Biomedical subjects

J A Higgins

Publications and source records attributed to J A Higgins.

131 records · Page 8Linked to original sources

PubMed1967

Fluid transfer in the everted human gallbladder.

The rates of fluid transfer across human gallbladders obtained at cholecystectomy for cholelithiasis were determined by the measurement of weight changes of everted preparations under controlled conditions. Active transport of fluid from the mucosal to the serosal surface was indicated since weight gain occurred with the same solution on both sides of the membrane and against hydrostatic, osmotic, and potential differences. With respect to sodium, the fluid transferred was isotonic to the bathing solutions. Metabolic inhibitors and temperature extremes inhibited weight gain. In addition, muscle contractions in this in vitro preparation were related to the rates and direction of fluid movement. Cholecystokinin increased muscle activity and caused weight loss in preparations that previously had gained weight. Norepinephrine caused weight gain or increased weight gain in all preparations tested. The direction of net fluid movement in the isolated everted human gallbladder was determined by the opposing forces of active mucosal transport and a filtration pressure generated by muscle contractions.

Biological Transport, Active↗

PubMed1967

Forces involved in chylomicron binding by isolated cells of rat liver.

The binding of chylomicrons by isolated liver cells has been found to decrease as temperature increases. It is greatest at the isoelectric point of the chylomicrons; although it occurs both above and below this pH, it decreases most rapidly as the pH is increased. Urea, guanidine hydrochloride, dimethylsulfoxide, dioxane, and sodium chloride at concentrations known to disrupt bonding in proteins have no effect on the removal (by centrifugation) of chylomicrons bound to liver cells. The binding is reduced by treatment of chylomicrons with phospholipase D or by addition of chylomicron "membrane" fraction, lecithin micelles, or lecithin-triglyceride-cholesterol micelles. This evidence implicates phospholipids in the binding. Treatment of liver cells with neuraminidase increases binding of chylomicrons but not the extent of lipolysis that accompanies the binding. Removal of divalent cations from the system with EDTA results in a rise both in chylomicron binding and lipolysis. It is suggested that the binding sites are accessible to the lipase that is responsible for hydrolysis.

Animals↗

PubMed1966

The uptake of lipids by rat liver cells.

1. Unesterified cholesterol, cholesterol esters and triglycerides of chylomicrons were taken up at the same rate by isolated hepatic parenchymal cells. 2. On incubation of hepatic cells, isolated 2min. after the injection of chylomicrons in vivo, the chylomicron triglyceride associated with the cells underwent hydrolysis. 3. In cells isolated 5min. after the injection of chylomicrons, the chylomicron triglyceride bound to the hepatic cells was accessible to added clearing factor lipase. 4. ;Ghost' hepatic cells had the same binding capacity and lipolytic activity per cell as intact cells. 5. Of all subcellular fractions studied, the ;plasma membrane' fraction showed the greatest capacity per unit weight for non-esterified fatty acid and chylomicron triglyceride binding and for triglyceride hydrolysis. 6. Once non-esterified fatty acids entered the hepatic cell, they were apparently metabolized in the same manner, whether taken up from the circulation as such or derived from chylomicron triglyceride.

Animals↗

PubMedDate not supplied

Flea-borne rickettsioses: ecologic considerations.

Ecologic and economic factors, as well as changes in human behavior, have resulted in the emergence of new and the reemergence of existing but forgotten infectious diseases during the past 20 years. Flea-borne disease organisms (e.g., Yersinia pestis, Rickettsia typhi, R. felis, and Bartonella henselae) are widely distributed throughout the world in endemic-disease foci, where components of the enzootic cycle are present. However, flea-borne diseases could reemerge in epidemic form because of changes in vector-host ecology due to environmental and human behavior modification. The changing ecology of murine typhus in southern California and Texas over the past 30 years is a good example of urban and suburban expansion affecting infectious disease outbreaks. In these areas, the classic rat-flea-rat cycle of R. typhi has been replaced by a peridomestic animal cycle involving, e.g., free-ranging cats, dogs, and opossums and their fleas. In addition to the vector-host components of the murine typhus cycle, we have uncovered a second typhuslike rickettsia, R. felis. This agent was identified from the blood of a hospitalized febrile patient and from opossums and their fleas. We reviewed the ecology of R. typhi and R. felis and present recent data relevant to the vector biology, immunology, and molecular characterization and phylogeny of flea-borne rickettsioses.

Animals↗

PubMedDate not supplied

Regulation of the assembly and secretion of very low density lipoproteins by the liver.

Recent studies have suggested that there are three sites at which VLDL secretion by the liver may be controlled: (i) Newly synthesised apo-B either remains associated with the RER membrane and is degraded by the ubiquitin/proteasome system, or is translocated into the lumen and incorporated into lipid poor VLDL precursors; (ii) the lumenal apo-B is either degraded or moves on, and (iii) acquires the remaining VLDL lipids in the SER/cis-Golgi. Newly synthesised apo-B, at the cytosolic side of the RER, is stabilised and protected from degradation by the chaperone protein, hsp-70. Triacylglycerol, cholesterol ester and phospholipids have all been implicated in the translocation of apo-B and microsomal triglyceride protein plays a major role. If translocation does not occur then the apo-B is degraded. Dietary fish-oils, but not sunflower oil, inhibit movement of apo-B containing precursors from the RER and their assembly with lipids and target lumenal apo-B to degradation. This effect is reversed by inhibition of lumenal proteolysis, but not by inhibition of cytosolic proteolysis. Therefore lumenal degradation of apo-B and secretion appear to be in balance, so that if assembly of VLDL precursors is slowed, then degradation becomes predominant. If however, degradation is inhibited then VLDL assembly can proceed. These observations suggest that movement of VLDL precursors from the RER lumen to the second stage of assembly may be a further regulated step.

Animals↗