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Biomedical subjects

J A Diez

Publications and source records attributed to J A Diez.

At least 19 recordsLinked to original sources
PubMed2001

Contact line instabilities of thin liquid films.

We present results of fully nonlinear time-dependent simulations of a thin liquid film flowing down an inclined plane. Within the lubrication approximation, and assuming complete wetting, we find that varying the inclination angle considerably modifies the shape of the emerging patterns (fingers versus sawtooth). Our results strongly suggest that the shape of the patterns is not necessarily related to either partial or complete coverage of the substrate, a technologically important feature of the flow. We find quantitative agreement with reported experiments and suggest new ones.

Journal Article↗
PubMed2000

Global models for moving contact lines.

We consider thin film flows driven by surface tension and gravity. Within the framework of the lubrication approximation, we study the contact line motion using global models where either precursor film or slip are allowed. We show that completely wetting films can be simulated under both conditions without requiring direct tracking of the contact line interface. We perform a comparative study of standard and positivity preserving numerical methods for these problems in one space dimension, with the ultimate goal of choosing the best method applicable to two-dimensional problems. We find a considerable computational advantage of the precursor film model over the slipping models.

Journal Article↗
PubMed1999

Synthesis and assembly of connexins in vitro into homomeric and heteromeric functional gap junction hemichannels.

The biogenesis of connexins and their assembly into functional gap junction hemichannels (connexons) was studied with the use of a cell-free transcription/translation system. Velocity sedimentation on sucrose gradients showed that a small proportion of connexin (Cx) 26 and Cx32 that were co-translationally translocated into microsomes were oligomers of Cx26 and Cx32. Chemical cross-linking studies showed that these corresponded to hexameric connexons. Reconstitution of connexons synthesized in vitro into liposomes induced permeability properties consistent with the view that open gap junction hemichannels were produced. By using an immunoprecipitation approach, a simultaneous translation of Cx26 and Cx32 incorporated into microsomes resulted in homomeric connexons. However, supplementation of the translation system in vitro with liver Golgi membranes produced heteromeric connexons constructed of Cx32 and Cx26, and also resulted in an increased oligomerization especially of Cx32. All of the connexins analysed were inserted co-translationally into canine pancreatic microsomal membranes. In addition, Cx26 and Cx43, but not Cx32, were also inserted into microsomal membranes post-translationally. Analysis of various connexin constructs in which the cytoplasmic carboxy tails were transposed, the cytoplasmic tail of Cx43 was truncated or a reporter protein, aequorin, was attached to the C-terminus showed that tail length was not the major determinant of the post-translational membrane insertion of connexins.

Animals↗
PubMed1999

Assembly of heteromeric connexons in guinea-pig liver en route to the Golgi apparatus, plasma membrane and gap junctions.

Guinea-pig liver gap junctions are constructed from approximately equal amounts of connexins 26 and 32. The assembly of these connexins into connexon hemichannels and gap junctions was studied using antibodies specific to each connexin. Intracellular membranes were shown to contain low amounts of connexin 26 relative to connexin 32 in contrast to the equal connexin ratios detected in lateral plasma membranes and gap junctions. Assembly of gap junctions requires oligomerization of connexins into connexons that may be homomeric or heteromeric. Immunoprecipitation using antibodies to connexins 26 and 32 showed that liver gap junctions were heteromeric. A chemical cross-linking procedure showed that connexons solubilized from guinea-pig liver gap junctions were constructed of hexameric assemblies of connexin subunits. The intracellular site of oligomerization of connexins was investigated by velocity sedimentation in sucrose-detergent gradients. Oligomers of connexins 26 and 32 were extensively present in Golgi membranes and oligomeric intermediates, especially of connexin 26, were detected in the endoplasmic reticulum-Golgi intermediate subcellular fraction. Two intracellular trafficking pathways that may account for the delivery of connexin 26 to the plasma membrane and explain the heteromeric nature of liver gap junctions are discussed.

Animals↗
PubMed1990

The need of drainage after cholecystectomy.

In an attempt to rationalize the use of intraperitoneal drainage of the subhepatic space after simple, elective cholecystectomy, a prospective study was designed to compare the post-operative course with and without drainage. There was a higher incidence of postoperative fever of unknown origin and wound infection in the drained group. In the group without drainage the hospital postoperative stay was shorter and there were no complications. The results suggest that routine surgical drainage after uncomplicated cholecystectomy is unnecessary and could be a source of postoperative fever and a higher incidence of wound infection.

Adolescent↗
PubMed1983

Monoaminergic antagonists which block naloxone-induced release of luteinizing hormone bind selectively to hypothalamic opiate receptors.

The possibility that adrenergic receptor antagonists which prevent naloxone-induced release of luteinizing hormone (LH) in vivo exert their action by direct competition with naloxone for hypothalamic opiate receptors was investigated in vitro in immature female rats. First, 26-day-old rats were injected with prazosin, an alpha 1-adrenergic blocker, or yohimbine, an alpha 2-adrenergic blocker, before receiving naloxone (2.5 mg/kg body wt.). Both adrenergic antagonists prevented naloxone-provoked LH secretion in a dose-dependent manner with yohimbine exhibiting a slightly greater potency. In a separate experiment hypothalami from 26-day-old rats were removed, membrane pellets prepared and incubated with [3H]naloxone in the presence of increasing concentrations of naloxone or various monoamine-active substances. Phentolamine, prazosin and yohimbine were the most effective competitors for naloxone binding sites while pronethalol, methysergide and metergoline were far less effective. These findings parallel the relative inhibitory potencies of these compounds in vivo for preventing naloxone-induced LH release as shown here and in a previous report. Clonidine and L-phenylephrine, both alpha-adrenergic agonists, also showed activity in the binding assay. Surprisingly, alpha-methyl-p-tyrosine and 5-hydroxytryptophan, substances which substitute for monoamine precursors early in the biosynthetic pathway, also displaced [3H]naloxone from hypothalamic receptors. These results offer a mechanism for the modulating effects of monoamine-active drugs on opiate antagonist-induced LH release and may have significance for inhibition of LH secretion by endogenous opiates.

Animals↗
PubMed1977

Lack of effect of chronically administered thyrotropin-releasing hormone (TRH) on regional rat brain tyrosine hydroxylase activity.

Chronic treatment of adult male rats with TRH (1 or 10 mg/kg IP) for 5 or 9 days failed to alter the activity of tyrosine hydroxylase (TH), the enzyme regulating the rate-limiting step in catecholamine biosynthesis. In contrast, as previously described, chronic reserpine administration (0.5 mg/kg IP: 9 days) resulted in a significant rise in TH activity in midbrain, hypothalamus, pons-medulla and forebrain. These results suggest that the enhanced brain norepinephrine turnover reported to occur after treatment with TRH is not due to synthesis of new TH enzyme protein.

Animals↗
PubMed1976

Postnatal development of mouse plasma and brain corticosterone levels: new findings contingent upon the use of a competitive protein-binding assay.

A competitive protein-binding (CPB) assay, suitable for measuring corticosterone levels in 20 mul of mouse plasma or 100 mg of brain, is described. The postnatal development of adrenocortical function was determined in C57BL/10 and DBA/1 mice by CPB assay of basal and stressinduced levels of plasma corticosterone and resting levels of brain corticosterone. Marked increases in both basal and stressed levels of plasma corticosterone were found beginning at day 12 after birth: mean basal levels rose from about 1 mug/u99 ml on day 12 to peak values of about 10-15 mug/100 ml on days 18-20, and then declined by day 30 to the 13-day level of 2.6 mug/100 ml. This pattern differs significantly from results obtained with standard fluorometric assays for corticosterone; it was determined that a major part of this discrepancy is due to the lack of specificity of the fluorometric assay. The developmental change in brain corticosterone was similar to the pattern found in plasma. Only the stress-induced levels of plasma corticosterone showed significant genetic variation, and this did not appear until about one week after the end of the relative stress-nonresponsive period. These findings should be useful in evaluating hypotheses concerning the developmental regulation of adrenocortical function and the action of glucocorticoids in regulating the biochemical differentiation of other tissues.

Age Factors↗