Unsuccessful treatment of CAPD peritonitis caused by Alcaligenes xylosoxidans subsp. denitrificans.
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Biomedical subjects
Publications and source records attributed to M Roth.
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Budesonide is a topical steroid which after intestinal absorption is rapidly degraded into inactive metabolites in the liver. Its systemic bioavailability is only 10-15%. In the present open trial the efficiency and safety of oral pH-modified release budesonide were assessed in patients with active Crohn's ileocolitis. This report describes the results of the first 30 of 78 patients. After 6 weeks of treatment with 3 x 3 mg budesonide/day 67% of the patients were in clinical remission. Typical steroid-related side effects were observed in only one patient. Budesonide therefore seems to be suited as an alternative for classical steroids in patients with Crohn's ileocolitis. Its clinical efficacy is comparable with classical steroids but it's rate of steroid-related side effects is lower.
The crystal structure of the ferredoxin I from the sulfate-reducing bacterium Desulfovibrio africanus (DaFdI) has been solved and refined by X-ray diffraction. The crystals are orthorhombic with a = 96.6 A, b = 58.1 A, and c = 20.7 A, space group P2(1)2(1)2, and two ferredoxin molecules per asymmetric unit. The initial electron density map has been obtained by combining phasing by molecular replacement methods, anomalous scattering, and noncrystallographic averaging. The final crystallographic R factor is 0.182 with 10-2.3 A resolution data. In parallel, the amino acid sequence was redetermined. This showed that DaFdI contains 64 residues (instead of 61) including one free cysteine, one histidine, and one tryptophan in the C-terminal part of the molecule. The current molecular model includes the two molecules of the asymmetric unit, 67 water molecules, and one sulfate ion. The DaFdI overall folding very closely resembles that of ferredoxins of known structure. Comparisons with the single cluster ferredoxins from Desulfovibrio gigas and Bacillus thermoproteolyticus show that the presence or the absence of a disulfide bridge does not significantly affect the folding of the other half of the molecule, including the characteristic alpha-helix of the single cluster ferreddoxins. Like other ferredoxins or analogs, the [4Fe-4S] iron--sulfur cluster presents, at 2.3 A resolution, a cubane-like geometry. By contrast, its immediate environment is different as it includes, besides the four cysteic sulfur ligands, the sulfur atom of the free cysteine. This sulfur atom, which is buried within the protein, is in van der Waals contact with one labile sulfur of the cluster and one liganded cysteic sulfur. The association of a [4Fe-4S] cluster with one free cysteic sulfur is similar to that previously found in both X-ray structures of Azotobacter vinelandii and Peptococcus aerogenes [Stout, C. D. (1989) J. Mol. Biol. 205, 545-555; Backes, G., et al. (1991) J. Am. Chem. Soc. 113, 2055-2064]. Chemical sequence analysis suggests that this characteristic [4Fe-4S] cluster sulfur environment is widely distributed among ferredoxins.
While normal adult tau protein is found typically in axons, paired helical filament (PHF) tau has been shown immunohistochemically to be in the somatodendritic compartment in Alzheimer's disease (AD). The small amount of PHF-tau (8-11%) found in white matter with immunochemical methods is shown here by immunoelectron microscopy to be located in axons. It is localized to straight filament variants of PHFs. The small amount of PHF-tau in white matter, therefore, appears not to result from the contamination of immunochemical preparations but to be an integral constituent of affected axons in AD.
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DNA topoisomerases have been purified from Streptomyces noursei. DNA gyrase and topoisomerase I show a differential sensitivity against quinolones and coumarins compared to the E. coli enzymes. Streptomyces gyrase is resistant to much higher levels of various drugs than is the E. coli enzyme. The observed differences between the gyrases from streptomycetes and E. coli are discussed in the light of present literature data.
Growing evidence suggests that cytokine expression is influenced by locally produced mediators, thus modifying the pluripotential effects of cytokines toward a tissue-specific inflammatory reaction. The granulocyte inhibitory protein (GIP), a 23-kDa protein found to be significantly overexpressed in patients with chronic renal failure, increases autocrine transcription and expression of interleukin (IL) 6 and IL-8 in human mesangial cells. Moreover, GIP alone induced the transcription of c-jun mRNA; however, in combination with IL-6, it stimulated de novo synthesis of DNA and the transcription of both c-jun and c-fos genes. The data suggest that the overall effect of GIP results in the modulation of the glomerular response to injury and contributes to the progression of glomerulosclerosis.
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The nervous supply of the vascular wall in its organ entirety represents the felt-like 'nervous skeleton'. Its growth is more vulnerable than that of any other tissue component of the developing vessel wall. Selective growth impairment of the vascular nervous skeleton should result in developmental vascular stenosis. Escape of the epithelial or smooth muscle cells from the confines of the nervous skeleton should be taken into account as a possible common denominator of carcinogenesis and atherogenesis.
OBJECTIVE: Human mononuclear cells from a previously sensitized donor generate procoagulant activity (PCA) following stimulation with purified protein derivative (PPD). Lymphocytes of tuberculous pleural effusions are also highly responsive to PPD stimulation. We examined the influence of cryopreservation on lymphocytes following stimulation with PPD. DESIGN: Peripheral blood lymphocytes of 5 healthy PPD skin test positive subjects were incubated with either PPD, thromboplastin, or concanavalin A (Con A) at concentrations of 0, 1, and 10 micrograms/ml. PCA was determined by measuring the recalcification time. Tests were repeated following cryopreservation for 4 weeks. RESULTS: Incubation of fresh lymphocytes led to a dose dependent shortening of recalcification time: PPD (0-1-10 micrograms/ml: 100-84-65%), thromboplastin (0-1-10 micrograms/ml: 100-85-62%), and Con A (0-1-10 micrograms/ml: 100-85-42%). These results were highly reproducible when tests were repeated 6 weeks later. Cryopreservation did not significantly affect the expression of PCA following incubation with PPD and with thromboplastin. In contrast, cryopreservation significantly diminished the degree of Con A generated PCA. CONCLUSION: Cryopreservation and storage of human lymphocytes is possible without alteration of PCA expression following their incubation with PPD or thromboplastin.
Rheumatoid arthritis (RA) usually requires lifelong treatment and sometimes surgery. Metacarpophalangeal joint (MCPJ) implant arthroplasty is one surgical treatment for patients with severe RA malformation of the finger joints. Although not a cure, MCPJ implant arthroplasty can enhance patients' quality of life by improving their performance of independent activities of daily living. The silicone implant acts as a spacer until tendons and connective tissues are able to control the joint's functions. Comprehensive preoperative and postoperative patient teaching and aggressive physical therapy are needed to achieve optimal outcomes in patients who undergo this surgical procedure.
Antibodies to different phosphorylated and non-phosphorylated tau epitopes have been used to identify three histologically distinct types of neurofibrillary tangles in Alzheimer's disease. Intracellular tangles (Type 1) were identified by antibodies recognizing epitopes throughout the tau molecule, including the NH2-terminus. Compact extracellular tangles (Type 2) were characterized by the loss of NH2-terminal immunoreactivity and retention of other tau epitopes. Dispersed extracellular tangles (Type 3) were characterized by the presence of epitopes associated with the microtubule binding region and the COOH-terminus. These three types of tangles, found in situ in hippocampus, could be created experimentally by proteolytic treatment of brain sections. These findings suggest that three stages of neurofibrillary degeneration can be understood as a sequential stripping of paired helical filaments in which the loss of amino-terminus epitopes, followed by loss of phosphorylated epitopes, results in the appearance of dispersed extracellular tangles containing PHF-core epitopes.
The aim of this study was to compare the intensity of typical late complications in diabetic patients (n = 65, 28 type I, 37 type II) who were not on glycoside drugs with low vs. high serum levels of digoxin-like immunoreactive factor (DLIF: group I, n = 42, DLIF < or = the detection limit of 0.2 ng ml-1; and group II, n = 23, mean +/- SEM: 1.17 +/- 0.31 [0.25-4.96] ng ml-1). For detection of nephropathy, urinary albumin excretion (24 h) and creatinine clearance tests were used. For coronary heart disease a questionnaire and standard ECG; for peripheral occlusive vascular disease a questionnaire; for eye disease a fundoscopy; for neuropathy a neurological score system; and for autonomic neuropathy a standardized test battery was employed. Patients with high DLIF levels showed better test results in vibratory perception (95.7 +/- 1.5 vs. 82.8 +/- 3.8%, normal finding = 100%, 2p = 0.016), had better percentile localizations concerning maximal pupillary area in darkness (28.4 +/- 6.6 vs. 8.1 +/- 1.8%, 2p = 0.0004), contraction velocity at 1 s (21.5 +/- 5.8 vs. 8.0 +/- 2.2%, 2p = 0.012), and dilation velocity at 6 s (23.0 +/- 6.8 vs. 10.5 +/- 2.5%, 2p = 0.041), had less retinopathy (with retinopathy: 26.1% vs. 64.3%, 2p = 0.0028), and better percentile localizations in the respiratory sinus arrhythmia test (68.4 +/- 7.3 vs. 44.1 +/- 4.9%, 2p = 0.0064). There was no difference concerning nephropathy, blood pressure, coronary heart disease and peripheral vascular disease. Separate analysis according to the type of diabetes confirmed the results in each group.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac hypertrophy is largely due to cardiac fibroblast growth and increased synthesis of extracellular matrix. This study has investigated the contribution of the vasoactive hormone, angiotensin II, toward this hypertrophic process. We have demonstrated that cultures of adult rat cardiac fibroblasts express AT1 but not AT2 receptors for angiotensin II. The ability of angiotensin II to stimulate phosphoinositide catabolism and to elevate intracellular calcium concentrations in these cells was blocked by losartan, a specific AT1 receptor antagonist, but not by the AT2 receptor antagonist CGP 42112. Exposure of adult cardiac fibroblasts to angiotensin II resulted in the induction of several growth-related metabolic events including c-fos protooncogene expression and increased synthesis of DNA, RNA, and protein. Angiotensin II was also found to induce collagen type I, alpha 1 chain transcript expression in cardiac fibroblasts as well as the synthesis and secretion of collagen by these cells. The data demonstrate that angiotensin II, via AT1 receptors, can stimulate cardiac fibroblast growth and increase collagen synthesis in cardiac tissue. Thus, angiotensin II may contribute toward the development of cardiac hypertrophy in conditions of hypertension that are associated with elevated concentrations of angiotensin II.
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A case of Allergic Fungal Sinusitis successfully controlled with oral corticosteroids followed by endoscopic sinus surgery is presented. The clinical diagnosis of AFS is emphasized. Endoscopic sinus surgery is preferable to open sinus techniques since the underlying mucosal disease is reversible. A prospective study is needed to determine the most appropriate treatment for this unique clinical disorder.
Case reports are given of a deforming ankylosis of the distal interphalangeal joints in two juvenile cattle of the breed German Simmental. In one animal all distal interphalangeal joints were affected; in the second animal the coffin joints of the forelimbs and the lateral coffin joints of the hindlimbs were ankylosed or in the process of being bridged by bone. The condition was painful, resulting in lameness and loss of weight. Clinical, radiological and pathological-anatomical features are described.
Although platelet-activating factor has been implicated in the pathogenesis of neutrophil-induced reperfusion injury, it has other mechanisms of direct deleterious hemodynamic effect. In this study we evaluated the definitive role of platelet-activating factor in myocardial reperfusion injury. Porcine hearts that underwent 60 minutes of normothermic ischemia with cardioplegia and 60 minutes of reperfusion under cardiopulmonary bypass were divided into three groups according to the methods of 15 minutes of controlled reperfusion: whole blood reperfusion group (n = 6), leukocyte-depleted reperfusion group (n = 6), and platelet-activating factor receptor antagonist (CV-3988) group (n = 6). At 60 minutes of reperfusion, the percentage of recovery of maximum slope of the pressure-volume relationship measured with intraventricular balloon, malondialdehyde value in coronary sinus blood, tissue adenosine triphosphate, and percentage of spontaneous defibrillation were evaluated. The receptor antagonist group showed significantly better recovery of maximum slope of the pressure-volume relationship than did the whole blood reperfusion group. Moreover, the receptor antagonist group showed significantly less release of malondialdehyde in the coronary sinus, higher values of adenosine triphosphate in the myocardium, and a higher percentage of spontaneous defibrillation than did the whole blood reperfusion group. On the other hand, the leukocyte-depleted reperfusion group showed no significant differences of maximum slope of the pressure-volume relationship, malondialdehyde, adenosine triphosphate, or spontaneous defibrillation as compared with the whole blood group. These results suggest that platelet-activating factor receptor antagonist attenuated severe damage in whole blood reperfusion of the myocardium as compared with leukocyte-depleted reperfusion, which also suggests that platelet-activating factor may play a more important role in myocardial reperfusion injury than do neutrophils.