B Soudan, D Tetaert, M Hublart, A Racadot, D Croix, A Boersma
{"title":"Experimental \"chronic\" African trypanosomiasis: endocrine dysfunctions generated by parasitic components released during the tryptanolytic phase in rats.","authors":"B Soudan, D Tetaert, M Hublart, A Racadot, D Croix, A Boersma","doi":"10.1055/s-0029-1211225","DOIUrl":"https://doi.org/10.1055/s-0029-1211225","url":null,"abstract":"<p><p>The disorders of the gonadotropic axis have been studied during the course of a \"chronic\" african trypanosomiasis induced experimentally in rats inoculated by the variant Trypanosoma brucei brucei AnTat 1.1.E. The levels of serum and pituitary LH as well as serum testosterone and corticosterone have been determined, during the infestation, at a particular period of the circadian cycle, in regard to the parasitemia variations. In addition, the inoculation of trypanosomal component fractions [obtained by concanavalin-A sepharose chromatography (conA-components)], has been performed in an attempt to define more exactly the nature of factor(s) producing the hypotestosteronemia in rats. This work evidenced that the hormonal parameter levels were predominantly decreased at the trypanolytic phase during the evolution of the disease. The action towards the hypothalamo-pituitary gonadal axis was attributed not only to peculiar trypanosomal enzyme(s) [a serine, thiol-dependent, cation sensitive endoprotease with a post-proline cleaving activity (purified from unretained conA fraction)], but also to protein and/or glycoprotein factor(s) released by the trypanosomes (components with affinity to the lectin).</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"166-72"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Lerchl, K A Stokkan, K O Nonaka, M K Vaughan, R J Reiter
{"title":"Type II iodothyronine 5'-deiodinase in mouse brown adipose tissue is stimulated by a single injection of isoproterenol in an oil/water emulsion.","authors":"A Lerchl, K A Stokkan, K O Nonaka, M K Vaughan, R J Reiter","doi":"10.1055/s-0029-1211232","DOIUrl":"https://doi.org/10.1055/s-0029-1211232","url":null,"abstract":"A single subcutaneous morning injection of the beta-adrenergic agonist isoproterenol (ISO) (10 mg/kg body weight) in an oil/water emulsion (70/30; v/v) caused a marked increase in the activity of the enzyme type II iodothyronine 5'-deiodinase (5'-D II) in the interscapular brown adipose tissue of BDF-1 mice. After a delay of 4 hours, the 5'-D II activity began to rise in an almost linear fashion and was increased 3-fold after 8 hours, when compared to the control values. The results indicate that this method of ISO administration may be a valid tool for artificial stimulation of brown adipose tissue in animals by beta-adrenergic agonists.","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"197-9"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211232","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endocrine markers in malignant tumor cells producing parathyroid hormone-related protein.","authors":"M Zabel, M Dietel","doi":"10.1055/s-0029-1211247","DOIUrl":"https://doi.org/10.1055/s-0029-1211247","url":null,"abstract":"<p><p>Humoral hypercalcemia of malignancy may reflect the synthesis and secretion of biologically active parathyroid hormone-related protein (PTHrP) by a given tumor. In the present study we investigated 25 human non-endocrine carcinomas which were clinically associated with hypercalcemia (Ca > 11 mg%). By applying PTHrP-specific immunocytochemistry, PTHrP could be detected in all tumors. The intra-tumorous distribution was heterogeneous with strong positivity in relatively few cells or weak positivity in the majority of cells. Surprisingly, in the PTHrP producing cells none of the marker proteins typical of endocrine cells (neuron-specific enolase, Leu-7 antigen, chromogranin, synaptophysin and endocrine granule constituent) was found. On the other hand, PTHrP producing cells of endocrine origin, such as medullary cancer, or normal and adenomatous parathyroid glands, all produce these endocrine markers. Thus for the first time, the existence of peptide hormone producing tumor cells is reported without expression of endocrine markers. This indicates a special mechanism of PTHrP secretion.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 5","pages":"297-302"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211247","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"In vivo assessment of insulin binding in different organs of growing and adult glutamate-induced obese rats.","authors":"P Nenoff, H Remke, F Müller, T Arndt, T Mothes","doi":"10.1055/s-0029-1211235","DOIUrl":"https://doi.org/10.1055/s-0029-1211235","url":null,"abstract":"Injection of Na-L-glutamate into neonate Wistar-rats (2 mg/g body mass s.c.; day 1-5 of life) induces hypothalamic lesions, which are followed by hypoplastic-hypertrophic obesity despite normophagia. In contrast to other animal models of obesity, these rats develop obesity under peripheral normoinsulinemic conditions. However, beginning at an age of 2 months (growing rats), peripheral insulin concentration rises gradually and at an age of 6 months (adults rats) hyperinsulinemia becomes manifest. Surprisingly, adult rats show normoglycemia, pointing to alterations in insulin sensitivity. In continuation to previous work, insulin binding of different organs of growing and adult rats was investigated using the in vivo radioreceptor assay described by Whitcomb et al. in 1985. In contrast to in vitro methods, this assay works under real metabolic and hormonal conditions in plasma of lean and obese rats. Insulin binding of liver, pancreas, adrenals, stomach, duodenum, spleen, and heart muscles was found to be not statistically different between lean and obese rats of both age groups. Thus, liver insulin binding was 6323 +/- 458 pg/g wet organ in growing, and 7586 +/- 959 pg/g in adult lean rats. Corresponding values for obese rats were 5755 +/- 445 pg/g and 7830 +/- 526 pg/g, respectively. Organ specific down regulation of insulin binding in obese rats was not detected, suggesting unalterated insulin sensitivity. It is concluded that hyperinsulinemia of adult glutamate-induced obese rats cannot be explained by diminished insulin binding and reduced organ specific insulin clearance.","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 4","pages":"215-21"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18904121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Quality of life in patients with Addison's disease: effects of different cortisol replacement modes.","authors":"M Riedel, A Wiese, T H Schürmeyer, G Brabant","doi":"10.1055/s-0029-1211215","DOIUrl":"https://doi.org/10.1055/s-0029-1211215","url":null,"abstract":"<p><p>This study compares the impact of different modes of cortisol replacement therapy on the health perception and general well-being in patients with primary adrenocortical failure. 14 adults (8 female, 6 male) with Addison's disease on chronic cortisol replacement participated in the study. In a randomized double-blind cross-over design, all patients were treated with 3 modes of cortisol replacement for one week each (mode I: 20 mg hydrocortisone (HC) at 0700 h and 10 mg HC at 1900 h; mode II: 30 mg HC at 0700 h and placebo at 1900 h; mode III: placebo at 0700 h and 30 mg HC at 1900 h). Following the third week, the replacement modes were repeated in a different random order. For quality-of-life assessment the patients completed three different questionnaires (Addison-questionnaire, Basler Befindlichkeits-Skala, Beschwerde-Liste) and were interviewed about their general contentment at the last day of each treatment week. General well-being in terms of subjective contentment was best established during mode I (in 64% of patients) and less often stated with mode II (in 29%) and III (in 14%) (p < 0.05 mode I vs III). With the twice-daily replacement (mode I), sum scores of all questionnaires were changed towards improvement compared to both once-daily regimens (p < 0.05 vs mode II and III), but did not reach normal values of healthy subjects. Differences between mode II and III were insignificant. We conclude that quality of life in Addison patients is mainly influenced by the mode of cortisol replacement therapy.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 2","pages":"106-11"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211215","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19390454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Genetic screening for multiple endocrine neoplasia type 2.","authors":"B A Ponder","doi":"10.1055/s-0029-1211208","DOIUrl":"https://doi.org/10.1055/s-0029-1211208","url":null,"abstract":"Multiple endocrine neoplasia type 2 (MEN 2) is a dominantly inherited cancer syndrome, in which the component tumours involve the C cells of the thyroid, the adrenal medulla, and the parathyroid. Three inherited varieties are distinguished on clinical grounds. Current evidence suggests that at least two of these are due to mutation at the same or closely adjacent loci on chromosome 10 (Norum et al., 1990). Men 2A. This is the commonest form (Table 1). It is important to note that not everyone who inherits the MEN 2 gene develops clinically significant disease. Figure 1 gives the ageincidence curves for presentation of MEN 2A with clinical disease and for detection by biochemical screening (Easton","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 1","pages":"53-6"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211208","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19459870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Perspectives in gene therapy with recombinant adenoviruses.","authors":"W Siegfried","doi":"10.1055/s-0029-1211201","DOIUrl":"https://doi.org/10.1055/s-0029-1211201","url":null,"abstract":"The cure of inherited disease in man at the genetic level is a dream of modern medicine that becomes closer every day with the development of more precise and faster methods in molecular biology. Already this year, we can expect the first experimental therapy with recombinant adenoviruses in individuals suffering from cystic fibrosis (CF), after the NIH Recombinant DNA Advisory Committee (RAC), in December 1992, gave full approvai to begin treating humans.","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 1","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19459871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E F Adams, M Buchfelder, A Hüttner, S Moreth, R Fahlbusch
{"title":"Recent advances in the molecular biology of growth-hormone secreting human pituitary tumours.","authors":"E F Adams, M Buchfelder, A Hüttner, S Moreth, R Fahlbusch","doi":"10.1055/s-0029-1211202","DOIUrl":"https://doi.org/10.1055/s-0029-1211202","url":null,"abstract":"<p><p>The application of DNA technology has led to significant progress in our understanding of the aetiology of GH-secreting pituitary tumours. X-chromosome inactivation and RFLP analysis has revealed that GH-secreting tumours are monoclonal in origin and thus arise as a consequence of a somatic mutation within a single cell. Using PCR and sequence analysis, such a mutation has been identified in 30-40% of tumours. This is the so-called gsp mutation in which the gene for the alpha s subunit of the Gs protein is converted to an oncogene the expression of which results in constitutive adenyl cyclase activity and thus excessive cAMP production. In our own studies, we demonstrate that it is unlikely that a defect within the promoter region of the GH gene will prove to be a cause of excessive GH secretion in acromegaly. In contrast, we have shown that the GH gene is hypomethylated in tumour derived DNA and this may account, at least in part, for abnormal GH gene expression.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 1","pages":"12-6"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211202","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19461263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H L Fehm, E Späth-Schwalbe, R Pietrowsky, W Kern, J Born
{"title":"Entrainment of nocturnal pituitary-adrenocortical activity to sleep processes in man--a hypothesis.","authors":"H L Fehm, E Späth-Schwalbe, R Pietrowsky, W Kern, J Born","doi":"10.1055/s-0029-1211243","DOIUrl":"https://doi.org/10.1055/s-0029-1211243","url":null,"abstract":"<p><p>The 24 hr patterns of plasma ACTH and cortisol concentrations are characterized by prominent circadian and ultradian oscillations. Usually both, nadir and acrophase of the circadian rhythm occur during sleep. This led us to re-evaluated the temporal relationship between sleep processes and nocturnal plasma ACTH and cortisol levels and the impact of several types of sleep manipulation (sleep delay, sleep disruption, sleep prolongation, sleep deprivation, and reversal of the sleep-wake cycle). Pituitary-adrenocortical activity appeared to be linked to the cyclic process of nocturnal sleep with inhibitory influences present during the first two sleep cycles. After initiation of the third sleep cycle stimulatory effects of sleep prevailed, lasting until awakening. The sleep associated influences appeared to act in concert with influences of circadian oscillators and resulted in an amplification of the circadian rhythm of pituitary-adrenal activity; they were strong enough to entrain the circadian rhythm of the pituitary-adrenal system to the sleep-wake cycle, as long as phase delays were moderate. However, with acute sleep-wake reversals the sleep associated influences were masked by the dominant effects of the circadian clock. In contrast, GH secretion appeared to be controlled primarily be sleep-associated mechanism with only minor circadian influences.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 5","pages":"267-76"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of protein deficiency on luteinizing hormone releasing hormone (LHRH), gonadotropin releasing hormone associated peptide (GAP) and luteinizing hormone (LH) immunocytochemistry in the hypothalamus and pituitary gland of prepubertal ewes.","authors":"J Polkowska, F Przekop","doi":"10.1055/s-0029-1211237","DOIUrl":"https://doi.org/10.1055/s-0029-1211237","url":null,"abstract":"<p><p>Growing female lambs were fed diets containing 14.2% (standard) or 8.1% (protein restricted) of proteins to determine their effects on puberty and luteinizing hormone releasing hormone (LHRH), gonadotropin hormone associated peptide (GAP), luteinizing hormone (LH) hormonal system. At the end of the experiment (30-34 weeks of age), hypothalamic LHRH, GAP and pituitary LH were analysed by immunocytochemical methods using specific antibodies. Plasma LH were determined by radioimmunoassay at 21 weeks of age. It was found that lowering of the dietary proteins content decreased the concentration of basal plasma LH significantly in lambs of 21 weeks of age. None of the sheep of this group reached sexual maturity at the same time as the animals of the standard group. However, immunoreactive (ir) LHRH neuronal system of protein restricted lambs was normally developed: Numerous irLHRH perikarya, dense network of axons and abundant material stored in the nerve terminals were well visualized in the typical sites of the preoptico-septal area, hypothalamus and the median eminence (ME). Gonadotropin associated peptide (GAP) of the LHRH precursor was present in the same populations of neurons that contained LHRH in the sheep brain. The proportion of pituitary LH-cells was three fold higher in pituitaries of the nutritionally restricted group. They displayed hypertrophy and very strong immunoreaction. These results show that protein deficiency in diets of growing female sheep delays their puberty but does not impair the synthesis and processing of LHRH in the brain neurons and synthesis of LH in pituitary cells.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 4","pages":"230-7"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211237","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19295487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}