Biomedical subjects

J Tarara

Publications and source records attributed to J Tarara.

3 recordsLinked to original sources

PubMed2003

A quick, reliable, and automated method for fat cell sizing.

Mean diameters of fat cells from abdominal tissues from 31 volunteers were determined by three methods based on fat cell isolation after collagenase digestion and methylene blue staining. The three methods were direct microscopy (Micro), manual measurement of diameters from digital images by using the public domain NIH Image program (Scion), and automated measurement of diameters from digital images using a customized program developed by Biomedical Imaging Resource at Mayo Clinic (AdCount). There was excellent agreement between the methods' measurement of mean abdominal fat cell diameter (concordance correlation coefficient >0.84). The Scion method gave slightly but systematically lower mean abdominal fat cell diameters than did either AdCount or Micro. The AdCount approach produced results that are comparable to those from Micro. Comparison of AdCount and Micro in measuring diameters of fat cells from thigh confirmed the good comparability between the two methods independent of fat depot. AdCount is very reliable, and the quickest and most objective of the three methods in measuring fat cell diameters from various depots.

Adipocytes↗

PubMed1993

The volatile anesthetic isoflurane attenuates Ca++ mobilization in cultured vascular smooth muscle cells.

Isoflurane is a volatile anesthetic which decreases vascular tone. Experiments were designed to determine whether isoflurane attenuated agonist-induced signaling in cultured vascular smooth muscle cells (A7r5). Cells were preincubated for 15 to 20 min with clinically relevant concentrations of isoflurane--0.5 to 2% in the gas phase and stimulated with 10(-9) or 10(-7) M vasopressin or with 3.3 x 10(-9) M platelet-derived growth factor. The two agonists are believed to act via differing signaling pathways. Total inositol phosphate formation was measured by column chromatography. Apparent intracellular free Ca++ concentration (1) [Ca++]i was estimated using indo-1 and flow cytometry. Isoflurane attenuated increases in [Ca++]i evoked by both agonists. Isoflurane 2.0% inhibited [Ca++]i responses evoked by vasopressin by 35 to 41%. Responses due to Ca++ release from intracellular stores were particularly sensitive to inhibition by isoflurane. The anesthetic attenuated inositol phosphate generation evoked by vasopressin and platelet-derived growth factor, suggesting a mechanism for isoflurane action on Ca++ release. Surprisingly, the anesthetic only modestly inhibited increases in [Ca++]i due to Ca++ entry. Isoflurane's effect on Ca++ influx after emptying of Ca++ stores was probed using thapsigargin. Inhibition of Ca++ influx was modest. It is suggested that isoflurane attenuates total inositol phosphate formation and Ca++ release evoked by vasopressin and platelet-derived growth factor while having limited effects on agonist-induced Ca++ entry.

Animals↗

PubMed1991

Halothane inhibits agonist-induced inositol phosphate and Ca2+ signaling in A7r5 cultured vascular smooth muscle cells.

Halothane, an anesthetic with marked depressant effects on the circulation, was studied for its ability to inhibit inositol phosphate and Ca2+ signaling evoked by the vasoactive hormone arginine vasopressin (AVP) and Ca2+ responses elicited by platelet-derived growth factor and by thapsigargin in cultured A7r5 vascular smooth muscle cells. Changes in apparent [Ca2+]i were measured using the indicator indo-1 and flow cytometry, whereas inositol phosphate levels were determined using myo-[3H]inositol and column chromatography. Preincubation with clinically relevant concentrations of halothane resulted in dose-dependent depression of [Ca2+]i responses evoked on stimulation with AVP. Halothane (2.0%) inhibited the increases in [Ca2+]i by 34-45%. In cells incubated in Ca(2+)-free medium plus 0.5 mM ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, the halothane effect was more marked, with 1.5% halothane inhibiting the responses by approximately 53-61%. However, when Ca2+ influx was stimulated by addition of 5 mM Ca2+ in the continued presence of the agonist, the [Ca2+]i response was inhibited by only 15%, suggesting that release of Ca2+ rather than Ca2+ influx is more sensitive to inhibition by the anesthetic. The effects of halothane on Ca2+ homeostasis are not explained solely by anesthetic-induced depletion of Ca2+ from intracellular stores, because the anesthetic inhibited increases in [Ca2+]i elicited by thapsigargin in cells suspended in Ca(2+)-free medium by only 31%. Halothane inhibited inositol phosphate formation elicited by AVP, suggesting an additional means by which the anesthetic may alter agonist-induced Ca2+ responses. The current results also demonstrate that halothane actions are not specific solely to responses evoked by AVP, which acts via a guanine nucleotide-binding protein-linked signaling pathway, but include responses stimulated by platelet-derived growth factor, an agonist that elevates [Ca2+]i via receptor-latent tyrosine kinase activity. The current results demonstrate that, in vascular smooth muscle cells, halothane alters Ca2+ homeostasis, an action that may underlie the in vivo vasodilator effects of the anesthetic.

Animals↗