[Proceedings: Comparative electron microscopy studies of dog hearts following various forms of ischemia].
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Biomedical subjects
Publications and source records attributed to M Stolte.
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A report is given on all 11-weeek-old male child who, after normal development, suddenly became critically ill and died within 8 hours. The autopsy revealed a rare aetiologically and in its pathogenesis unclarified, always lethal clinical picture of so-called "Arteriopathia calcificans infantum" (ACI). An analysis of 90 published cases revealed an average age of the diseased children of 150.9 days and a mean duration of the disease of 32.8 days; in the large majority of the cases (64.7%), death occurred at the latest within 3 days of the first symptoms. A statistical familial concentration of the disease could neither be shown nor excluded. No indication of an exogenous cause of the disease could be found in the reports on previous parental disease, in the history of the pregnancy, in the placenta findings, the case history of the children themselves or in the clinical data. The pathological-anatomical substrate of ACI comprised a calcification, predominantly of the muscular arteries, and located at the boundary between the intima and the media, within the course of the internal elastic lamina. Depending upon the stage of the disease, we first see a fragmentation of the elastic fibres, calcific dust deposits, calcific plaques and the complete replacement of the media by concentric, in part coarsely distingrating, calcific rings. As a result of proliferation of the intima a marked constriction of the lumen occurs in the diseased arteries. Most frequently involved at 90% are the coronary arteries. The genesis of this disease has a considerable similarity to experimental calciphylactic arteriopathy, but no sensitizer mechanism can be demonstrated for ACI. Morphological similarities also exist to generalised elastorrhexis, which is also very rare. There is probably a causal relationship between the two diseases. In a hypothesis on the aetiology of the ACI, it is suggested that this disease may be triggered by a congenital enzyme defect localised in the myointimal cells of the vascular wall. These cells produce incorrectly structured mucopolysaccharides, collagen and elastic material with pathologically increased calcipexy.
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Nonneoplastic disorders of the parotid gland, such as chronic recurrent parotitis, asymptomatic gland enlargement, or salivary fistulae, are therapeutic problems. Surgical removal of the gland is often difficult, since scar tissue may be present in these benign diseases. Therefore, alternative treatment methods, such as ligation of Stensen's duct, irradiation, or tympanic neurectomy, have been used to induce atrophy of gland parenchyma. This goal can also be attained by intraluminal duct occlusion, which involves instillation of a resorbable protein solution into the duct system, a procedure similar to sialographic injection. Intraluminal duct occlusion is a simple technique with rapid onset of atrophy and low morbidity, and with its use options remain open for other treatment modalities. The authors have used this method in the treatment of various diseases in 26 parotid glands and one submandibular gland. Their experience, which includes three-year patient follow-up data, suggests that this technique may be a useful alternative to salivary gland resection in certain nonneoplastic diseases.
In an experiment testing the resorption of Poly-l-lactate in the back muscles of Cara rats a foreign body sarcoma occurred in two rats. 20 months after implantation of a body of high molecular weight poly-l-lactate a malignant fibrous histiocytoma developed in one rat. A soft tissue tumor, which was classified according to the immune-histiochemical analysis as a neurogenic sarcoma, developed 23 months after the implantation of a body of injection-casted poly-l-lactate of high molecular weight in a second rat.
Sarcocystis dubeyella n. sp. and S. phacochoeri n. sp. from muscle fibers of the skeletal musculature of two warthogs in South Africa are described by light and and electron microscopy. Sarcocystis dubeyella sarcocysts are macroscopic (up to 12 mm long and 1 mm wide), with a parasite-induced encapsulation of the host muscle fiber in which the plasma membrane of the latter remained unaltered. The sarcocyst wall is characterized by evenly arranged, irregularly semicircular or rectangular villar protrusions (5.0 x 2.8-11.0 microns) with indented margins and no specific content. Sarcocystis phacochoeri formed filiform microcysts (up to 4 mm long and 0.13 mm wide). Its cyst wall is provided with tightly packed, molarlike villar protrusions (1.6-3.3 x 1.7-3.3 microns), with smooth margins, hollow on one side, and with longitudinal condensations of the fine granular matrix at various locations in the interior.
In this randomized, multicenter trial, we evaluated the effectiveness and side effect profile of a modified omeprazole-based triple therapy to cure Helicobacter pylori infection. The control group consisted of patients treated with standard dual therapy comprising omeprazole and amoxicillin. One hundred and fifty-seven H. pylori infected patients with duodenal ulcers were randomly assigned to receive either a combination of omeprazole 10 mg, clarithromycin 250 mg and metronidazole 400 mg (OCM) given three times daily for 10 days (n = 81), or a combination of omeprazole 20 mg and amoxicillin 1 g (OA) given twice daily for 14 days (n = 76). Prior to treatment and after 2 and 6 weeks, gastric biopsies from the antrum and corpus were obtained for histology and H. pylori culture. H. pylori infection was cured in 97.4% after OCM and in 65.8% after OA in the per-protocol analysis (p < 0.001) (intention-to-treat analysis: 93.4% and 63.2%, respectively). H. pylori was successfully cultured in 122 patients (77%). The overall rate of metronidazole resistance was 19.7% (24/122), no primary resistance to clarithromycin or amoxicillin was found. In the OCM group, all patients infected with metronidazole-sensitive H. pylori strains (n = 51) and those infected with strains of unknown susceptibility to metronidazole (n = 14) were cured (100%), while 77% (10/13) of those harboring metronidazole-resistant strains were cured of the infection (p = 0.36). Side effects leading to premature termination of treatment occurred in 2.5% of the patients in the OCM group and in 1.4% of the OA group. We conclude that combined treatment with omeprazole, clarithromycin and a higher dose of metronidazole is highly effective in curing H. pylori infection, and that this regimen remains very effective in the presence of metronidazole-resistant strains.
This prospective study was designed to validate a novel biopsy urease test as well as a simplified 13C-urea breath test for the detection of Helicobacter pylori. In addition, the hypothesis was tested that both the reaction velocity of the urease test and the 13CO2 excess of the urea breath test may allow a prediction of the severity of gastritis. Seventy dyspeptic patients with unknown H. pylori status were included. The H. pylori status was assessed by means of culture and histology after Warthin and Starry stain. One antral and one body biopsy specimen were separately analyzed by the novel biopsy urease test (HUT). Also, a 13C-urea breath test using 75 mg 13C-labelled urea and orange juice as test meal was performed in all patients. Forty-seven patients (67%) were H. pylori positive as judged from histology and culture. In 46 patients, H. pylori infection was also detected by the novel biopsy urease test and by the urea breath test as well (sensitivity 97.9%). False-positive results were not observed by either method (specificity 100%). Both the reaction velocity of the urease test and the 13CO2 excess of the breath test significantly correlated with H. pylori density and grade and activity of gastritis. The determination coefficients, however, indicated that both methods allow a reliable prediction of the severity of gastritis only in about 40-50% of the patients. In conclusion, the novel biopsy urease test and the simplified 13C-urea breath test proved to be highly accurate in diagnosing H. pylori infection. Despite a significant correlation, neither the reaction velocity of the urease test nor the 13CO2 excess of the breath test are clinically useful for the prediction of the severity of gastritis.
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In 110 patients with unknown Helicobacter pylori status and without anti-bacterial treatment submitted for routine endoscopy of the upper gastrointestinal tract biopsies were taken from the antral and body mucosa, which were assessed for H. pylori colonisation and/or gastritis by an urease test (Jatrox H. p.-Test), microscopy after methylene-blue staining of a mucosal smear, specific culture and histology (stains: haematoxylin & eosin and Warthin-Starry). In addition, a simplified 13C-urea breath test was validated. A complete set of data was available from 104 patients (64 women - 40 men, median of age: 55 years [range: 17-92 years], H. pylori positive histologically and/or culturally [goldstandard]: n = 67). The test criteria sensitivity, specificity, positive and negative predictive value were calculated to be 100%/100%/100%/100% for the urease test, 76.1%/100%/100%/69.8% for microscopy of a mucosal smear, and 92.5%/97.3%/98.4%/88.1% for 13C-urea breath test (two-point measurement). Statistical analysis demonstrated highly significant (p < 0.0001) correlations between the reaction velocity of the urease test, the histologically visible degree of Helicobacter pylori colonisation and the differences of the delta-values of the 13C-urea breath test on the one hand and between grade and activity of gastritis as well as between the gastritis and activity scores, respectively, and the semi-quantitatively categorized results of the urease test, the histological degree of H. pylori colonisation and the 13C-urea breath test on the other hand.(ABSTRACT TRUNCATED AT 250 WORDS)