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Biomedical subjects

S Borst

Publications and source records attributed to S Borst.

6 recordsLinked to original sources
PubMed2001

Influence of dialysis modalities on serum AGE levels in end-stage renal disease patients.

BACKGROUND: The accumulation of advanced glycation end-products (AGEs) in end-stage renal disease (ESRD) influenced by dialysis modalities is of current interest. Highly permeable membranes in haemodialysis or haemofiltration should be able to eliminate circulating AGEs as well as their AGE precursors more efficiently. METHODS: In our study, 10 non-diabetic and 10 diabetic ESRD patients were on haemodialysis with low-flux membranes (LF) followed by a cross-over haemodialysis with high-flux or super-flux polysulfone membranes (HF, SF) for 6 months each. We measured the protein-bound pentosidine and free pentosidine serum levels by high-performance liquid chromatography (HPLC) as well as the serum AGE peptide, AGE-beta(2)-microglobulin and beta(2)-microglobulin concentrations, using ELISA assays. RESULTS: All parameters investigated were significantly higher in dialysis patients than in healthy subjects. The reduction rates during a single dialysis session were found to be higher using the SF than those obtained with the HF (free pentosidine 82.4+/-7.3 vs 76.6+/- 8.7%; AGE peptides 79.7+/-7.7 vs 62.3+/-14.7%; AGE-beta(2)-microglobulin 64.0+/-16.5 vs 45.4+/-17.7%; beta(2)-microglobulin 70.5+/-5.6 vs 58.2+/-6.0%). The protein-bound pentosidine levels remained constant over the respective dialysis sessions. In the 6-month treatment period with the SF, decreased pre-dialysis serum levels of protein-bound pentosidine, free pentosidine and AGE peptides were observed in non-diabetics and diabetics as compared with values obtained with the LF. The respective pre-dialysis AGE-beta(2)-microglobulin concentrations decreased insignificantly, whereas those of beta(2)-microglobulin were significantly lower. Using the HF dialyser, only moderate changes of the parameters measured were noted. CONCLUSION: Treatment with the biocompatible polysulfone SF dialyser seems to be better suited to lower serum AGE levels and to eliminate their precursors.

Adult↗
PubMed1994

Thermoregulation with age: role of thermogenesis and uncoupling protein expression in brown adipose tissue.

To investigate whether attenuation of thermogenesis in interscapular brown adipose tissue (IBAT) may account for the loss of thermoregulation with age, we examined two indices of thermogenesis after two types of cold exposure: one in which the senescent rats maintained homeothermy and the other in which the senescent rats became hypothermic. To this end, we assessed body temperature, guanosine 5'-diphosphate (GDP) binding to the IBAT mitochondrial uncoupling protein (UCP) and the induction of UCP mRNA after both 1-hr and 48-hr mild cold exposures at 8 degrees C and after a more severe, 1-hr cold exposure at 4 degrees C in 3- and 24-month-old F-344 rats. Thermoneutrality was determined to occur at an ambient temperature of 26 degrees C in rats of both ages. In the 1-hr mild cold-exposed rats, there was no significant increase in GDP binding to IBAT UCP. However, after 48 hr of mild cold exposure, there was a 3-fold increase in GDP binding and a 5-fold increase in the expression of UCP mRNA despite no hypothermia in either the young or old rats. During the more severe cold exposure, the senescent rats, but not the young rats, became hypothermic. GDP binding to UCP increased 75% following cold exposure and, surprisingly was the same in young and old rats. UCP transcripts did not increase during the 1-hr cold exposure. These data, coupled with our previous findings of diminished beta 3-agonist-stimulated IBAT thermogenesis, suggest that (i) IBAT thermogenesis, at least in the senescent rats, may be mediated by other than beta 3-adrenergic receptors, and (ii) that altered heat dissipation or impaired thermogenesis at some site other than interscapular BAT is responsible for the observed hypothermia.

Adaptation, Physiological↗
PubMed1988

Calcium dependence of beta-adrenoceptor mediated cyclic AMP accumulation in human lymphocytes.

In intact human lymphocytes, cyclic AMP accumulation in response to isoproterenol was inhibited by 5 mM EDTA, by deletion of calcium ions from the medium and by 1 mM lanthanum chloride, but not by 1 microM verapamil or by 10 microM nifedipine. A23187 caused a modest increase in cyclic AMP content. Exposure of lymphocytes to 5 microM 1-isoproterenol desensitized the cells to subsequent beta-adrenergic stimulation, reducing cyclic AMP accumulation. With higher concentrations of 1-isoproterenol (50 microM), receptor density was reduced as well. None of the above agents attenuated losses in agonist-stimulated cyclic AMP accumulation induced by treatment with 5 microM isoproterenol for 90 min. These data suggest that calcium ions, both those present in the extracellular medium and those bound to the plasma membrane, are required for isoproterenol-stimulation of adenylate cyclase. In addition, it appears that neither the presence of extracellular calcium ions nor full activation of adenylate cyclase are required for desensitization.

1-Methyl-3-isobutylxanthine↗
PubMed1987

The effects of tetramethylpyrazine on the human platelet alpha 2 adrenergic receptor adenylate cyclase system.

The binding properties of tetramethylpyrazine (TMPZ), a commonly used cardiovascular drug in China, to alpha 2 adrenergic receptors in human platelets were investigated. Increasing concentrations of TMPZ inhibited [3H]-yohimbine binding in intact platelets. The displacement curve was parallel to those of clonidine and yohimbine, with a Ki of 7.7 X 10(-5) M and an IC50 of 1.2 X 10(-4) M. In platelet membranes, increasing concentrations of TMPZ shifted the saturation binding curves of [3H]-yohimbine to the right and caused the dissociation constant (KD) to increase gradually. Higher concentrations of [3H]-yohimbine overcame the inhibition of TMPZ. Furthermore, in platelet cyclic AMP generation experiments, higher concentrations of TMPZ (10(-4)M-10(-6)M) inhibited the cyclic AMP increases induced by 10(-5) M PGE1. However, in the presence of an alpha 2 adrenergic receptor agonist (L-epinephrine), TMPZ blocked the inhibitory effect of L-epinephrine on cyclic AMP increases induced by PGE1. These properties suggested that TMPZ is an alpha 2 adrenergic receptor partial agonist. These effects may provide potential mechanisms for the cardiovascular actions of TMPZ.

Adenylyl Cyclase Inhibitors↗