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Biomedical subjects

J E Phillips

Publications and source records attributed to J E Phillips.

At least 55 records · Page 3Linked to original sources
PubMed1986

Basolateral K channels in an insect epithelium. Channel density, conductance, and block by barium.

K channels in the basolateral membrane of insect hindgut were studied using current fluctuation analysis and microelectrodes. Locust recta were mounted in Ussing-type chambers containing Cl-free saline and cyclic AMP (cAMP). A transepithelial K current was induced by raising serosal [K] under short-circuit conditions. Adding Ba to the mucosal (luminal) side under these conditions had no effect; however, serosal Ba reversibly inhibited the short-circuit current (Isc), increased transepithelial resistance (Rt), and added a Lorentzian component to power density spectra of the Isc. A nonlinear relationship between corner frequency and serosal [Ba] was observed, which suggests that the rate constant for Ba association with basolateral channels increased as [Ba] was elevated. Microelectrode experiments revealed that the basolateral membrane hyperpolarized when Ba was added: this change in membrane potential could explain the nonlinearity of the 2 pi fc vs. [Ba] relationship if external Ba sensed about three-quarters of the basolateral membrane field. Conventional microelectrodes were used to determine the correspondence between transepithelially measured current noise and basolateral membrane conductance fluctuations, and ion-sensitive microelectrodes were used to measure intracellular K activity (acK). From the relationship between the net electrochemical potential for K across the basolateral membrane and the single channel current calculated from noise analysis, we estimate that the conductance of basolateral K channels is approximately 60 pS, and that there are approximately 180 million channels per square centimeter of tissue area.

Animals↗
PubMed1986

Characterization and identification of bovine and ovine Pasteurellaceae isolated from the oral cavity and rumen of apparently normal cattle and sheep.

Reinvestigations of 121 strains previously described as Actinobacillus lignieresii showed that only fifteen strains (12%) had phenotypic characters compatible with A. lignieresii sensu stricto. Four strains were diagnosed as Pasteurella multocida and nine strains as P. haemolytica biogroup 1. The remaining organisms had phenotypic characters compatible with Pasteurellaceae, but could not be classified with accepted species. Fifty-one of the strains investigated had phenotypic characters allowing classification with P. haemolytica biogroups 6 through 9. In addition 19 strains made up at least two new biogroups within the bovine and ovine P. haemolytica complex. Twenty-seven unclassified ovine isolates formed a heterogeneous group provisionally designated taxon 18. At least four biovars were demonstrated within taxon 18. The taxonomic significance of characters separating the P. haemolytica complex and taxon 18 as well as characters separating biogroups within these groups remains to be investigated genetically. The necessity of extended phenotypic characterization within the family Pasteurellaceae Pohl 1981 is underlined by the present findings.

Actinobacillus↗
PubMed1985

Cellular mechanism of HCO-3 and Cl- transport in insect salt gland.

Active HCO-3 secretion in the anterior rectal salt gland of the mosquito larva, Aedes dorsalis, is mediated by a 1:1 Cl-/HCO-3 exchanger. The cellular mechanisms of HCO-3 and Cl- transport are examined using ion- and voltage-sensitive microelectrodes in conjunction with a microperfused preparation which allowed rapid saline changes. Addition of DIDS or acetazolamide to, or removal of CO2 and HCO-3 from, the serosal bath caused large (20 to 50 mV) hyperpolarizations of apical membrane potential (Va) and had little effect on basolateral potential (Vbl). Changes in luminal Cl- concentration altered Va in a rapid, linear manner with a slope of 42.2 mV/decalog a1Cl-. Intracellular Cl- activity was 23.5 mM and was approximately 10 mM lower than that predicted for a passive distribution across the apical membrane. Changes in serosal Cl- concentration had no effect on Vbl, indicating an electrically silent basolateral Cl- exit step. Intracellular pH in anterior rectal cells was 7.67 and the calculated acHCO-3 was 14.4 mM. These results show that under control conditions HCO-3 enters the anterior rectal cell by an active mechanism against an electrochemical gradient of 77.1 mV and exits the cell at the apical membrane down a favorable electrochemical gradient of 27.6 mV. A tentative cellular model is proposed in which Cl- enters the apical membrane of the anterior rectal cells by passive, electrodiffusive movement through a Cl- -selective channel, and HCO-3 exits the cell by an active or passive electrogenic transport mechanism. The electrically silent nature of basolateral Cl- exit and HCO-3 entry, and the effects of serosal addition of the Cl-/HCO-3 exchange inhibitor, DIDS, on JCO2net and transepithelial potential (Vte) suggest strongly that the basolateral membrane is the site of a direct coupling between Cl- and HCO-3 movements.

Aedes↗
PubMed1984

Mechanisms of CO2 transport in rectal salt gland of aedes. I. Ionic requirements of CO2 secretion.

Rectal salt glands of Aedes dorsalis can be successfully isolated and microperfused in vitro. Microperfused salt glands maintain a large, stable transepithelial potential (-40 to -50 mV, lumen negative) and secrete total CO2 at high and stable rates [CO2 net flux ( JCO2net ) = 799 +/- 57 pmol . min-1 . mm-1]. Bilateral Na+ and K+ or serosal Cl- substitutions and serosal addition of 1.0 mM ouabain, 2.0 mM amiloride, or 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid had no effect on JCO2net . Removal of luminal Cl- inhibited JCO2net by 80%, whereas serosal addition of 1.0 mM acetazolamide or 0.5 mM 4,4'-diisothiocyano-2,2'-disulfonic acid inhibited JCO2net by 80 and 40%, respectively. Net Cl- reabsorption ( JClnet = -888 +/- 57 pmol . min-1 . mm-1) was equivalent to total CO2 secretion, suggesting that CO2 transport was mediated by a 1:1 exchange of luminal Cl- for serosal HCO-3.

Aedes↗
PubMed1984

Mechanisms of CO2 transport in rectal salt gland of Aedes. II. Site of Cl(-)-HCO3(-) exchange.

In the previous paper [Am. J. Physiol. 246 (Regulatory Integrative Comp. Physiol. 15): R727 - R734 , 1984] evidence was presented that indicated HCO3(-) transport in the microperfused rectal salt gland of Aedes dorslis larvae is mediated by a 1:1 exchange of luminal Cl(-) for serosal HCO3(-). The present work demonstrates clearly that the anterior segment is the site of Cl(-)HCO3(-) exchange. Changes in total CO2 concentration of collected perfusates are the same in perfused anterior segments as in whole, perfused salt glands. Furthermore Cl(-) reabsorption in the perfused anterior segment is equivalent to total CO2 secretion and is completely inhibited by bilateral CO2 and HCO3(-) removal. Contrary to a previous hypothesis, both salt gland segments are capable of secreting strongly hyperosmotic fluids containing high concentrations of Na+, Cl(-), and HCO3(-)-CO3(2-).

Aedes↗
PubMed1984

On the mechanism of lactate dehydrogenase leakage from normal and D-galactosamine-treated hepatocytes in monolayer culture.

Synthesis, degradation and leakage of lactate dehydrogenase and of total protein was measured using D-galactosamine-treated rat hepatocytes in monolayer culture. The kinetics of [3H]leucine incorporation into trichloroacetic acid-precipitable material and into isolated lactate dehydrogenase of cells and of the extra-cellular space revealed a similar extent of inhibition of both synthesis and leakage following exposure to D-galactosamine. Hepatocyte cultures that had been labeled before D-galactosamine treatment lost intracellular protein-associated radioactivity almost as rapidly as control cells up to the time of measurable enzyme leakage; thereafter, the rate of 3H-loss increased in the treated cells. Lactate dehydrogenase present in the medium is degraded less rapidly than the enzyme in the intracellular space. This explains the apparent increase of total lactate dehydrogenase activity in D-galactosamine-treated as compared to control cultures. Following [3H]leucine addition to D-galactosamine-treated cultures, the specific radioactivity of the leaked lactate dehydrogenase in the medium was never greater than that of the enzyme in the cytosolic compartment. The data rule out a direct excretion of newly synthesized enzyme as a result of D-galactosamine action.

Animals↗
PubMed1983

Mechanism and control of salt absorption in locust rectum.

The rectum is the main reabsorptive site in the excretory system of locusts. The primary urine entering this organ from the Malpighian tubules is rich in K+ (140 mM) and Cl- (90 mM), and most of this fluid is normally reabsorbed. Fluid and active Cl- reabsorption in the rectum are regulated by neuropeptide hormones from the corpus cardiacum. We have studied the mechanism of KCl reabsorption using voltage clamp, tracers, double-barreled ion-sensitive microelectrodes, and ion substitutions. Locust Cl- absorption differs from vertebrate systems in that it is not dependent on Na+ or HCO-3/CO2, and it is insensitive to normal inhibitors of Cl- transport. Entry of Cl- into rectal cells is active, electrogenic, and stimulated by luminal K+. This cation substantially increases the electrochemical gradient across the apical membrane against which Cl- is pumped; therefore K+ does not act solely and indirectly by electrical coupling. Kinetic studies also suggest that K+ activates the Cl- pump. Consequently at least two levels of control are exerted during cAMP stimulation; K+ permeability of the epithelium and the transepithelial potential generated by active Cl- transport both increase. The enhanced net K+ absorption from the lumen side after stimulation is largely passive, being electrically coupled to Cl- transport. However, this general increase in KCl absorption is "fine tuned" by K+ itself, through its direct effect on the Cl- pump.

Animals↗
PubMed1983

Cellular mechanisms and control of KCl absorption in insect hindgut.

The hindgut of the desert locust possesses an unusual chloride transport system. The isolated locust rectum absorbs chloride from the mucosal (lumen) to the serosal (haemolymph) side at a rate which is equal to the short-circuit current (Isc). Net chloride transport (JClnet) persists in nominally Na-free or HCO3(CO2)-free saline, is insensitive to normal inhibitors of NaCl co-transport and anion exchange, and is independent of the net electrochemical gradient for sodium across the apical membrane. However, active chloride transport is strongly dependent on mucosal potassium (Ka = 5.3 mM-K). Chloride entry across the apical membrane is active, whereas the net electrochemical gradient across the apical membrane is active, whereas the net electrochemical gradient across the basal membrane favours passive Cl exit from the cell. Although mucosal potassium directly stimulates 'uphill' chloride entry, there is no evidence for coupled KCl co-transport, nor would co-entry with potassium be advantageous energetically. Net chloride absorption and Isc are stimulated by a peptide hormone from the central nervous system which acts via cyclic-AMP. Cyclic-AMP increases Isc and JClnet approximately 1000% and transepithelial conductance (Gt) approximately 100%. Approximately half of the delta Gt during stimulation results from increased Cl conductance at the basal cell border. This increase is also reflected in a shift of the basal membrane e.m.f. towards the Nernst potential for chloride. The remainder of the cAMP-induced delta Gt is due to an elevation of apical membrane K conductance, which causes a 400% increase in transepithelial potassium permeability as estimated by radiotracer diffusion. Because of this stimulation of K conductance, potassium serves as the principal counterion for active chloride transport under open-circuit conditions. Very high luminal levels of K oppose the stimulatory actions of cAMP on active Cl transport and K conductance. These and other results have been incorporated into a cellular model for KCl absorption across this insect epithelium.

Animals↗
PubMed1982

Electrogenic, K+-dependent chloride transport in locust hindgut.

Potassium chloride is the major salt recycled in most insect secretory systems. Ion and water reabsorption occur in the rectum by active transport of Cl- and largely passive movement of K+. Both these processes are stimulated several fold by a neuropeptide hormone acting via cyclic AMP (cAMP). This Cl- transport process was investigated by using intracellular ion-sensitive microelectrodes, radiotracer flux measurements, voltage clamping, ion substitutions and inhibitors. the mucosal entry step for Cl- is energy-requiring and highly-selective, and is stimulated directly by cAMP and luminal K+. Under some experimental conditions, measured electrochemical potentials for cations across the mucosal membrane are too small to drive C;- entry by NaCl or KCl cotransport mechanisms; moreover, net 36Cl- flux is independent of the apical Na+ potential. Similarly no evidence for a HCO3- -Cl- exchange was obtained. We conclude that Cl- transport in locust gut is different from mechanisms currently proposed for vertebrate tissues.

Animals↗
PubMed1982

Hormonal control of renal functions in insects.

Insect Malpighian tubules secrete an isosmotic, KCl-rich primary urine containing low concentrations of most other blood solutes. Neuropeptide diuretic hormones (DH), possibly related to vasopressin, stimulate tubular fluid secretion by 2- to 200-fold in response to water loading, e.g., feeding. DH acts on tubules through cyclic AMP (cAMP) to stimulate salt transport without measurable change in osmotic permeability. Changes in composition of tubular secretion after stimulation and the possible control of DH release are discussed. Most of the water, ions, and metabolites in tubular secretion are normally reabsorbed by active mechanisms in the rectum, where the urine may finally become either hyposmotic or strongly hyperosmotic to the blood. A newly discovered neuropeptide, chloride transport-stimulating hormone, controls (via cAMP) reabsorption of the principal salt by stimulating K-dependent, electrogenic transport of Cl- across the apical cell border. Passive net absorption of K+ is thereby enhanced. Diuretic and antidiuretic factors may control osmotic permeability of the rectal wall and thereby influence the osmotic concentrations of the rectal absorbate and final urine. The increased recycling of a KCl-rich fluid through the Malpighian tubule-rectal system after feeding probably serves to clear the body of unwanted substances ingested with, and produced by, metabolism of the meal.

Animals↗
PubMed1980

The Rochester plan.

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Education, Medical, Undergraduate↗
PubMed1980

On nonscience premedical education: surprising evidence and a call for clarification.

Critics decrying inadequacies in the training of physicians note a lack of "humanistic" education. This deficiency is cited as the cause of a variety of problems perceived among modern physicians. Yet the content of "humanistic" education is rarely specified, and typically little or no data are presented about what medical students actually study during their premedical years. Proposals for change thus do not have an empirical base and instead derive from observations of "symptoms." The present authors report an analysis of the undergraduate transcripts of 465 students from the University of Rochester who applied to medical school. Results indicate a surprising breadth in undergraduate training which is inconsistent with the claims of narrowness. The authors call upon medical educators for further specification of the desired role of the social sciences and humanities in the undergraduate preparation of future physicians.

Education, Premedical↗