No abstract

We report associations between IAP and the serum adenosine and IL-10 levels providing new tools for the laboratory monitoring of IAH as well as further understanding of the pathomechanisms contributing to ACS.

No abstract

No abstract

No abstract

In the present study the signal transduction of the formyl-Met-Leu-Phe receptor was studied in granulocytes obtained from control subjects and patients with elevated low density lipoprotein levels. According to our results, 10 n M formyl-Met-Leu-Phe in control cells activates phospholipase C inducing a pronounced inositol phosphate production followed by a Ca 2 ؉ signal from intracellular pools. The pertussis toxin-sensitive O 2 ؊ generation and leukotriene synthesis were moderate. In contrast, in granulocytes from hypercholesterolemic patients, formyl-Met-Leu-Phe triggered an intensive pertussis toxin-insensitive oxidative burst and leukotriene synthesis. The inositol trisphosphate and Ca 2 ؉ signals were decreased significantly in granulocytes of hypercholesterolemic patients and seem to be dependent on the extracellular Ca 2 ؉ content. Furthermore, in the resting granulocytes of hypercholesterolemic patients the [Ca 2 ؉ ]i and the membrane-bound protein kinase C activity were higher than in controls, the time of normalization after the low Ca 2 ؉ signal was delayed, while the membrane fluidity was decreased. Our results suggest that in these ex vivo experiments, the high level of circulating low density lipoprotein in patients can affect the membrane composition of granulocytes leading to altered signal transduction by the formyl-Met-Leu-Phe receptor, to altered Ca 2 ؉ pump-activity, and protein kinase C translocation. -

Catecholamines are important elements of neuroendocrine regulation, and their concentrations in dental pulp are of interest. Two groups of teeth were used in this study: (i) healthy teeth and (ii) periodontally diseased teeth. After the processing of dental pulp obtained from the extracted teeth, the samples were analyzed in a computer-controlled Merck-Hitachi HPLC system at 280 nm wavelength. The external and internal standard methods of the HPLC Manager Program were used for validation. In healthy teeth the norepinephrine level of dental pulp was 4.86 +/- 0.96 micrograms/g, whereas the epinephrine level was 8.1 +/- 1.18 micrograms/g. In periodontally diseased teeth norepinephrine and epinephrine levels were significantly higher (p < 0.01) at 13.98 +/- 21.13 micrograms/g and 1.42 +/- 0.32 micrograms/g, respectively. Dopamine could not be demonstrated in 87% of the pulps. Summing up we succeeded in demonstrating norepinephrine and epinephrine in human pulp, but in most cases we could not demonstrate dopamine. Further investigations are needed on pulp tissue infected because of caries.

Objective: We compared different signal transduction pathways through thyroid stimulating hormone receptor (TSH-R) in porcine thyroid cells (PTC) following stimulation with thyroid stimulating hormone (TSH) and 11 thyroid stimulating immunoglobulin samples (TSI) obtained from patients with Graves' disease. Design: Following stimulation with TSI, the level of inositol trisphosphate (IP 3 ) and [Ca 2þ ] i , as well as the membrane bound protein kinase C (PKC) activity and the intensity of the arachidonic acid (AA) cascade, were determined in PTC.Results: Seven out of eleven TSI samples activated PTC through IP 3 generation, elevated [Ca 2þ ] i from the intracellular pools, exhibited verapamil-insensitive membrane-bound PKC activation, and enhanced release of [ 14 C]AA derivates (however, one of the samples was also able to take up Ca 2þ from the extracellular space). Four out of eleven TSI samples did not activate the phospholipase C (PLC) system in which case the Ca 2þ signal occurred only in the presence of extracellular Ca 2þ , the membrane bound PKC activation was verapamil sensitive, and in two of these four TSI samples, the AA release was extremely high. Conclusions:The simultaneous examination of the majority of the known signal pathways using TSI samples showed that TSI samples from different patients activate thyroid cells through different pathways. Their effects differ from that of TSH and, to a certain extent, from each other. The results give a certain new insight into the intracellular mechanisms exerted by TSI.