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Biomedical subjects

R Meier

Publications and source records attributed to R Meier.

At least 163 records · Page 9Linked to original sources
PubMed1990

[Diarrhea in returning travellers (etiology, diagnosis and therapy)].

International tourism is constantly expanding and traveller's diarrhea has become a common disease. Although traveller's diarrhea may already have ceased after return, more and more general practitioners are confronted with patients complaining of GUT-symptoms associated with the journey. To manage these patients the precise knowledge of the etiology of traveller's diarrhea and the forms leading to chronic diarrhea is mandatory. This review deals with the etiology of diarrhea after returning home from tropical/subtropical areas and gives special emphasis on adequate diagnosis and treatment. It also points to the importance of parasites as cause of chronic traveller's diarrhea. Parasitic disease needs more often antibiotic treatment than infectious diarrhea due to bacterial agents. We summarize the etiology, the diagnostic and therapeutic approach.

Algorithms↗
PubMed1989

CGP 31358 binds to a site on the NMDA receptor that is coupled to both the transmitter recognition site and the channel domain.

CGP 31358, a novel triazole, inhibited the binding of L-[3H]glutamate and [3H]MK-801 to the N-methyl-D-aspartate (NMDA) receptor complex in rat brain synaptic membrane fractions, and showed anticonvulsant activity in mice. It had no effect on the strychnine-insensitive binding of [3H]glycine. Saturation and Hill analyses indicated that CGP 31358 binds to a site on the NMDA receptor which is separate from, but coupled to, both the transmitter recognition site and the channel domain. Available data indicate that this site is distinct from those with which tricyclic antidepressants and ifenprodil interact. CGP 31358 is a new chemical entity with a novel mechanism of action at the NMDA receptor, and as such may form a tool for understanding the molecular pharmacology of this receptor-channel complex.

Animals↗
PubMed1989

Induction of glia-derived nexin after lesion of a peripheral nerve.

Glia-derived nexin (GDN), also known as protease nexin I, is a serine protease inhibitor of deduced relative molecular mass 41,700, identified in conditioned media of glioma cells by its neurite-promoting activity. GDN can promote neurite outgrowth in vitro from neuroblastoma cells, sympathetic neurons and hippocampal neurons (L. Farmer et al., manuscript in preparation). In vivo, GDN is constitutively expressed in all parts of the olfactory system, where axonal regeneration and neurogenesis occur continuously throughout life. This observation indicates that GDN could be important for axonal regeneration in vivo. To investigate this possibility, we have taken advantage of the fact that damage to nerves in the peripheral nervous system leads to their regeneration, whereas in the central nervous system no such regeneration can occur. Here we report that after lesion of the rat sciatic nerve there is a large transient increase in the amount of GDN messenger RNA and of released GDN. The cells showing GDN immunoreactivity are mainly localized distal to the lesion site. These results further support the suggestion that GDN is important for axonal regeneration in vivo, and indicate that protease inhibitors could have a role in Wallerian degeneration and peripheral nerve regeneration.

Amyloid beta-Protein Precursor↗
PubMed1989

[Stress ulcer disease and its prevention].

The incidence and prophylaxis of stress ulcer disease are analyzed. Acute gastroduodenal stress lesions are frequently encountered in critically ill patients, yet the incidence of stress ulcer bleeding has decreased. It is still difficult to describe the risk in an individual patient in spite of the fact that patient groups prone to development of stress ulcer disease have been well defined (e.g. patients on mechanical ventilation). Prophylaxis with antacids, H2-receptor antagonist, pirenzepine and sucralfate seems to be equally effective and capable of reducing the incidence of stress ulcer bleeding. Its efficacy does not really correlate with the capability of a drug to keep gastric pH above 4. The higher the incidence of stress ulcer bleeding under placebo, the better the efficacy of prophylactic treatment. There is evidence that blockers of gastric acid secretion may be associated with an increased incidence of nosocomial pneumonia, but more data are needed in this regard.

Antacids↗
PubMed1988

[Acute bacterial sacroiliitis caused by Salmonella cholerae-suis].

A 17-year-old schoolboy was admitted to hospital because of one-sided pelvic pain of uncertain aetiology and fever gradually rising over several days. Bacteriological analysis of blood cultures, skeletal scintigraphy and computed tomography revealed sacroiliitis caused by Salmonella cholerae-suis. Specific antibiotic treatment quickly stopped all symptoms and cured the infection. Radiologically there remained sclerosis of the sacro-iliac joint.

Acute Disease↗
PubMed1988

Detection of glia-derived nexin in the olfactory system of the rat.

Glia-derived nexin (GDN) is a 43 kd cell-secreted protease inhibitor with neurite promoting activity. We have raised specific polyclonal antisera to rat GDN. These antibodies stain a single band at 43 kd on immunoblots of concentrated C6 glioma-conditioned medium and have been used to demonstrate that GDN is present in the olfactory system of the rat. One band at 43 kd is recognized by the GDN antibodies on immunoblots of olfactory bulb homogenate. Immunohistochemistry shows that GDN occurs predominantly in the olfactory nerve layer of the olfactory bulb and in the olfactory submucosa. Comparative studies with antibodies against vimentin, GFAP, and fibronectin suggest that anti-GDN recognizes cells associated with the olfactory system, but not exclusively the olfactory neurons themselves. Data from the immunohistochemical studies were confirmed by RNA blots and GDN mRNA expression throughout development of the olfactory bulb. The high levels of GDN in the rat olfactory system may be related to the continuous degeneration and regeneration phenomena taking place in these structures.

Amyloid beta-Protein Precursor↗
PubMed1988

Treatment of hepatic encephalopathy (HE) with the benzodiazepine antagonist flumazenil: a pilot study.

In experimental animal studies the benzodiazepine antagonist (BZA) flumazenil reversed galactosamine-induced fulminant liver failure. Based on this observation, we treated three patients (two male, one female), mean age 41 yrs (34-52 yrs) with five episodes (ep) of hepatic encephalopathy (HE) with i.v. BZA over 24 h. The efficacy of BZA in reversing HE was evaluated. On admission all patients had elevated plasma ammonia levels. The patients were in coma stage II (n = 3 ep) and stage III (n = 2 ep); the modified Glasgow score was less than 10 (n = 1 ep), 10-15 (n = 2 ep), 15-20 (n = 2 ep). No evidence for benzodiazepine, barbiturate or opiate intake was found in the urine. Two patients with HE episode stage II showed an immediate recovery within 1 h, which continued without any therapy other than BZA. After 24 h BZA was given orally, 30 mg q.i.d. One patient with an HE episode stage II showed no effect over 12 h. After this time he progressed to HE stage III; BA therapy was stopped. After discontinuation of BZA the Glasgow score rapidly deteriorated. Twenty-eight hours later BZA was given again with i.v. mannitol (20%) and oral lactulose and Fordtran solution. The patient then recovered within the next day. Another patient with a HE episode stage III showed a short lasting improvement after BA bolus injection. Then impairment of the Glasgow score was noted again. Lactulose and Fordtran solution was added orally and mannitol (20%) was given i.v. The patient recovered within 24 h to HE stage II and after 72 h to normal. BZA seems to improve hepatic encephalopathy, especially at an early stage (II). It appears less effective in stage III, most of all when there is evidence of brain oedema. No specific side-effects were observed during BZA therapy.

Adult↗
PubMed1987

cDNA sequence coding for a rat glia-derived nexin and its homology to members of the serpin superfamily.

Rat glial cells release a neurite-promoting factor with serine protease inhibitory activity. By using a rat glioma cDNA clone as a probe, it was possible to isolate rat cDNAs containing the entire sequence coding for this neurite-promoting factor. The largest rat cDNA (approximately 2100 bp) was characterized by DNA sequencing. It contained the entire coding region, 135 bp of the 5' nontranslated region, and about 750 bp of the 3' nontranslated region. The open reading frame coded for 397 amino acids including a putative signal peptide of 19 amino acids. The correct identity of the coding sequence was substantiated by the fact that the sequence of tryptic peptides, derived from the purified rat factor, matched exactly with the deduced amino acid sequence. The rat protein sequence had 84% homology with the corresponding protein from human glioma cells. Both amino acid sequences indicated that the proteins belong to the protease nexins [Baker, B.J., Low, D. A., Simmer, R. L., & Cunningham, D.D. (1980) Cell (Cambridge, Mass.) 21, 37-45] and therefore can be defined as glia-derived nexins (GDNs). Further analysis showed that both rat and human GDN belong to the serpin superfamily and share 41%, 32%, and 25% homology with human endothelial-cell-type plasminogen activator inhibitor, antithrombin III, and alpha-1 proteinase inhibitor, respectively.

Amino Acid Sequence↗