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Biomedical subjects

J Pfeilschifter

Publications and source records attributed to J Pfeilschifter.

281 records · Page 16Linked to original sources
PubMed1985

Inflammation-mediated osteopenia in the rat: the effects of artificial granuloma and sham operation on cortical and trabecular bone.

Recent studies have established that generalized loss of trabecular bone occurs in the growing rat following day-to-day inflammatory irritation for a period of 3 wk. We can now demonstrate that there are similar effects on bone in milder but more prolonged chronic inflammation (14 wk). Thus, there were significant decreases in trabecular bone mass as well as in cortical bone after weekly subcutaneous injections or implantations of nonspecific irritants. Osteopenia, induced by a single but extensive inflammatory lesion, remained apparent even 14 wk after induction. This indicates that inflammation-mediated osteopenia is at least incompletely reversible. A less pronounced but similar reduction of cortical and trabecular bone was observed in rats following sham operation. This might be of importance in all animal studies on bone metabolism that include surgical procedures.

Animals↗
PubMed1985

Hypoxia enhances prostaglandin synthesis in renal mesangial cell cultures.

In view of recent findings which suggest that renal prostaglandins mediate the effect of hypoxia on erythropoietin production, we have studied whether hypoxia is a stimulus for in vitro prostaglandin synthesis. Studies were carried out in rat renal mesangial cell cultures which produce erythropoietin in an oxygen-dependent manner. Production rates of PGE2 and in specified samples also of 6-keto-PGF1 alpha, as a measure of PGI2, and PGF2 alpha were determined by radioimmunoassay after incubation at either 20% O2 (normoxic) or 2% O2 (hypoxic) in gas permeable dishes for 24 hrs. Considerable variation in PGE2 production was noted among independent cell lines. PGE2 production appeared to be inversely correlated to the cellular density of the cultures. In addition, PGE2 production was enhanced in hypoxic cell cultures. The mean increase was 50 to 60%. PGF2 alpha and 6-keto-PGF1 alpha increased by about the same rate. These results indicate that hypoxia is a stimulus for in vitro prostaglandin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Role of prostaglandins in hypoxia-stimulated erythropoietin production.

The role of prostaglandins in the mediation of hypoxia-stimulated erythropoietin (Ep) production by cultured rat renal mesangial cells was examined. It was found that an increase in prostaglandin E2 (PGE2) production accompanied the rise in Ep due to hypoxia (2% O2). The hypoxia-stimulated increase in Ep production was abolished in the presence of the cyclooxygenase inhibitor indomethacin (10(-5) M). When PGE2 (10(-6) M was added simultaneously with indomethacin, however, no diminution in hypoxia-stimulated Ep production was observed. Addition of arachidonic acid (AA, 10(-5) M), PGE2 (10(-6) M), or PGI2 (10(-4) M) enhanced Ep production under normoxic conditions (20% O2), while PGF2 alpha (10(-6) M) had no effect on Ep production. AA, PGE2, and PGI2 were found to stimulate adenosine 3',5'-cyclic monophosphate formation by the cultured mesangial cells. Enhancement of adenylate cyclase activity by forskolin (10(-5) M) also increased Ep production in the cell cultures. Our results suggest that hypoxia-stimulated Ep production by cultured mesangial cells is mediated by prostaglandins with subsequent stimulation of adenylate cyclase activity.

Adenylyl Cyclases↗
PubMed1984

Activation of phospholipase C and prostaglandin synthesis by [arginine]vasopressin in cultures.

[Arginine]vasopressin (AVP) stimulates maximal prostaglandin E2 production in cultured rat renal mesangial cells within 2 min. As early as 10s after addition of AVP (10(-6)M) a significant loss of radioactivity from phosphatidylinositol 4,5-bisphosphate but not from phosphatidylinositol 4-phosphate and phosphatidylinositol was observed in cells prelabelled with 32Pi. Cells labelled with [14C]arachidonic acid showed an increase of label in 1,2-diacylglycerol after 15 s and in phosphatidic acid after 30 s upon stimulation with AVP. Pretreatment of the cells with indomethacin (10(-5)M) did not abolish the effect of AVP on the increased labelling of phosphatidic acid.

Animals↗
PubMed1984

Is renin secretion governed by the calcium permeability of the juxtaglomerular cell membrane?

Using cell cultures rich in renal juxtaglomerular cells we found that a change of the intracellular c-AMP concentration is not a prerequisite for an alteration of the renin secretion rate. Modulators of renin secretion including activators of the adenylate cyclase, however, altered the calcium permeability of the cellular plasma membrane in a way that stimulators of renin secretion lowered the calcium permeability and vice versa. Our results suggest that renin secretion is controlled by the intracellular calcium concentration and not by c-AMP. We postulate that modulators of renin secretion act by changing the calcium permeability of the cell membrane.

Angiotensin II↗
PubMed1984

Inflammation-mediated osteopenia in the rat: a new animal model for pathological loss of bone mass.

We have developed a rat model of inflammation-mediated osteopenia. Generalized loss of trabecular bone occurs in the rat after sc injection of nonspecific irritants such as talcum (magnesium silicate) and cotton wool (Cellulose). Although it appears likely that a systemic mediator of bone resorption is responsible for these effects, the loss of bone was not due to increased PTH secretion, since it occurred in parathyroidectomized rats, nor due to excessive 1,25-dihydroxyvitamin-D3 production. In parathyroidectomized rats, this inflammation was associated with significant increase in serum calcium within 4-7 days independent of its cause. Identification and characterization of this mechanism may provide insight into the bone loss associated with chronic inflammatory diseases such as rheumatoid arthritis and periodontal disease.

Animals↗
PubMed1981

[Pretherapeutic metastases diagnosis in bronchial cancer with special reference to nuclear medicine procedures].

In a retrospective study of 280 patients with histologically verified bronchogenic carcinoma, pretherapeutic diagnosis using scanning procedures yielded 13.6% skeletal metastases, 8.6% liver metastases and 3.6% brain metastases. The total 23.9% of hematogenous metastases proved to be dependent on the histological type of tumor: it was highest in small cell anaplastic carcinomas (38.8%) and large cell carcinomas (32.5%), and lowest in epidermoid carcinomas (13.3%). If the localization of metastases was also taken into account, the highest rates of metastases in the skeleton (17.5% and 22.5%) the liver (15%) and the brain (7.5%) were always found with small cell anaplastic and large cell carcinomas. Besides the histopathological type of tumor, the frequency of metastases depended also on the local stage of bronchial cancer. While scanning of the skeleton and the liver for clinical staging of bronchogenic carcinoma should always be regarded as an essential part of primary diagnosis (alternatively ultrasonography and computed tomography of liver) the necessity for brain scan and/or computed tomography depends on the neurological findings and the histomorphological type of tumor.

Bone Neoplasms↗
PubMedDate not supplied

Bone matrix insulin-like growth factor (IGF)-I, IGF-II and transforming growth factor (TGF)-beta1 levels in men and postmenopausal women with osteoporosis: lack of association with circulating growth factors and bone mineral density.

Previous clinical studies have suggested a positive correlation between serum insulin-like growth factor components and bone mass in both men and women with or without osteoporosis. The aim of the present study was to analyze the relationship between the skeletal levels of insulin-like growth factors and transforming growth factor-b1 and bone mineral density in a group of men and postmenopausal women in whom osteoporosis was diagnosed previously. Bone matrix extraction was achieved by passive dialysis against tetrasodium EDTA-guanidine-HCL. IGF's were quantified by radioimmunoassay. TGF-b1 was assessed by a specific enzyme-linked immunoassay. No correlation between BMD and the concentration of IGF-I, IGF-II and TGF-b1 in bone matrix was detected in either men or postmenopausal women with osteoporosis. In addition, circulating growth factors levels failed to be associated with the concentration of IGF-I, IGF-II and TGF-b1 in the skeleton. Thus, our study provides no evidence for a major role of bone matrix IGF's or TGF-b1 as determinants of bone mass in men or postmenopausal women with osteoporosis.

Algorithms↗
PubMedDate not supplied

Immunocharacterization of protein kinase C isoenzymes in rat kidney glomeruli, and cultured glomerular epithelial and mesangial cells.

Protein kinase C (PKC) is a key enzyme in the signalling pathways that regulate glomerular functions. To understand the role of PKC in renal homeostasis, the expression and localization of PKC isoenzymes have been investigated. The isoforms of PKC present in rat kidney glomeruli, primary cultures and cell lines of glomerular epithelial and mesangial cells, were identified by immunoblot analysis with isotype-specific antibodies. Glomeruli were isolated from rat kidney cortex by differential sieving and found to express five PKC isoenzymes, PKC-alpha, -beta, -delta, -epsilon and -zeta. No PKC-gamma isoenzyme was detected. Outgrowth of cells from isolated glomeruli after 5 days in culture, considered to be mainly epithelial in nature, displayed strong immunoreactivity to PKC-alpha, -delta, -epsilon and zeta isoenzymes. No PKC-beta and -gamma isoforms were detectable. Outgrowth from isolated glomeruli after 21 days of culture, considered to be mainly mesangial cells, similarly expressed PKC-alpha, -delta, -epsilon and -zeta isotypes, but not PKC-beta and -gamma isoforms. The PKC isoenzyme content of a stable cell line of rat kidney glomerular parietal epithelial cells was also characterized. We have demonstrated previously that a cloned rat mesangial cell line expresses PKC-alpha, -delta, -epsilon and -zeta isoenzymes. Here we report that a cloned parietal epithelial cell line also expressed PKC-alpha, -delta, -epsilon and -zeta isoforms. No beta- and gamma-isoenzymes of PKC were detected. Subcellular distribution of PKC isotypes displayed clear differences, depending on the cell type and the isoenzyme examined. Phorbol 12-myristate 13-acetate stimulation of PKC caused down-regulation of PKC-alpha, -delta and -epsilon isoenzymes in epithelial and mesangial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗