Biomedical subjects

W Kranewitter

Publications and source records attributed to W Kranewitter.

6 recordsLinked to original sources

PubMed2002

[Fever and weight loss as leading symptoms of infection with giardia lamblia].

Infections, malignancies and autoimmune diseases are the most important causes of fever of unknown origin.A case report of a 80-year old patient is described, who was admitted to our hospital because of fever lasting more than 2 weeks, weight loss and lack of appetite. Physical examination did not provide any relevant information, laboratory tests revealed an elevation of inflammation markers and anemia. Serological tests for infectious and autoimmune diseases and cultures of stool, blood and urine were all negative. Imaging did not show any pathological findings, colonoscopy and gastroscopy were macroscopically normal. Surprisingly, histology showed massive giardiasis of the duodenum. After initiation of therapy with metronidazol, fever and inflammation markers declined and the patient could be discharged from hospital without complaints on the 15(th) day after admission. Giardia lamblia is one of the most common intestinal pathogens worldwide. Infection can cause acute diarrhea, but may also be responsible for chronic abdominal complaints or may stay asymptomatic. To our knowledge, giardiasis has not been described as differential diagnosis of fever of unknown origin so far. In synopsis of clinical presentation and outcome after antibiotic therapy, we postulate that Giardia lamblia was the relevant cause of fever and weight loss in this case. In patients presenting with these symptoms, Giardia lamblia should be considered as differential diagnosis.

Aged↗

PubMed2002

[Obstructive jaundice and acute pancreatitis due to an obstruction of the afferent loop after billroth-II-resection].

An obstruction of the afferent loop after Billroth-II-resection is an extremely rare late complication of this procedure. We report on a 76-year-old female patient with a history of Billroth-II-resection 11 years ago who was admitted due to acute pancreatitis and obstructive jaundice. Abdominal sonography lead to the suspicion of a dilated afferent loop, which could be proven by means of magnetic resonance imaging. A tumorous lesion as cause of the obstructive jaundice was not detectable. Intraoperatively a volvulus of the small intestine and strangling adhesions near the Braun's anastomosis were seen, causing the obstruction of the afferent loop. Following reposition of the small intestine and adhesiolysis the patient gained a quick relief of symptoms and the jaundice disappeared completely.

Acute Disease↗

PubMed1998

CH domains revisited.

A sequence motif of about 100 amino acids, termed the 'calponin homology domain' has been suggested to confer actin binding to a variety of cytoskeletal and signalling molecules. Here we analyse and compare the sequences of all calponin homology domain-containing proteins identified to date. We propose that single calponin homology domains do not confer actin-binding per se and that the actin-binding motifs of cross-linking proteins, which comprise two disparate calponin homology domains, represent a unique protein module.

Actins↗

PubMed1997

Organ-specific expression pattern of the human growth hormone/placental lactogen gene-cluster in the testis.

In addition to testosterone, the essential paracrine factor for spermatogenesis, a number of potential auto/paracrine regulatory substances such as beta-endorphins, enkephalins, chorionic gonadotropin beta, growth hormone-releasing hormone (GHRH) and insulin-like growth factor I (IGF-I) have been identified in the testis of various mammalian species. The latter findings prompted us to investigate a possible eutopic production of GH, placental lactogen (PL) and PRL in human testes. Specific expression of testicular GH/PL mRNA (n = 20) was shown by reverse transcription-polymerase chain reaction (RT-PCR) using a pair of primers designed to non-selectively amplify any transcript of the five GH/PL genes (GH-N, GH-V, PL-A, PL-B, PL-L). In contrast to the classical sites of production, the pituitary (exclusively GH-N transcripts) and the placenta (PL-A/B > 99%, GH-V < 1%), radioactive semiquantitative restriction enzyme analysis of the PCR-products revealed, that the testis has its own organ-specific pattern of GH/PL gene expression: PL-A/B > GH-V > or = PL-L = GH-N. All three organs express the single PRL gene, and testis and placenta show the alternative splice variant GH-V2. Immunological analyses by immunofluorometric assays for hPL-A/B, hGH-N and hPRL, demonstrated significant amounts of protein hormones in all testicular cytosolic homogenates (means: hPL 1.0 ng/g, hGH 5.1 ng/g and hPRL 58.7 ng/g tissue wet weight). Most noteworthy, hPL serum levels in an elderly age-matched healthy subjects (n = 18) were < 0.02 ng/ml. The concept of purely endocrine functions of placental and pituitary-derived GH/PL needs to be reassessed, since human testicular synthesis of these molecules suggest auto/paracrine functions in the male reproductive tract.

Aged↗

PubMed1996

[The testis as eutopic production site of human growth hormone, placental lactogen and prolactin: possible autocrine/paracrine effects on testicular function].

The human (h) protein hormones, growth hormone (hGH-N) and prolactin (hPRL), are mainly produced in the pituitary, whereas the human placenta expresses the other four members of the protein hormone gene family, designated placental lactogens (PL-A, PL-B, PL-L) and growth hormone variant (GH-V), GH-N stimulates somatic growth, supports nitrogen-, phosphate- and potassium retention and promotes lipolytic and anabolic metabolism, whereas PRL acts on the mammary gland and induces mammogenesis, lactogenesis and galactopoesis. Both hyperprolactinemia and growth hormone deficiency affect the onset of puberty and reproduction in man and mice. In addition to the glycoprotein hormones, these hormones play a role in the maintenance of testicular function. Our group previously demonstrated eutopic production of glycoprotein hormones hLH (human luteinizing hormone) and hCG (human chorionic gonadotropin) in the testis. We have now extended our investigations to the local testicular expression of protein hormones. By means of the molecular biology techniques of the reverse transcription-polymerase chain reaction (RT-PCR), Southern blot and by restriction endonuclease analyses of the generated PCR products we demonstrated the eutopic expression of genes coding for the protein hormones. GH-N gene transcripts were detected only in the pituitary and abundant PL-A/B and a few GH-V gene transcripts were demonstrable in the placenta. In contrast, in the testis GH/PL and PRL genes are transcribed. Since testicular protein hormone gene expression is rather low, these hormones may act locally and not as systemic factors; they presumably modulate the LH/CG-mediated testosterone biosynthesis and/or may act on the spermatogenesis.

Animals↗

PubMed1994

Eutopic production of human chorionic gonadotropin beta (hCG beta) and luteinizing hormone beta (hLH beta) in the human testis.

The classical pregnancy and tumor marker hCG has long been considered to be only accidentally expressed ectopically, e.g. by tumors. The biological functions of low levels of hCG beta, hCG alpha and holo-hCG in the sera of nonpregnant healthy individuals remained unclear. Immunological analyses by our ultrasensitive time-resolved fluoroimmunoassays revealed a concentration gradient from < 5 pg hCG beta/ml in cubital vein serum versus up to 480 pg hCG beta/ml in the corresponding benign testicular hydrocele fluids. Moreover, hCG beta and its cognate molecule luteinizing hormone beta (LH beta) were present in cytosolic extracts of normal human testes. Both hCG beta and hLH beta are eutopically produced as proven by RT-PCR and subsequent Southern and dot blot analyses. Thus, the view of a purely systemic hormonal function of hLH, and of hCG during pregnancy needs a reassessement as hCG beta and hLH beta are synthesized in the human testis and autocrine/paracrine actions seem to be likely.

Base Sequence↗