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Biomedical subjects

M Siebels

Publications and source records attributed to M Siebels.

29 records · Page 2Linked to original sources
PubMed1995

[Panarteritis nodosa with kidney and spleen rupture: diagnostic and therapeutic possibilities].

Classic polyarteritis nodosa is a necrotizing vasculitis affecting medium- and small-sized arteries. Renal involvement from aneurysm formation is common and can result in perirenal or intrarenal bleeding. The gold standard of diagnostic procedures is the arteriography. Treatment of choice is a combination of steroids and cyclophosphamide, but in the case of severe hemorrhage surgery is mandatory. Patients with PAN need at least 2 years of long-term therapy; repeated arteriography will establish the efficacy of therapy.

Adult↗
PubMed1995

CD80-transfected human breast and ovarian tumor cell lines: improved immunogenicity and induction of cytolytic CD8+ T lymphocytes.

Human tumor cell lines derived from breast and ovarian carcinomas have been found to be ineffective in stimulating the induction phase of an immune response such as T cell proliferation in allogeneic mixed tumor cell lymphocyte cultures. Since representative tumor cell lines are effectively lysed by activated T lymphocytes, the induction of an effector phase is not impaired. In order to reconstitute the potential to induce primary T cell activation, we transfected CD80 into a breast (KS) and an ovarian carcinoma (GG) cell line. CD80 expression in KS cells resulted in improved primary T cell activation, whereas it was ineffective in the case of GG cells. However, treatment of CD80-transfected GG cells with INF-gamma rendered them immunogenic, and resulted in T cell proliferation. Likewise, TNF-alpha and/or INF-gamma augmented T cell proliferation induced by CD80-transfected KS cells. Furthermore, T lymphocytes stimulated with cytokine-treated CD80+ KS cells gave rise to a long term proliferating CD8+ CTL line with class I MHC restricted cytolytic antitumor activity. These studies emphasize the requirement for costimulation in generating tumor-specific immunity, and demonstrate the efficacy of CD80 in generating CD8+ cytolytic T lymphocytes.

Antigens, CD↗
PubMed1994

Renal involvement in type II diabetes.

The incidence and prevalence of renal failure from type II diabetes have been seriously underestimated in the past. Currently, the incidence of uremia in patients with type II diabetes has increased continuously in Europe and the United States, mainly because of better patient survival (ie, they now live until nephropathy develops) and possibly because of a rising prevalence of type II diabetes in the general population (ie, more patients are at risk of developing nephropathy). Generally, renal hemodynamics and glomerular lesions are similar in type I and type II diabetes, but glomerular histology is more diverse in type II diabetes. Given the high prevalence of diabetes and renal failure from various causes in the elderly, coexistence of the two (even in the absence of glomerulosclerosis) occurs in approximately 20% of uremic type II diabetic patients. The development of nephropathy is controlled by strong genetic determinants, but these have not been further characterized.

Animals↗
PubMed1993

Pathophysiology of hypertensive renal damage.

The kidney may contribute to and be damaged by hypertension. Evidence from studies of renal transplant recipients and familial studies suggests a genetic component for the occurrence of hypertension and nephrosclerosis. Glomerular injury may result from glomerular hypertension caused by loss of autoregulation and afferent renal vasodilatation. Glomerular injury may be mediated by injury to endothelial cells, which, having lost their thromboresistance, may initiate intravascular coagulation and alter the balance between endothelin and endothelium-derived relaxing factor. Increased transit of protein-laden fluid into the mesangial space also may mediate hypertensive nephrosclerosis. Several studies have provided encouraging evidence that antihypertensive therapy, particularly with angiotensin-converting enzyme inhibitors or calcium antagonists, can slow the progression of renal damage.

Animals↗
PubMed1993

[Silicosis and systemic diseases].

We present case histories of 5 patients with silicosis who developed systemic lupus erythematosus and microscopic polyarteritis in two cases each, and rapidly progressive glomerulonephritis (limited Wegener's granulomatosis) in one case. An association between silica exposure and autoimmune disease is emphasized.

Aged↗
PubMed1992

Dose dependent suppression of mineralocorticoid metabolism by different heparin fractions.

One neglected side effect of heparin therapy is the inhibition of adrenal aldosterone production leading to occasionally life-threatening hyperkalaemia. This is only reported with (therapeutic) high doses (greater than or equal to 20.000 IU). The complex interplay of mineralocorticoid metabolites was studied in 29 subjects with unfractionated (UFH) and low molecular weight heparin (LMWH). Both heparins altered mineralocorticoid metabolism in a dose dependent manner. Whereas no effect was observed with UFH 2 x 5000 IU sc/day or LMWH 2500 a FXa U sc/day, higher doses significantly suppressed aldosterone and 18-hydroxycorticosterone production in plasma and urine. Three out of seven patients receiving UFH 3 x 7500 IU sc/day developed hyperkalaemia. This study shows the threshold dosage of UFH leading to suppression of mineralocorticoid metabolism in man and provides information that LMWH as well as UFH can suppress mineralocorticoid production. With respect to therapeutic implications it is important that LMWH at 2500 a FXa U sc/d had no effect on mineralocorticoid metabolism in contrast to UFH at a dosage currently used for prevention of thromboembolism (3 x 5000 IU sc/d).

Adult↗