Biomedical subjects

A Torbati

Publications and source records attributed to A Torbati.

8 recordsLinked to original sources

PubMed2000

The lactoperoxidase system functions in bacterial clearance of airways.

Airway mucus is a complex mixture of secretory products that provides a multifaceted defense against pulmonary infection. Mucus contains antimicrobial peptides (e.g., defensins) and enzymes (e.g., lysozyme) although the contribution of these to airway sterility has not been tested in vivo. We have previously shown that an enzymatically active, heme-containing peroxidase comprises 1% of the soluble protein in sheep airway secretions, and it has been hypothesized that this airway peroxidase may function as a biocidal system. In this study, we show that sheep airway peroxidase is identical to milk lactoperoxidase (LPO) and that sheep airway secretions contain thiocyanate (SCN(-)) at concentrations necessary and sufficient for a functional peroxidase system that can protect against infection. We also show that airway LPO, like milk LPO, produces the biocidal compound hypothiocyanite (OSCN(-)) in vitro. Finally, we show that in vivo inhibition of airway LPO in sheep leads to a significant decrease in bacterial clearance from the airways. The data suggest that the LPO system is a major contributor to airway defenses. This discovery may have significant implications for chronic airway colonization seen in respiratory diseases such as cystic fibrosis.

Amino Acid Sequence↗

PubMed1998

Retrievable cemented implant restorations.

Prostheses can be attached to implants or implant abutments by screw retention, cementation, or with the use of set-screws. The indications for non-screw-retained restorations are discussed with respect to implant body position and surgical limitations for implant placement. The advantages and disadvantages of each method are outlined. A technique that uses a screw threaded into the implant restoration to displace the cemented restoration is presented. Use of this technique will allow predictable removal of the cemented restorations without damage to the prosthesis or abutment.

Cementation↗

PubMed1994

Differentiation of intrahepatic membrane-bound and secretory apolipoprotein B by monoclonal antibodies: membrane-bound apolipoprotein B is more glycosylated.

Most apolipoprotein B (apoB) in rat hepatocytes membrane is membrane-bound. The purpose of this study was to determine whether differences existed between membrane-bound and plasma apolipoprotein B, which could be detected using monoclonal antibodies. Detergent-solubilized microsomal membrane-bound apoB was probed with two previously characterized monoclonal antibodies (LRB 200, LRB 220) and compared to a monospecific polyclonal antibody. LRB 200 (capable of binding 71% of plasma apoB) was able to recognize less than 20% of microsomal apoB compared to LRB 220 (a pan-apoB monoclonal antibody capable of binding 100% plasma apoB). To test the hypothesis that the immunologic difference detected by the monoclonal antibodies was due to increased glycosylation of the membrane-bound apolipoprotein B, plasma lipoproteins were incubated with neuraminidase. A progressive increase was found in antibody binding by LRB 200 but not by LRB 220 or the polyclonal antibodies. Inhibition of N-glycosylation by tunicamycin also increased the binding of monoclonal antibody LRB 200 to hepatocyte apoB. Inhibition of trimming of N-linked sugar by incubating hepatocytes with the inhibitors of glucosidase I and mannosidase I eliminated antibody binding by LRB 200 but not by LRB 220 or the polyclonal antibody. When N-linked sugars were removed by peptide: N-glycosidase F, antibody binding by monoclonal antibody LRB 200 was increased. Double-labeling experiments using 3H-mannose and 35S-methionine showed that cellular apoB contained twice the amount of mannose as medium apoB. These data suggest that membrane-bound apoB is more glycosylated than plasma lipoprotein apoB.

Amidohydrolases↗

PubMed1991

Human T-cell leukemia virus (HTLV) type II Rex protein binds specifically to RNA sequences of the HTLV long terminal repeat but poorly to the human immunodeficiency virus type 1 Rev-responsive element.

The human T-cell leukemia viruses (HTLVs) encode a trans-regulatory protein, Rex, which differentially regulates viral gene expression by controlling the cytoplasmic accumulation of viral mRNAs. Because of insufficient amounts of purified protein, biochemical characterization of Rex activity has not previously been performed. Here, utilizing the baculovirus expression system, we purified HTLV type II (HTLV-II) Rex from the cytoplasmic fraction of recombinant baculovirus-infected insect cells by heparin-agarose chromatography. We directly demonstrated that Rex specifically bound HTLV-II 5' long terminal repeat RNA in both gel mobility shift and immunobinding assays. Sequences sufficient for Rex binding were localized to the R-U5 region of the HTLV-II 5' long terminal repeat and correlate with the region required for Rex function. The human immunodeficiency virus type 1 (HIV-1), has an analogous regulatory protein, Rev, which directly binds to and mediates its action through the Rev-responsive element located within the HIV-1 env gene. We demonstrated that HTLV-II Rex rescued an HIV-1JR-CSF Rev-deficient mutant, although inefficiently. This result is consistent with a weak binding activity to the HIV-1 Rev-responsive element under conditions in which it efficiently bound the HTLV-II long terminal repeat RNA.

Animals↗

PubMed1990

Stimulation of the phosphorylation of uridine in skeletal muscle by insulin and vanadate.

The action of insulin and sodium vanadate on the phosphorylation of uridine by skeletal muscle was studied in vitro. Insulin significantly increased the incorporation of 3H-uridine into uracil nucleotides by pieces of rat diaphragm incubated for 15 min in a phosphate-buffered medium. This action of the hormone was exceptionally consistent when MgATP was added to the incubation medium. In experiments in which pieces of psoas muscle were incubated in TRIS buffer in the presence and absence of insulin, the hormone caused a significant activation of uridine kinase measured in cytosolic extracts of the incubated tissue. In experiments with rat diaphragm similar to those with insulin, the vanadate ion caused a significant increase in phosphorylation of uridine. The results of these experiments provide preliminary support for the proposal that uracil nucleotide metabolism is regulated by insulin and that insulin activates uridine kinase, the limiting enzyme in the synthesis of uracil nucleotides from uridine by the salvage pathway.

Animals↗

PubMed1986

Blood glucose as a predictive measure for central nervous system oxygen toxicity in conscious rats.

Blood glucose concentration was measured during continuous electrocorticographic (ECoG) recording in conscious rats exposed to 3 and 5 atmosphere absolute oxygen (ATA O2). The preconvulsive oxygen-induced ECoG changes included increased slow wave activity in delta range, followed by the appearance of successive paroxysmal electrical discharges. A correlation between increases in blood glucose concentration and ECoG changes was observed at both 3 and 5 ATA O2. No significant changes in blood glucose concentration were found in the absence of the ECoG changes. Equivalent periods of exposure to N2-O2 normoxic pressures of 1, 3, and 5 ATA did not produce changes either in ECoG or blood glucose concentration. It is therefore considered possible that an increase in blood glucose concentration may be a useful predictive measure of the ECoG manifestations of oxygen toxicity in conscious unrestrained rats. The possible mechanisms for increase in blood glucose concentration during development of brain oxygen toxicity are discussed.

Animals↗

PubMed1986

Metabolic effects of acarbose in normal and diabetic rats: long- and short-term administration.

The effects of acarbose administration to normal and streptozotocin-diabetic rats were studied in animals given the drug for 3 or 21 days. The acarbose was incorporated into control diets or diets fortified with sucrose and starch. After extirpating the hearts, they were perfused by the Langendorff procedure and ventricular rate and isometric force of contraction were recorded in the presence or absence of isoproterenol. Frozen samples of heart and liver were used for metabolic measurements. At a low dose of isoproterenol (0.01 microgram) the positive inotropic response was the same in control and diabetic animals. With a higher dose of the amine (0.1 microgram) the contractile response was increased further in hearts from normal animals but not enhanced in hearts from diabetic rats. Cardiac phosphorylase activation by isoproterenol was accentuated by diabetes only when the smaller dose of the amine was given. The markedly elevated heart glycogen content of diabetic rats was decreased in response to a high carbohydrate diet. Inclusion of acarbose in the diet prevented this diminution in cardiac glycogen. In normal and diabetic rats fed the high carbohydrate diet for 3 weeks, liver glycogen was elevated. The increase in hepatic glycogen was not observed when acarbose was present in the diet. A comparison of the results of the short- and long term-administration of acarbose show that the onset of action of the drug is prompt and that the effect of the treatment is undiminished over an extended period of time.

Acarbose↗

PubMed1984

Metabolic effects of acarbose administration in normal and diabetic rats.

The effect of acarbose on cardiac and hepatic metabolism was investigated in normal and diabetic rats. Groups of rats were fed one of the three following diets for 7 days: (1) ground Purina chow, (2) ground Purina chow fortified with raw corn starch and sucrose, and (3) the above high carbohydrate diet, with added acarbose (40 mg/100 g food). At the end of the dietary period the rats were decapitated, and a sample of liver tissue was removed and frozen in liquid nitrogen. The heart was extirpated for subsequent perfusion by the Langendorff technique. Increases in liver and heart glycogen produced by the high carbohydrate diet in the normal rats were prevented completely when acarbose was incorporated into the food. In diabetic animals, liver glycogen was uniformly lower than normal, irrespective of the diet or the presence of acarbose. With animals fed the control diet, cardiac glycogen was higher in diabetic than in normal rats. The high carbohydrate diet caused a lowering of heart glycogen in diabetic rats and this reduction in glycogen content was reversed by including acarbose in the diet. Effects of isoproterenol on myocardial phosphorylase a activity were determined in hearts from normal and diabetic rats given one of the three diets. The high carbohydrate diet decreased the enzymatic response to the catecholamine in hearts from both normal and diabetic animals, and this phenomenon was prevented by the presence of acarbose in the diet. In diabetic rats fed any of the three diets, the activation of cardiac phosphorylase by isoproterenol was greatly accentuated. Measurements of heart uridine kinase showed that the activity of this enzyme was lower than normal in hearts from diabetic rats given either the control or the high carbohydrate diet. The presence of acarbose in the latter diet resulted in a significant decrease in cardiac uridine kinase activity in hearts from normal rats. The results of this study demonstrate the effectiveness of acarbose in modulating tissue metabolism in normal and diabetic animals.

Acarbose↗