Biomedical subjects

T Mauerhoff

Publications and source records attributed to T Mauerhoff.

6 recordsLinked to original sources

PubMed1991

De novo HLA class II and enhanced HLA class I molecule expression in SV40 transfected human thyroid epithelial cells.

Human thyroid follicular cells normally synthesize and express HLA Class I molecules but in glands affected by autoimmune or neoplastic diseases they express Class II molecules. We have investigated the effect of SV40 virus transformation on the expression of MHC molecules in human thyrocytes. Primary cultures of human thyroid from two different glands were transfected with the plasmid pX-8, containing the 'early' region of SV40 virus, and two continuous lines of thyrocytes were obtained. The cell lines maintained features of parental thyroid epithelial cells showing the characteristic cytokeratin filament network, microvillar protrusion and tight junctions. In addition, the SV40-transfected cells responded to graded doses of TSH with increased c-AMP production. Thyrocytes from both cell lines hyperexpressed Class I molecules and a significant proportion of them also acquired constitutive Class II expression, as determined by indirect immunofluorescence (IFL), flow cytometry and Northern blotting hybridization using a DR beta probe. These cells were found to be normally up-regulated by interferon (IFN)-gamma. Indirect IFL and flow cytometry analysis were used to detect and quantify the expression of HLA-DR, DP and DQ subregions. A co-ordinated expression (DR greater than DP much greater than DQ), reminiscent of the inappropriate HLA expression found in thyroid autoimmune disease in vivo and of the in vitro regulation in normal thyrocytes, was observed. Clones derived from these cell lines differed in their level of constitutive Class II expression and in their sensitivity to Class II induction by IFN-gamma. In conclusion, these thyroid cell lines could provide a useful tool for further investigation of HLA gene regulation in thyroid cells and for elucidating on the mechanism involved in the inappropriate HLA expression described in autoimmune and neoplastic diseases of the thyroid.

Autoantigens↗

PubMed1991

Spontaneous pituitary apoplexy with transient panhypopituitarism and diabetes insipidus.

A 40-year-old patient presented with intractable headache, panhypopituitarism and diabetes insipidus 5 months after a severe shock syndrome. The magnetic resonance imaging of the brain confirmed a hemorragic necrosis of the pituitary gland. On follow-up, the patient recovered a normal pituitary function, except for the persistence of a partial ACTH deficiency. The pituitary image also normalized. Pituitary apoplexy is a rare disease of severe prognosis due to its neurological and endocrine consequences. It can now be more easily recognized by the new imaging techniques.

Adult↗

PubMed1991

[Emphysematous pyelonephritis in a diabetic patient. Literature review apropos of a case].

We report the history of a 65-year-old woman, diabetic for 25 years who presented progressive alteration of consciousness with hyperthermia, right upper quadrant pain and vomiting. Bacteriological and radiographic investigations, especially computerized tomography scan of the abdomen, led to the diagnosis of emphysematous pyelonephritis caused by Escherichia coli. Despite a large spectrum antibiotic therapy and surgical drainage of the gas collection, the patient remained septic. An emergency nephrectomy was eventually performed. We review the characteristics of emphysematous pyelonephritis. Early diagnosis is essential because without early nephrectomy mortality rates reach 75%.

Aged↗

PubMed1991

Evidence that pretranslational and translational defects decrease serum insulin-like growth factor-I concentrations during dietary protein restriction.

Dietary protein restriction causes GH resistance and decreases serum insulin-like growth factor-I (IGF-I) concentrations. To determine whether pretranslational or translational defects are involved in the decline of serum IGF-I concentrations during protein restriction, we measured hepatic IGF-I mRNA abundance together with the serum IGF-I peptide response to exogenous GH after 1 week of protein restriction (5% casein in diet; P5) in hypophysectomized rats. We compared these responses with those of hypophysectomized rats fed a protein-sufficient diet (15% casein in diet; P15) and given exogenous GH. A single injection of rat GH (200 micrograms/100 g BW) produced a comparable IGF-I mRNA increment in both groups (at 6 h, 7.8 +/- 1.1 arbitrary units in P5 vs. 8.2 +/- 1.1 in P15), but failed to raise serum IGF-I normally in the P5 group (at 6 h, 90 +/- 15 ng/ml in P5 vs. 216 +/- 63 in P15; P less than 0.01). The post-GH decline of the 7.5-kilobase (kb) IGF-I mRNA abundance was faster in P5 than in P15 animals. In another experiment in intact rats subjected to protein restriction, injections of pharmacological doses of rat GH (400 micrograms/100 g BW.day) for 1 week restored liver IGF-I mRNA abundance to normal without normalization of serum IGF-I (403 +/- 91 vs. 713 +/- 53 ng/ml; P less than 0.01). Our data suggest that 1) the machinery involved in the transcription of the liver IGF-I gene is intact in protein-restricted rats, because these animals retain the ability to muster normal IGF-I mRNA responses to high doses of exogenous GH; 2) the stability of the 7.5-kb IGF-I mRNA is probably decreased by the protein restriction, as suggested by the faster decline of the 7.5-kb transcript in P5 than in P15 hypophysectomized rats; and 3) the discrepancy between normal liver IGF-I mRNA abundance and low serum and liver IGF-I peptide concentrations suggests that translational stalling of the IGF-I mRNAs or increased serum IGF-I clearance is involved in the low serum IGF-I concentrations during dietary protein restriction.

Animals↗

PubMed1988

Differential expression and regulation of major histocompatibility complex (MHC) products in neural and glial cells of the human fetal brain.

The cells of the central nervous system (CNS) have the peculiarity of physiologically expressing very low levels of HLA molecules. In multiple sclerosis (MS), however, as in endocrine autoimmune diseases, there is a marked increase of HLA expression in the tissue (i.e. the plaques) and this is attributable not only to infiltrating cells but also to the astrocytes. To gain an insight into the regulation of HLA in the different cell types in the CNS and to compare it to that observed in the endocrine organs, we have studied the effect of the lympho/monokines interferon (IFN)-alpha and -gamma, tumour necrosis factor (TNF)-alpha, and interleukin (IL)-2 and other agents on this aspect of the biology of human fetal brain cells in culture. A two-colour immunofluorescence technique which combines antibodies to diverse CNS cell markers and monoclonal antibodies (MoAbs) to the non-polymorphic region of HLA molecules was used throughout this study. In control cultures, only astrocytes expressed MHC class I, but after incubation with either IFN-gamma or TNF-alpha oligodendrocytes acquired class I expression. Surprisingly, astrocytes became spontaneously class II positive in culture and this was greatly enhanced by IFN-gamma. Other agents such as IL-2, epidermal growth factor, phorbolmyristate acetate and lectins had no effect. The expression of HLA molecules in the cells of the CNS both in basal conditions and in response to lymphokines is therefore selective and highly heterogenous, thus reflecting their intrinsic biological diversity. These findings may help to explain the features of the immunopathology of MS and also of latent viral infections of neural cells.

Astrocytes↗

PubMed1986

Effect of glibenclamide in insulin-treated diabetic patients with a residual insulin secretion.

We have studied the effect of the combination of a sulfonylurea (Hb 420 or glibenclamide) with insulin in 22 type II diabetic patients, treated with insulin and with residual insulin secretion (fasting plasma C peptide level greater than 0.2 pmol/ml). After a 3 week run-in period, the patients received either glibenclamide (7 mg of Hb 420 before breakfast and 3.5 mg before supper) or placebo in double blind fashion. Clinical and biological parameters (body weight, number of hypoglycemic episodes, daily insulin dose, fasting and postprandial glucose and C peptide levels after a standard meal) were collected during the basal (run-in) period and after 8 and 16 weeks of treatment. In the glibenclamide group, a significant increase in the number of hypoglycemic episodes was observed in spite of a 8 to 10% reduction in insulin requirements. A 18% reduction of both fasting and postprandial plasma glucose levels was found after 8 and 16 weeks of glibenclamide therapy. Concomitantly, a 35% increase of fasting and postprandial plasma C peptide levels occurred. The data suggest that the use of combined sulfonylurea and insulin therapy may be beneficial to type II diabetic patients with residual insulin secretion and poor glycemic control under insulin therapy alone.

Blood Glucose↗