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Biomedical subjects

D Mayer

Publications and source records attributed to D Mayer.

At least 145 records · Page 8Linked to original sources
PubMed1990

Arterialization of the liver. III. Influence of systemic and portal pressure gradients following heterotopic partial liver transplantation.

An acute study was designed to compare blood pressures across a heterotopically transplanted partial liver graft using arterialized and nonarterialized models. Eight partial liver transplants (PLT) were done in each group, using Wistar rats. The data gathered from them are the basis for the results obtained herein. Whereas there was no significant difference (P greater than 0.01) in inflow, outflow, or the pressure difference across the PLT between nonarterialized and arterialized groups, host portal venous pressures were significantly higher (P less than 0.01) in the arterialized group. A 1 mm arteriovenous fistula (AVF) was used to arterialize the PLTs in this study. It was proved that arterializing a PLT using a 1 mm AVF did not alter the pressure difference across the transplanted liver compared with the situation in the nonarterialized setting.

Animals↗
PubMed1990

Expression of key enzymes of purine and pyrimidine metabolism in a hepatocyte-derived cell line at different phases of the growth cycle.

The effect of growth phase on enzymatic activities of the de novo and salvage pathways for purine and pyrimidine nucleotide synthesis was studied in a hepatocyte-derived cell line from the rat. The cells were in lag phase after plating for 36 h; log phase started at 48 h and persisted up to 120 h of culture. Then the cells stopped growing and entered into plateau phase (144 h). In non-proliferating cells (144 h of culture) the basal activities of the enzymes of purine de novo biosynthesis were 1.7- to 6.8-fold higher than in normal rat liver, those of pyrimidine de novo synthesis showed 0.6- to 30-fold increase in activity. The purine salvage enzymes were unchanged, and the pyrimidine salvage enzymes were 3.1- to 7.4-fold higher compared to normal liver. During the growth cycle all enzymes except the purine salvage enzymes, which did not change, showed a peak in activity at 72 h of culture (log phase). The increase in activity in log phase compared to plateau phase was 1.3- to 2.4-fold for purine de novo synthetic enzymes, 1.1- to 2.4-fold for pyrimidine de novo enzymes, and 1.4- to 4.7-fold for pyrimidine salvage enzymes. The specific activities of the enzymes in exponentially growing cells were comparable either to that in 24-h regenerating liver, or to that in hepatomas of low or medium growth rate. It was concluded that the enzymatic pattern and metabolic state of the cells shared some features with regenerating liver, others with tumors, although they were not tumorigenic after transplantation into athymic nude mice.

Animals↗
PubMed1990

Absence of genotoxic activity of penbutolol in bacterial and mammalian cell screening systems.

The genotoxic potential of the beta-adrenergic blocker penbutolol was assessed using the Ames and HGPRT tests, unscheduled DNA synthesis (UDS) and alkaline elution assays. In the Ames test, penbutolol was tested for cytotoxicity and genotoxic activity in concentration ranges of 0.8-500 micrograms/plate and 0.1-125 micrograms/ml in the HGPRT, UDS and alkaline elution assays. In the Ames test penbutolol showed significant toxicity above 500 micrograms/plate. In the mammalian cells (V79) used for the HGPRT test and A459 cells used for alkaline elution and UDS assays, penbutolol was cytotoxic at concentrations above 30 micrograms/ml. In another series of experiments, male Wistar rats were treated i.p. with penbutolol (1, 10 and 100 mg/kg) and after 2 h liver nuclei were isolated and formation of single DNA-strand breaks was measured. The results of the present study demonstrate the absence of genotoxic activity of penbutolol in the 5 strains of Salmonella typhimurium (TA98, TA100, TA1535, TA1537 and TA1538) and in the strain of Escherichia coli WP2 uvrA in the presence or absence of metabolic activation. In V79 cells, penbutolol showed no mutagenic effects at the HGPRT locus in the presence or absence of metabolic activation. Additionally, no significant incorporation of [3H]thymidine into the DNA in the UDS test or formation of DNA-strand breaks in the alkaline elution assay was detected in the non-toxic concentration range of penbutolol with or without metabolic activation. Furthermore, penbutolol did not cause DNA damage in liver nuclei isolated from penbutolol-treated rats.

Animals↗
PubMed1990

Summary of safety evaluation toxicity studies of glufosinate ammonium.

This article reviews the results of toxicity studies to evaluate the safety of the herbicide glufosinate ammonium (GLA) and its formulation (200 g/litre) in laboratory animals. The data show that GLA and its formulation are slightly toxic following oral exposure. In addition, the formulation induced GLA and its formulation are slightly toxic following oral exposure. In addition, the formulation induced slight dermal toxicity and eye irritation. Testing for teratogenicity in rats and rabbits indicated no teratogenic potential, and numerous mutagenicity tests showed GLA to be non-genotoxic. Chronic toxicity testing in rats and dogs yielded no-observable-effect levels of 2 and 5 mg/kg body weight/day, respectively. Oncogenicity studies in rats and mice revealed no carcinogenic potential. On the basis of these toxicity data it is concluded that this herbicide is safe under conditions of recommended use.

Aminobutyrates↗
PubMed1990

A model preclinical, clinical, and graduate educational curriculum in emergency medicine for medical students and rotating residents.

The Society for Academic Emergency Medicine model curriculum for medical students and rotating residents was developed over a two-year period. The document was created as a complementary work to the undergraduate Core Content to provide appropriate emphasis, structure, and suggestions on the teaching of emergency medicine core curriculum topics at all levels. Consensus on the curriculum contents was reached from a national sample of emergency medicine educators. An educational matrix format was used to enhance flexibility based on the educational level of the learner and the instructional strengths of the teacher, and allowing for incorporation of a problem-based learning format. An outline of document contents and representative samples from each section are included; the entire document is available from SAEM.

Curriculum↗
PubMed1990

Analyzing clinical case distributions to improve an emergency medicine clerkship.

Recommendations for a core curriculum for undergraduate emergency medicine education have been published. It is expected that a combination of bedside teaching and didactic sessions will cover all aspects of the curriculum, but this has not been demonstrated. This study describes a method of using the distribution of clinical cases to shape the mix of clinical and didactic learning in an emergency medicine clerkship. All senior students at the Albany Medical College participate in a four-week emergency medicine rotation. A brief log describing each clinical encounter is maintained by the students. Data from one year were sorted into 32 categories adapted from American College of Emergency Physicians guidelines and were tabulated. A criterion of 80% of students encountering at least one case in each category was chosen to ensure a reasonable level of exposure to a particular case or topic. One hundred twenty-three students were exposed to an average of 63.7 +/- 27.5 (SD) patients. Seven categories met the criterion, and the remaining 25 categories failed the criterion. Results indicate that exposure to certain categories of patients with appropriate monitoring can be reasonably ensured in our clinical setting. The didactic portion of the curriculum can be adjusted so that categories not meeting the clinical criterion will be emphasized, whereas those meeting the criterion will be de-emphasized. A method has been described that identifies gaps in the clinical exposure of students and permits appropriate identification of didactic sessions to create a clerkship more consistent with recommended guidelines.

Clinical Clerkship↗
PubMed1990

Refusal of care and discharging 'difficult' patients from the emergency department.

Patients generally have the right to refuse medical care, a right based on certain legal precedents. Its application in the emergency department leads to difficult decisions for the emergency physician. A model that allows the emergency physician to determine the capacity of a patient to refuse care is presented. Certain types of patients regularly present problems in their treatment. These include psychiatric patients, narcotics abusers, alcoholics, "street people," and some patients with migraine headaches. They represent some of our most difficult decisions because the treatment required for the patient is often clear and the patient refuses care or demands inappropriate care.

Comprehension↗
PubMed1990

[Effect of chronic renal failure and hemodialysis on the pancreas-specific enzyme pattern in the serum].

Amylase concentration in serum is frequently found increased in chronic renal insufficiency without being associated with pancreatic diseases. A prospective study was performed in 71 patients with chronic renal insufficiency undergoing hemodialysis for comparison of different pancreatic enzymes in serum. 7 patients were not considered in this comparative study because of chronic pancreatitis-like-changes in ultrasound. Increased serum concentrations were found for total amylase in 27 patients (42.2%), pancreatic amylase in 26 patients (25.0%), lipase in 50 patients (78.1%), immunoreactive trypsin in 61 patients (95.3%) and for elastase 1 in 7 patients (10.9%). Hemodialysis did not affect any of the investigated pancreatic serum-enzymes. Elastase 1 determination in serum appears superior to the other pancreatic serum-enzymes because of higher specificity, not limited by renal insufficiency. The different serum concentration of elastase 1 and trypsin, which have a similar molecular weight, points towards a completely different clearance mechanism for these enzymes.

Adolescent↗
PubMed1990

Subchronic and chronic toxicity of the new antibiotic cefpirome in rats.

Subchronic and chronic toxicity studies in rats were performed with 3-[(2,3-Cyclopenteno-1-pyridinium)-methyl]- 7-[2-syn-methoximino-2-(2-aminothiazol-4-yl)-acetamido] -ceph-3-em-4- carboxylate (cefpirome, HR 810), a new cephalosporin derivative. In subchronic (14 day) studies cefpirome was intravenously administered in dose levels up to 1500 mg/kg/d with good kidney tolerance. Signs of renal functional impairment were observed (800 and 1500 mg/kg) but histologically no morphological changes could be detected. The chronic intraperitoneal administration (90 day) of cefpirome at dose levels of 400 or 1600 mg/kg/d resulted in some reversible changes in hematology (slight anemia), serum-chemistry parameters (liver), urinalysis (proteinuria), and histopathology (increased numbers and enlargement of lysosomes in proximal tubular epithelia of the kidneys and pigment deposits in follicle epithelia of the thyroids), predominantly in high-dose animals. The "no effect level" is considered to be 100 mg/kg/d in this study.

Animals↗
PubMed1989

[Bismuth aluminate in gastroenterology. Therapeutic effects in chronic erosive Campylobacter pylori-associated gastritis].

14 patients with epigastric pain and chronic active gastritis as well as endoscopically proven erosions underwent an open therapeutic trial with bismuth aluminate (3 x 300 mg/day) for three weeks. Prior to and after treatment five biopsy specimens were taken from the antral mucosa 2 and 4 cm proximal to the pylorus for histological scoring of inflammatory activity and C. pylori detection, for urease quick test (CUT) and culture. Before treatment C. pylori was detected histologically and by CUT in all patients, whereas in culture, C. pylori was not detected in one case. After three weeks of treatment, 9 patients (64%) were C. pylori-negative in culture, and 8 patients (57%) had negative results both on histology and CUT. In 86% (12 patients) chronic erosions were no longer detectable and histological evidence of inflammation was reduced (p less than 0.01). All patients reported symptomatic relief. Complete elimination of C. pylori was observed in just over half the patients. These results confirm the effectiveness of bismuth aluminate in the short-term treatment of chronic active gastritis.

Adult↗
PubMed1989

Ethanol-induced inhibition of leukotriene degradation by omega-oxidation.

omega-Oxidation of leukotrienes is a major pathway in the degradation and inactivation of these proinflammatory mediators. Ethanol inhibited this process in vivo and in vitro. In rat liver in vivo the catabolism of LTE4 to omega-carboxylated leukotrienes was inhibited by 57% by an ethanol dose of 25 mmol/kg body mass administered intragastrically. The site of inhibition was the oxidation of omega-hydroxy-N-acetyl-LTE4 to omega-carboxy-N-acetyl-LTE4 resulting in an accumulation of omega-hydroxy-N-acetyl-LTE4 and of N-acetyl-LTE4. Analogous results were obtained for the oxidative degradation of LTB4 and omega-hydroxy-LTB4 in rat hepatocyte suspensions. Ethanol, at a concentration of 12.5 mmol/l (0.07%; by vol.), caused 68% inhibition of the oxidation of omega-hydroxy-LTB4 by 50% in hepatocyte suspensions. The conversion of omega-hydroxy-LTB4 to omega-carboxy-LTB4 by rat and human liver cytosol was inhibited by ethanol with half maximal concentrations of 100 mumols/l and 300 mumols/l, respectively. Our measurements indicate that direct interference by ethanol of the omega-oxidation of leukotrienes as well as an increased NADH/NAD+ ratio induced by ethanol led to the inhibition of leukotriene degradation. The impairment of leukotriene inactivation in the liver by ethanol may contribute to the development of the inflammatory reaction in acute alcoholic liver disease.

Animals↗
PubMed1989

Glucose 6-phosphate plays a central role in the regulation of glycogen synthesis in a glycogen-storing liver cell line.

Two substrains of the epithelial liver cell line C1I, one storing large amounts of glycogen, the other one being very poor in glycogen were used as a model for studying glycogen synthesis. The glycogen content of glycogen-rich cells doubled during the proliferative phase and remained high in plateau phase although glycogen synthase I activity was not significantly altered during growth cycle and was too low to account for the increase in glycogen. However, the activity of the glucose 6-phosphate (Glc6-P)-dependent synthase rose continuously during growth cycle, and intracellular Glc6-P-concentration increased about 10-fold in log phase cells to 0.72 mumol g-1 wet weight. A0.5 of synthase for Glc6-P was 0.79 mM. It was also found that in contrast to the enzyme from normal liver, glycogen phosphorylase a from C1I cells was inhibited by Glc6-P, the apparent Ki being 0.45 mM. It was concluded that glycogen accumulation in C1I cells was due to stimulation of synthase and inhibition of phosphorylase by Glc6-P. Findings from the glycogen-poor cell line which revealed similar specific activities of synthase and phosphorylase but only low Glc6-P (0.056 mumol g-1 wet weight) supported this conclusion. Addition of glucose to starved cells resulted in a transient activation of synthase in both cell lines. Net glycogen synthesis, was, however, only observed in the cells with a high Glc6-P-content. Thus, modulation of synthase and phosphorylase by Glc6-P and not activation/inactivation of the enzymes seems to play a predominant role in glycogen accumulation in this cell line.

Animals↗
PubMed1989

Peroxidative damage and nephrotoxicity of dichlorovinylcysteine in mice.

Male NMRI mice were treated i.p. with dichlorovinylcysteine (DCVC) in a dosage of 2.5-500 mg/kg-1 and renal cortical slices from naive mice were incubated with 0-125 micrograms/ml-1 DCVC. The effects of DCVC on blood urea nitrogen (BUN), reduced glutathione (GSH) content, malondialdehyde (MDA) production, p-aminohippuric acid (PAH)- and tetraethylammonium (TEA)-accumulation and glucose synthesis (gluconeogenesis) were measured. DCVC depleted GSH in a time- and dose-dependent manner. Depletion of renal cortical GSH by DCVC was more pronounced in the kidney cortex than in the liver. DCVC caused a dose-dependent increase of ethane exhalation and of MDA production in the renal cortex. When animals were kept in a closed system, decrease in oxygen concentration increased the peroxidative damage. No increase of MDA concentration was observed in the liver. Treatment of mice with DCVC induced a dose-dependent increase in BUN and decreased the accumulation of PAH and TEA in renal cortical slices. Pretreatment of mice with aminooxyacetic acid (AOAA) and (+) cyanidanol-3 (CY) caused a significant reduction in DCVC-induced lipid peroxidation and nephrotoxicity. In vitro incubation of renal cortical slices of naive mice with DCVC resulted in a concentration-dependent increase in MDA and a concentration-dependent decrease in the accumulations of PAH, TEA and of gluconeogenesis. In conclusion, the interaction of DCVC and/or its metabolites with membrane lipids may be responsible for lipid peroxidation and nephrotoxicity. The formation of lipid peroxidation products was greater under hypoxic conditions and appeared to be related to the DCVC-induced nephrotoxicity. This data suggests lipid peroxidation as a possible mechanism of DCVC-induced nephrotoxicity.

Animals↗
PubMed1989

Adrenal cortical foci and nodules in Sprague-Dawley rats treated with N-nitrosomorpholine. Light and electron microscopic findings.

Treatment of male Sprague-Dawley rats with N-nitrosomorpholine (NNM) in the drinking water at a dose of 120 mg/l for 7 weeks resulted in a subsequent enhanced development of focal and nodular lesions in the adrenal cortex. Sequential observation revealed that focal lesions in the zona reticularis/fasciculata or the zona glomerulosa developed both earlier and at a significantly higher incidence in animals treated with carcinogen than in untreated controls. Foci observed within or adjacent to the zona glomerulosa were all of pale cell appearance and contained large numbers of electron-dense cytoplasmic granules similar to those observed in normal granulosa cells. The foci and nodules which arose in the zona reticularis/fasciculata were, in contrast, characterized by a reduction or loss of the dense osmiophilic droplets normally seen in the cells of this region of the adrenal cortex, a pronounced increase in pleomorphic mitochondria of atypical appearance and the development of vacuoles.

Adrenal Cortex Neoplasms↗
PubMed1989

Lipid peroxidation: a possible mechanism of trichloroethylene-induced nephrotoxicity.

The purpose of this study was to investigate whether lipid peroxidation plays a role in (TCE) trichloroethylene-induced nephrotoxicity in mice at different oxygen concentrations. Male NMRI mice (25-30 g) were treated i.p. with TCE in a dosage of 125-1000 mg/kg in sesame oil. To determine the TCE-induced depletion of reduced glutathione (GSH) in the kidney cortex and liver tissue, mice were given 1000 mg/kg TCE i.p., then killed between 0 and 6 h after TCE administration and GSH was measured was non-protein sulfhydryls. In another series of experiments, mice were administered 125 to 1000 mg/kg TCE i.p. with or without a 2 h i.p. pretreatment with 1500 mg/kg L-buthionine-S-R-sulfoximine (BSO). Mice were then exposed to a 10, 15, 20 or 100% oxygen atmosphere for 3 h and lipid peroxidation in vivo was measured as exhalation of ethane. Subsequently, mice were killed and malondialdehyde (MDA) generation was measured in the liver and kidney cortex. Ethane evolution was estimated by gas chromatography and MDA was determined as thiobarbituric acid reactive substances. In a further series of experiments mice were treated in the same manner as for ethane and MDA determination and the changes in blood urea nitrogen (BUN) and accumulation of the organic ion p-aminohippurate (PAH) were determined. PAH accumulation by renal cortical slices were measured as the slice to medium (S/M) ratio. Six hours after administration of 1000 mg/kg TCE to mice, GSH was significantly depleted to about 60% of control in the kidney cortex but not in the liver. Three hours after TCE administration, MDA content in the kidney cortex and ethane exhalation increased in a dose-dependent manner only under a 10% oxygen atmosphere. Under the same experimental conditions, MDA content remained unchanged in the liver. BSO depletion of GSH prior TCE administration induced an increase of the MDA content in the kidney cortex and an increase of the ethane exhalation in vivo. At 10% oxygen concentration, TCE induced a dose-dependent increase in BUN and a dose-dependent decrease of PAH accumulation by the renal cortical slices. Thus, the results of the present study suggest that, under hypoxic conditions, lipid peroxidation plays a role in TCE nephrotoxicity.

Animals↗
PubMed1989

Immunocytochemical demonstration of cytochrome c oxidase as a marker for renal oncocytes and oncocytomas.

Using an antibody raised against the mitochondrial enzyme cytochrome c oxidase (EC 1.9.3.1), it was possible to visualize microoncocytomas, oncocytic tubules and even single oncocytes in the renal cortex of rats treated with N-nitrosomorpholine, and to localize the lesions to the collecting duct of the nephron. In human specimens, the antibody also stained oncocytomas and oncocytic tubules in the surrounding macroscopically unaffected cortex. Thus, this antibody may be used for detection as well as for investigation of the development of oncocytic lesions in various species.

Animals↗