemical studies with antisera raised against the synthetic undecapeptide C-terminal fragment of drosulfakinin II from D. melanogaster, Asp-Gln-Phe-Asp-Asp-Tyr(SO3)- Gly-His-Met-Arg-Phe-NH2, revealed only four pairs of sulfakinin neurones in the brain of C. vomitoria and no others anywhere else in the neural, endocrine or gut tissues. In situ hybridisation studies with a digoxigenin-labelled sulfakinin gene probe (from the blowfly Lucilia cuprina) also revealed only four pairs of neurones in the brain. The perikarya of two pairs of cells are situated medially in the caudo-dorsal region, close to the roots of the ocellar nerve. The other perikarya are slightly more posterior and lateral. Although it has been suggested by several authors that the insect sulfakinins are homologous to the vertebrate peptides gastrin and cholecystokinin, such arguments (based essentially on C-terminal structural similarities) do not take account of important differences in the C-terminal tetrapeptide. His-Met-Arg-Phe-NH2 in the sulfakinins, compared with Trp-Met-Asp-Phe-NH2 in gastrin and cholecystokinin. Furthermore, whereas the sulfakinin neurons of C. vomitoria are small in number and have a very specialised location, a greater number of cells throughout the nervous system react positively to gastrin/cholecystokinin antisera. Chromatographic profiles of the present study also revealed peaks of gastrin/cholecystokinin-immunoreactive material separate from the sulfakinin peptides. This evidence suggests that the insect and vertebrate peptides may not necessarily be homologous.

Amino Acid Sequence↗
PubMed1994

Pathophysiology of failure to wean from mechanical ventilation.

Weaning patients from mechanical ventilation constitutes a major portion of the workload in an intensive care unit, as over 40% of total ventilator time is consumed by the weaning process. Several pathophysiological mechanisms may be responsible for weaning failure, but the precise role of each is incompletely understood. Patients who fail a weaning trial commonly develop hypercapnia, which appears to be due to decreased tidal volume rather than a primary decrease in respiratory drive. Respiratory muscle performance is impaired as a result of dynamic hyperinflation and paradoxic motion of the rib cage and abdomen. Worsening of pulmonary mechanics will cause further embarrassment of the respiratory muscles. However, the clinical importance of respiratory muscle fatigue remains unclear. Afferent stimuli arising in the lung parenchyma, respiratory muscles, or as a consequence of impaired gas exchange will be transmitted to the respiratory control centers and result in severe dyspnea in patients who fail a weaning trial.

Abdomen↗
PubMed1982

Hypercortisolism and insulin resistance: comparative effects of prednisone, hydrocortisone, and dexamethasone on insulin binding of human erythrocytes.

We have studied the effects of 3 days of hydrocortisone (30 mg every 8 h), dexamethasone (1 mg every 8 h), and prednisone (7.5 mg every 8 h) ingestion on glucose intolerance and insulin resistance in three groups of lean normal volunteers and compared these parameters to specific insulin binding in erythrocytes. All three glucocorticoids caused significant reduction of glucose tolerance as assessed by glucose and insulin areas under oral glucose tolerance text curves and insulin sensitivity in response to 0.1 U insulin/kg BW, iv. Although both hydrocortisone and dexamethasone caused significant reduction in insulin binding compared to that during the pretreatment period (11.0 +/- 0.7 vs. 9.0 +/- 0.5% (P less than 0.01) and 11.8 +/- 0.7 vs. 9.0 +/- 0.5% (P less than 0.05), respectively), prednisone ingestion did not significantly alter insulin binding (10.6 +/- 0.6 before vs. 9.4 +/- 0.5% after). Decreased insulin binding with hydrocortisone and dexamethasone was caused by decreased binding affinity rather than by a decreased number of receptors. In two subjects in whom receptor binding was measured daily for 3 days during prednisone (one subject) or hydrocortisone (one subject) ingestion, the inhibition of binding was highest on the first day, with subsequent reduction of this inhibited binding toward normal by the third day. We conclude that although hydrocortisone, dexamethasone, and prednisone all cause deterioration of glucose tolerance and decreased insulin sensitivity, only hydrocortisone and dexamethasone exhibit significant decreases in insulin binding to erythrocytes. This decreased binding is not due to changes in receptor numbers but to decreased affinity brought about by hyperinsulinemia. Prednisone ingestion caused significant insulin resistance with an insignificant decrease in insulin binding. We believe that other mechanisms, such as alteration of postreceptor events, may play a major role in the induction of insulin resistance in hypercortisolism in man.

Adult↗
PubMedDate not supplied

A low-cost computer-assisted teaching package for kidney dialysis: a preliminary report.

This paper describes a low-cost system, comprising software and a video interface unit, for interactive computer-aided learning for renal dialysis. The system is designed for use with IBM PC compatibles. The main aim of the package is to provide a teaching aid, to be used in conjunction with conventional techniques, for teaching the concepts relevant to renal dialysis. The system has been designed to be of benefit to groups such as patients, nurses and renal technicians and is suitable for users who have differing levels of expertise ranging from novice through to expert. The software is also designed to facilitate updating as new techniques and technologies become available.

Computer Systems↗