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Biomedical subjects

J Homann

Publications and source records attributed to J Homann.

At least 19 recordsLinked to original sources
PubMed2006

[Systemic mast cell disease with gastrointestinal symptoms--a diagnostic questionnaire].

Systemic mast cell disease often becomes clinically manifest as a mast cell mediator activation syndrome with episodic or chronic nonspecific abdominal symptoms. As a result of genetic alterations, pathological mast cells have an increased proliferation rate as well as accumulation within different organs with consequential effect on gastrointestinal secretion, absorption, pain perception and motility caused by release of their mediators. These changes may not be detected in routine laboratory or imaging methods. This report describes how the diagnosis systemic mast cell disease can be established with a diagnostic questionnaire based on a synopsis of clinical findings relevant to a mast cell mediator activation syndrome.

Diagnosis, Differential↗
PubMed2003

Localized lymphoid relapse in the pancreas following allogeneic hematopoietic stem cell transplant for chronic myelogenous leukemia.

The incidence of isolated extramedullary disease (EMD) following allogeneic hematopoietic stem cell transplant (allo-HSCT) for chronic myelogenous leukemia (CML) is not fully known. One review found the incidence of isolated myeloid EMD, or granulocytic sarcoma (GS), in an allo-HSCT treated CML/myelodysplastic subgroup to be just 0.22%. The incidence of lymphoid EMD in similar patients is extremely rare with only two cases reported in the literature. While the etiology of EMD in the post-transplant setting is not entirely clear, there may be inefficacy of immune surveillance function outside of the bone marrow cavity. Isolated CML GS following allo-HSCT carries a median interval to bone marrow relapse between 7 and 10 months and a median survival of 12 months. Less is known about lymphoid EMD. The treatment in these cases is ill defined with modalities ranging from involved field radiation to second allo-HSCT. We present a case of isolated pancreatic lymphoid EMD diagnosed 15 months after allo-HSCT for CML. Our patient was also treated with withdrawal of his immunosuppressive regimen. Unfortunately, at just over 4 months following pancreatic resection, he developed systemic relapse and died. While EMD can occur anywhere in the body, CML associated pancreatic EMD is not previously reported.

Adrenal Cortex Hormones↗
PubMed2000

[Knowledge about stroke among the German population].

BACKGROUND AND OBJECTIVE: Modern stroke therapy requires patients to correctly identify stroke symptoms and seek immediate hospital admission. US studies showed that only 57% of the population knew at least one stroke symptom. This is the first study about stroke knowledge among German populations. METHODS: Using a cross-sectional questionnaire survey, 300 working-age participants of the PROCAM study, the Prospective Cardiovascular Münster Study, and 95 senior citizens of the Augsburg Study, a follow-up project of the MONICA survey 1989/90, were asked about stroke symptoms and what to do if they occur. Good knowledge about stroke was defined as knowing at least two stroke symptoms and calling the emergency medical system or seeking immediate hospital admission in case of symptoms. RESULTS: Participation rate in the PROCAM study was 90%, while all senior citizens took part. The mean age of the working population was 41.2 years, the mean age of the retired population was 72.8 years. 35% of the working and 24.5% of the retired participants knew at least two stroke symptoms. Urgent hospital admission was selected by 78.2% of the occupational but only 41.5% of the retired participants. Good stroke knowledge was demonstrated by nearly a third of the workers but less than 10% of the elderly. Among the occupational population, being a white-collar worker or knowing someone with a stroke was a significant predictor of good stroke knowledge. Among senior citizens higher age and current smoking status were significant predictors. CONCLUSION: Our study shows significant information deficits about stroke in our population: education needs to be geared especially towards the elderly.

Adult↗
PubMed2000

Stroke knowledge among stroke support group members.

BACKGROUND AND PURPOSE: Community stroke education is needed to improve early stroke recognition and reduce delays in the referral of stroke patients. In some regions, stroke support groups are important promoters of regional stroke education. However, there are no data about the level of stroke knowledge among support group members that support this promotional role. METHODS: We performed a cross-sectional questionnaire survey among 11 German stroke support groups. The questionnaire asked for stroke knowledge and sociodemographic and medical data. Stroke knowledge was excellent if a participant knew (1) at least 2 stroke symptoms (good symptom knowledge) and (2) at least 2 stroke risk factors (good risk factor knowledge), as well as knowing (3) that immediate hospital admission or an emergency call is necessary in case of stroke (good action knowledge). RESULTS: A total of 133 members (96.2%) of 11 stroke support groups took part in the study. Mean age was 65.3 years (SD 11.2 years). Fifty-four percent of subjects were female, 72.8% were retired, and 69.8% were stroke patients. Of the participants, 80.3% had good symptom knowledge, 64.7% had good risk factor knowledge, and 79.7% had good action knowledge. Stroke knowledge was excellent in 44.0% of subjects. Logistic regression analysis showed that age <70 years and not having had a stroke were significant predictors for excellent stroke knowledge. CONCLUSIONS: Overall, members of stroke support groups are well informed about all aspects of modern stroke care. Because of their knowledge and personal experience, support groups should be viewed as important partners in community stroke education.

Aged↗
PubMed1999

Imidazoline recognition sites and stomach function.

Radioligand binding experiments carried out in cell membranes from rat and human stomach revealed the existence of non-adrenoceptor [3H]clonidine and [3H]idazoxan binding sites and of [3H]DTG (1,2-di-(2-tolyl)guanidine) binding sites. In rat stomach, specific binding was inhibited by imidazolines and guanidines and by non-imidazoline sigma-site ligands, respectively, at different rank orders of affinity, suggesting the existence of non-I1/non-I2 [3H]clonidine binding sites, I2-imidazoline binding sites as well as sigma 2-like-sites. These sites are not directly related to a postsynaptic contractile effect on rat gastric smooth muscle or to acid release from isolated gastric glands. Finally, we demonstrated that the gastric pathogen Helicobacter pylori is able to form and to release the endogenous imidazoline receptor ligand agmatine and that considerable amounts of agmatine are present in human gastric juice. The quantities of agmatine were higher in gastric juice from H. pylori-positive than H. pylori-negative patients.

Animals↗
PubMed1999

Potential relevance of agmatine as a virulence factor of Helicobacter pylori.

The polyamine agmatine is able to increase gastric acid secretion. Therefore, we investigated whether Helicobacter pylori is able to form and release agmatine in vitro and in the human stomach in vivo, and if so, whether a relationship exists among agmatine concentration in gastric juice, H. pylori infection, and gastroduodenal lesions. Agmatine was determined by means of HPLC. In the supernatant of H. pylori cultures, agmatine concentrations up to 1500 ng/ml (approximately 12 microM) were determined, depending on the number of the bacteria in the individual cultures. Agmatine concentration in gastric juice from H. pylori-positive patients was higher than in that from H. pylori-negative patients. Gastrin in blood was elevated in H. pylori-positive patients compared with H. pylori-negative patients. Agmatine concentration in gastric juice and serum gastrin level appeared to be related. In conclusion, H. pylori is able to form and to release agmatine in vitro and in vivo. This may be assumed to be relevant in vivo, since higher amounts of agmatine are present in gastric juice from H. pylori-positive than from H. pylori-negative patients. Accordingly, agmatine produced by H. pylori may be a virulence factor of this bacterium and may be involved in the pathogenesis of gastroduodenal lesions.

Agmatine↗
PubMed1986

Early detection of amatoxins in human mushroom poisoning.

Amatoxins were detected radioimmunologically as early as 90-120 min after ingestion in the gastric fluid and urine of a 15-year-old boy who tried to commit suicide by ingestion of wild mushrooms. This early detection of amatoxins in the urine is proof of rapid absorption from the intestinal tract and subsequent excretion by the kidneys in man.

Adolescent↗
PubMed1986

[Dose comparative study with ranitidine in the therapy and prevention of duodenal ulcer].

The clinical value of ranitidine, 75 b. d. versus 175 mg b. d. in 48 patients with endoscopically proven duodenal ulcer was evaluated in a randomised double-blind study. In the two groups of patients there was no significant difference of ulcer healing. After 4 weeks of treatment in each group healing of 79% and after 6 weeks of 92% of the ulcers was observed. After 8 weeks the healing rate was 96% in patients who received 75 mg b. d. and 100% in those receiving 150 mg of ranitidine b. d. Smoking prolonged ulcer healing in both groups. Upon ulcer healing in 34 patients a ranitidine dosis of 75 mg nocte for prophylaxis of ulcer recurrence was compared with a 150 mg dosis nocte. Within 12 months in the two groups recurrence of duodenal ulcer was found by endoscopy in 21% and 20% of the patients. 7 out of 8 patients with ulcer recurrence were smokers. According to the results of these studies it appears that the recommended standard dosis of ranitidine for treatment of duodenal ulcer could be reduced by one half. To confirm our conclusions, further studies with a greater number of duodenal ulcer cases are necessary.

Adult↗
PubMed1985

Parathion-provoked lethality in rats is reduced by diethyldithiocarbamate.

Intoxication of male rats with 5 mg/kg parathion reduces survival to 15%. Diethyldithiocarbamate (DDC), known to inhibit mixed-function oxidase activity, has no effect on survival rate when this compound is used in a dosage of 300 mg/kg 45 min before or 10 min after parathion intoxication. However, when DDC and parathion are administered simultaneously, the rate of survival rises to 53%.

Animals↗
PubMed1980

[Protective and curative effects of diethyldithiocarbamate on galactosamine hepatitis in the rat (author's transl)].

Diethyldithiocarbamate influences galactosamine induced hepatitis in the rat. Experimental liver damage produced by galactosamine is less severe when diethyldithiocarbamate is given before or after galactosamine application. Galactosamine induced hepatitis is nearly completely suppressed when diethyldithiocarbamate is applied 24 h after galactosamine administration.

Animals↗
PubMed1976

Comparative studies on isolated rat hepatocytes and AS-30D hepatoma cells with leucocidin from Pseudomonas aeruginosa.

Leucocidin, one of the cytotoxic principles of Pseudomonas aeruginosa induces potassium loss and swelling in isolated hepatocytes and in AS-30D ascites hepatoma cells in a dose and time dependent manner. Hepatoma cells are more sensitive than normal hepatocytes. As shown by scanning electron microscopy the volume increase of both types of cells is accompanied by disappearance of microvilli. In contrast to phalloidin poisoning no protrusions were formed when the cells were exposed to leucocidin under isotonic conditions.

Animals↗
PubMed1976

[Inhibition by diethyldithiocarbamate (DEDTC) of acute hepatotoxic effects induced by polyhalogenated hydrocarbons (PHHC)].

Hemoglobin-free perfused rat livers were treated with carbon tetrachloride, chloroform, trichloroethylene and halothane by equilibrium of the perfusion medium with the varorous PHHCs. The resulting swelling of liver tissue, the potassium loss and the decrease of the perfusion rates were reduced by DEDTC to a different degree: The decrease of swelling, potassium loss and of the microcirculatory alteration by DEDTC was dose dependent in the case of carbon tetrachloride and halothane, whereas the effects of chloroform and trichloroethylene were not markedly influenced. Glutathione was mostly ineffective when given in similar doses. Pretreatment of rats with phenobarbital for 3 days increased itself swelling, K+-loss and reduction of perfusion rates, when the livers were perfused in absence of PHHCs. The effects of PHHCs in livers from pretreated rats were seldom greater but often lower than additive ones. Chiefly the effects of halothane were not markedly influenced by treatment of rats with phenobarbital. Isolated parenchymal liver cells were exposed to gas mixtures of O2, CO2 and PHHCs under controled conditions. Changes of the shape and staining of the cells were used for additional information. In view of these latter effects chloroform appeared as the most toxic and halothane as a nontoxic agent. DEDTC inhibits all effects of PHHCs demonstrated in isolated hepatocytes.

Animals↗
PubMed1975

Glucose-6-phosphatase (EC 3.1.3.9) and esterase (EC 3.1.1.1) activities of microsomes prepared from perfused rat livers after partial outflow block or phalloidin poisoning.

Microsomes were prepared from perfused rat livers after different perfusion procedures. The yield of microsomal protein and the kinetic data (Km, Vmax) of glucose-6-phosphatase (3.1.3.9) and esterase (3.1.1.1) activities were analysed in each preparation. No marked differences were detected between conventionally prepared liver microsomes and those from livers perfused 1 hr with an erythrocytes-free medium under the conditions of open outflow. If the outflow pressure was increased artificially, the yield of microsomal protein decreased. The Vmax of both enzymes was markedly increased, whereas the Km values remained unchanged. The same microsomal alterations occurred when perfused rat livers were poisoned with phalloidin in vitro under the condition of open outflow. Our findings indicate that microsomal alterations in livers from poisoned animals might be due to microcirculatory disturbances, and not primary effects of the toxin on the endoplasmatic reticulum.

Animals↗