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Biomedical subjects

H Weber

Publications and source records attributed to H Weber.

At least 127 records · Page 7Linked to original sources
PubMed1997

Epidemiological features of Adamantiades-Behçet's disease in Germany and in Europe.

The German Registry of Adamantiades-Behçet's disease was founded in 1990 in Berlin and it provides current data on the epidemiology, the clinical manifestations and the course of the disease in Germany on a continuous basis. A total of 218 patients, including 89 German and 100 Turkish patients, had been reported to the German Registry until October 1997. One hundred and ninety-six patients fulfilled the criteria of the Behçet's disease classification tree. The prevalence of the disease evaluated in Berlin-West was 1.68/100,000 in 1989 and had risen to 2.26/100,000 by 1994. The median age of onset was 25 years (range 5 to 66 years; German-Turks, ns). Juvenile disease was recorded in 6.9% of patients. The complete clinical picture according to the criteria of the International Study Group of Behçet's Disease developed in 15.5 months. The interval between onset of the disease and diagnosis was 35 months, which was significantly longer than the duration of the development of the complete clinical picture (p < 0.0001). The disease was diagnosed later in German (48.5 months) than in Turkish patients (25.5 months, p = 0.003). While German patients presented an equal male-to-female ratio, a male predominance was shown in Turkish patients (M:F 2.1:1, p = 0.022). Familial occurrence was detected in 2.0% of German and 15.9% of Turkish patients (p = 0.013). The frequencies of major clinical manifestations were: oral ulcers 99%, skin lesions 76%, genital ulcers 75%, ocular manifestations 59%, arthritis 59%, and positive pathergy test 52%. Clinical differences between German and Turkish patients were only found in the frequency of ocular lesions (48% vs. 66%, p = 0.025). Oral ulcers were with 72% the most common onset symptom of the disease followed by erythema nodosum (9%), uveitis (7%), arthritis (7%), genital ulcers (3%), superficial thrombophlebitis (2%) and papules/sterile pustules (2%). Uveitis and erythema nodosum as onset symptoms shortened the median interval to diagnosis to 1.5 and 15 months, respectively, while arthritis delayed diagnosis (43.5 months; p = 0.029). A severe course developed in 25% of the patients; irreversible retinal vasculitis to blindness in 15%, sterile meningoencephalitis in 8%, severe arthritis in 5%, hemoptysis in 2%, lethal outcome in 2% and bowel perforation in 1%. The relative risk of HLA-B5 positive German natives developing the disease. HLA-B5 was confirmed as a marker of severe prognosis. Cardiolipin autoantibodies were associated with cutaneous vasculitis and superficial thrombophlebitis was correlated with systemic vessel involvement.

Adolescent↗
PubMed1997

[Prevalence of hepatitis G virus genome in blood donors].

The relevance of the GB virus C/hepatitis G virus (GBV-C/HGV) in blood banking results from its high prevalence in blood donors and the fact that it is present at a very high percentage (18%) in polytransfused and hemophiliac patients. Since there is no assay available for serological testing, we developed a sensitive PCR utilizing newly designed NS3 primers to investigate the prevalence in blood donors in Hessia. Testing 1,143 accepted blood donors with alaninaminotransferase (ALT) concentrations < 45 U/l we found 15 (1.3%) positive for GBV-C/HGV RNA. From 507 donors settling in urban Frankfurt areas, 10 (2.0%) were positive. Of those donors settling in rural hessian areas only 5/635 (0.8%) tested positive. By testing 100 excluded donors with ALT values > 45 U/l, 3% turned out to be positive. In 4 out of 9 recipients of GBV-C/HGV-positive blood products we detected the donor viral RNA as proved by sequencing and phylogenetic analysis. The virus was transmitted to 3 recipients by erythrocytes and to 1 recipient by platelets. Testing family members of the GBV-C/HGV-positive blood donors we could not detect any intrafamilial transmission.

Blood Banks↗
PubMed1996

Thrombin receptor activation elicits rapid protein tyrosine phosphorylation and stimulation of the raf-1/MAP kinase pathway preceding delayed mitogenesis in cultured rat aortic smooth muscle cells: evidence for an obligate autocrine mechanism promoting cell proliferation induced by G-protein-coupled receptor agonist.

Treatment of quiescent rat aortic smooth muscle cells with either alpha-thrombin or a thrombin receptor-derived agonist peptide (SFLLRNP) resulted in pronounced increases in [3H]thymidine incorporation that were concentration dependent and reached a maximum of approximately 15-fold above serum-starved controls. However, in contrast to FBS, PDGF-BB, or basic fibroblast growth factor (bFGF), that initiated DNA synthesis promptly after 16-19 h, thymidine incorporation in response to thrombin was delayed by an additional 3-6 h. Delayed mitogenesis correlated with the appearance of a potent mitogenic activity in conditioned media samples obtained from thrombin-stimulated rat aortic smooth muscle cells, as assayed using Swiss 3T3 fibroblasts. This activity was not inhibited by neutralizing antibodies directed against PDGF or bFGF. Furthermore, in the Swiss 3T3 cells, simple addition of either alpha-thrombin or SFLLRNP failed to elicit a significant mitogenic response. In signal transduction studies, both thrombin and SFLLRNP treatment led to rapid tyrosine phosphorylation of proteins with apparent molecular masses of 42, 44, 75, 120, and 190 kD, respectively, as assessed by antiphosphotyrosine immunoblotting. The overall pattern of protein tyrosine phosphorylation was distinct from that observed after PDGF-BB addition. Activation of Raf-1 and the mitogen-activated protein (MAP) kinases p44mapk and p42mapk was also observed. However, the time course and duration of Raf-1/MAP kinase activation after thrombin stimulation were similar to those elicited by PDGF-BB. Taken together, our results indicate that thrombin-stimulated vascular smooth muscle proliferation is delayed and requires the de novo expression of one or more autocrine mitogens. In addition, the rapid induction of discrete intracellular signaling mechanisms by thrombin, including the Raf-1/MAP kinase pathway, appears to be insufficient alone to promote vascular smooth muscle cell mitogenesis.

Animals↗
PubMed1996

Effects of procues on error rate and reaction times of antisaccades in human subjects.

In a gap paradigm, where the saccadic reaction times are usually short, the number of express saccades can be further increased and their latency decreased when a valid transient peripheral cue is given 100 ms before target occurrence. In the present study we measured the saccadic reaction times of seven human subjects who had been instructed to make antisaccades (saccades to the side opposite to stimulus presentation) in the gap paradigm. In the first experiment, we presented a 100% valid cue with 100 ms cue lead time. To explore whether the cue reduced the reaction times of the antisaccades, the cue was always presented on the opposite side to where the stimulus occurred (stimulus direction was randomized between 4 degrees to the left and right), and it was thus indicated in each trial to which side the antisaccade was required (procue). In the second set of experiments the cue was consistently presented on either the left or the right side in two different blocks; it was thus noninformative with respect to the direction of the antisaccade. In the first experiment, a significant increase in mean reaction times of correct antisaccades and a considerable increase in erratic prosaccades to the stimulus were obtained compared with a control session with no cue. In the two experimental blocks with noninformative cues, the reaction times of correct antisaccades were decreased when cue and stimulus were on at the same side, while large numbers of erratic prosaccades were again obtained when cue and stimulus were presented on opposite sides. These results suggest that the orienting mechanism elicited by a transient peripheral cue relates to the command and to the decision to make a pro- versus an antisaccade. Since the subjects reported that they could not prevent, or, moreover, in some cases did not even realize that they were making erratic prosaccades, we conclude that this orienting mechanism occurs automatically, being largely beyond voluntary control.

Attention↗
PubMed1996

Lesions of the Achilles tendon. A sonographic, biomechanical and histological study.

Thirty-four Achilles tendons were explanted post-mortem. The explanation took place less than 24 h after death. The tendons were examined by means of ultrasonography and after explanation assessed histologically and biomechanically. In the sonograms 19 changes in echogenicity were noted. Changes in form with an increase in the diameter of the tendon of up to 10 mm (compared with the contralateral side) were found in 6 tendons. The changes in echogenicity and form were found most frequently 2-4 cm from the insertion of the tendon at the os calcis. At a speed of 5 mm/min, the average force needed until rupture occurred was calculated as 27.6 N/mm2. The tear was located on average 29.7 mm from the bony insertion of the tendon at the calcaneus. Histologically, necroses could be found most frequently in all regions of the tendon, followed by scars and fissures. When there were differences of more than 25% in tensile strength between the right and left sides, there was a histological change in the weaker tendon at the site of the tear. Sonographic changes in form pointed to histological lesions in this region. Changes in the echogenicity led to the detection of degenerative changes of the tendon, but they have to be analysed carefully, as they are prone to artefacts. There was not statistically relevant correlation either with regard to tensile strength or to the site of the rupture for sonographically proven changes in the area of the rupture. However, when there was a sonographically abnormal finding in the course of a tendon, the tendon tore at an earlier point than those exhibiting no abnormality. Sonography proved to be a useful method in the detection of degenerative lesions of tendons. A direct influence on the biomechanics of the tendon could not be found.

Achilles Tendon↗
PubMed1996

Sucrose metabolism during cotyledon development of Vicia faba L. is controlled by the concerted action of both sucrose-phosphate synthase and sucrose synthase: expression patterns, metabolic regulation and implications for seed development.

The roles of sucrose-phosphate synthase (Sps) and sucrose synthase (Sus) in developing embryos of Vicia faba have been characterized. In the cotyledons the expression of both Sps and Sus is initiated in cells differentiating into storage tissue. This stage is characterized by a switch in the carbohydrate state from a high to a low hexoses to sucrose ratio. The carbohydrate state was found earlier to be controlled by seed coat-associated invertase. During cotyledon development the Sps-enzyme undergoes a cycle of deactivation and reactivation: the activated state is associated with the prestorage phase, desiccation and germination and the deactivated state with the storage phase. Sus activity is associated with the storage phase. Sps and Sus are differentially influenced by free sugars. Feeding hexoses to storage phase cotyledons increases levels of Sps-mRNA but not Sus-mRNA, Sps activity and Sps activation state and impairs storage functions evidenced by an increased sucrose to starch ratio and a downregulation of storage protein legumin B-mRNA. Sus enzyme activity is inhibited by free hexoses in vitro. It is proposed that the changing carbohydrate state during cotyledon development controls the ratio of Sps to Sus. Sps may have some significance for the initiation of the storage process possibly decreasing hexoses and/or increasing sucrose. The relevance of the changing carbohydrate state with respect to development and storage processes is discussed.

Base Sequence↗
PubMed1996

Hyperthermia induces heat shock protein expression and protection against cerulein-induced pancreatitis in rats.

BACKGROUND & AIMS: Heat shock proteins (HSPs) are part of the cellular stress response machinery. HSPs are expressed in the pancreas, but their protective potential has not been thoroughly investigated. The aim of this study was to characterize the pancreatic heat shock response both in vitro and in vivo and to study whether this response has protective effects. METHODS: For in vitro experiments, rat pancreatic acini were exposed to heat and protein expression was analyzed through 35S-methionine labeling or Western blots. In vivo, cerulein pancreatitis was induced after whole body hyperthermia (42 degrees C). RESULTS: After thermal stress (42 degrees C), acini increasingly expressed five proteins of 92, 72, 59, 58, and 30 kilodaltons, with HSP. 70 the most strongly induced 72-kilodalton protein. In vivo, increased expression of four isoforms of pancreatic HSP-70 was found. Isoform-specific antibodies identified the inducible and constitutively expressed (HSC-70) isoform of HSP-70. HSP-60 was also weakly induced after hyperthermia. Concomitantly, cerulein-induced pancreatic organ damage was greatly reduced after whole-body hyperthermia. The time course and strength of HSP induction correlated well with the time course and degree of protection against cerulein-induced pancreatitis. CONCLUSIONS: A causal relation between hyperthermia-induced HSP expression and organ protection seems possible.

Animals↗
PubMed1996

Urine delivery of cyromazine for suppressing house and stable flies (diptera: muscidae) in outdoor dairy calf hutches.

In a series of 4 trials, dairy calves housed in outdoor hutches were administered technical cyromazine daily at rates of 0, 0.1, 0.5, and 1.0 mg/kg body weight. Cyromazine was excreted primarily in the urine. The 2 highest rates prevented the development of immature stages of both the house fly, Musca domestica L., and the stable fly, Stomoxys calcitrans (L.). Analysis of calf body tissues for cyromazine and its metabolite, melamine, indicated that highest combined residues ( < or = 0.35 ppm) were found in the kidney. Lower levels of residues were found in kidney fat and liver, and occasionally in round muscle.

Administration, Oral↗
PubMed1996

Prediction of permanent work disability in a follow-up study of early rheumatoid arthritis: results of a tree structured analysis using RECPAM.

The objectives of this study are: (a) to determine the occurrence of permanent work disability (PWD) in early rheumatoid arthritis (RA); (b) to identify prognostic groups of patients; (c) to assess the employment rates for these groups over time. Seventy-three gainfully employed consecutive out-patients with early RA (> or = 5 ARA 1958 criteria, disease duration < or = 12 months) at time one (T1) were re-examined at time two (T2) after a mean follow-up of 6 yr (S.D. +/- 2 yr). Potential risk factors, identified at T1, for PWD at T2 were entered in a tree structured survival analysis using RECPAM (RECursive Partition and AMalgamation). Cumulative 3 yr employment rates (3-yrER +/- S.E.M.) were computed from the resulting Kaplan-Meier curves. At T2, PWD occurred in 27 of the 73 patients (37%). The fastest decline in the employment rate was found within the first 3 yr of the disease onset, with a 3-yrER reduced to 73 +/- 5%. The group with the poorest prognosis (n = 14; 3-yrER 14 +/- 9%) was defined by age > or = 50 yr with either ESR > or = 60 mm/h or the combination of modified functional class (1-7) > or = 4 with a disease duration > or = 7 months. An intermediate group (n = 38; 3-yrER 79 +/- 6%) was defined by (a) age > or = 50 yr and low or moderate disease activity, (b) age < 50 yr and more strenuous job-related physical requirements, (c) age < 50 yr and less strenuous work, but joint count > or = 15. No case of PWD occurred in 21 individuals aged < 50 yr with a joint count < 15 and less physically demanding jobs. PWD occurs early in a substantial number of patients with RA. RECPAM defines risk profiles that can readily be applied in actual clinical situations and allow an estimation of the risk of PWD at different time points using the resulting Kaplan-Meier curves.

Adult↗
PubMed1996

Cobalt chromium molybdenum metal combination for modular hip prostheses.

The development of a metal combination for modular hip systems was motivated by the following observations: (1) wear particles from polyethylene acetabular components can lead to a foreign body reaction and late aseptic loosening and (2) well designed all metal hip prostheses had very low wear rates, usually causing no osteolytic problems. The following challenges had to be met: (1) metal alloy with the maximum wear resistance; (2) the optimal clearance (difference in diameter) between 28-mm ball head and acetabular component; and (3) equipping modern, modular hip systems with metal combinations while maintaining compatibility with existing components. The realization of a metal combination consisted of the stable anchoring of a standard metal lining in a polyethylene insert that, combined, is intended to provide adequate load transfer and fit to either the bone cement bed or the titanium shell. The metal lining is manufactured from a carbide containing cobalt chromium molybdenum wrought alloy (Protasul-21WF). From 1988 to 1995, approximately 40,000 metal combinations (Metasul) were implanted. From these, 44 single components, with a maximum time in situ of 5.5 years, were retrieved and examined. The total linear wear rate averaged 2 to 5 micrometers per year per component after the initial conditioning phase. Under these conditions, particle induced late aseptic loosening is not to be expected.

Biomechanical Phenomena↗
PubMed1996

Renal and depressor activity of C-natriuretic peptide in conscious monkeys: effects of enzyme inhibitors.

The depressor and renal responses to C-type natriuretic peptide (CNP) were determined in conscious cynomolgus monkeys treated with vehicle or inhibitors of neutral endopeptidase EC 3.4.24.11 (NEP) and angiotensin-converting enzyme (ACE). The NEP inhibitor SQ 28603 (100 mumol/kg intravenously, i.v.) significantly (p < 0.05) enhanced the depressor responses to 1 and 10 nmol/ kg i.v. CNP from -2 +/- 3 to -22 +/- 10 mm Hg and from -16 +/- 4 to -66 +/- 4 mm Hg, respectively. SQ 28603 also significantly increased the cyclic GMP responses to 1 and 10 nmol/kg CNP from 1.4 +/- 1.6 to 11.0 +/- 2.0 nmol/2 h and from 4.2 +/- 0.5 to 53.3 +/- 12.1 nmol/2 h, respectively. Furthermore, the NEP inhibitor significantly increased the natriuretic activity of 1 and 10 nmol/kg i.v. CNP from 235 +/- 99 to 760 +/- 60 microEq/2 h and from 399 +/- 208 to 1,036 +/- 79 microEq/2 h, respectively. A positive correlation between the cumulative natriuretic and cyclic GMP responses suggested a cyclic GMP-mediated mechanism. These data are consistent with the protection of CNP from degradation by renal NEP. Inhibition of ACE by 100 mumol/kg i.v. captopril did not significantly alter the depressor or renal activities of 1 nmol/kg of CNP, neither did it alter the potentiation of CNP activity by SQ 28603. The potentiation of the depressor, cyclic GMP, and natriuretic responses to CNP in nonhuman primates by SQ 28603 suggested that NEP is an important mechanism for in vivo inactivation of natriuretic peptides, including CNP.

Alanine↗
PubMed1996

Three-point bending strength of ceramics fused to cast titanium.

Titanium requires special ceramic systems for veneering. This study compared the three-point bending strength of three commercially available titanium ceramic systems with a NiCr-alloy with conventional ceramics. Three-point bend specimens 25 x 5 x 0.5 mm were cast from polyethylene patterns. After alpha-case removal, they were veneered with 8 x 5 x 1 mm of ceramics at the center of the bar. Specimens were tested in a universal testing machine without ageing, after thermocycling, and after 90 d storage in an electrolyte solution. Titanium-ceramic systems were found to have a significantly lower bond strength in comparison to the NiCr-ceramic system. One of the titanium ceramic systems had a significantly lower bond strength in comparison to the other systems investigated. It could be concluded that bonding between titanium and ceramics is obtainable; however, the achievable bonds strengths did not match the NiCr-ceramic control.

Analysis of Variance↗
PubMed1996

Stereospecific Biohydroxylations of Protected Carboxylic Acids with Cunninghamella blakesleeana.

Cunninghamella blakesleeana DSM 1906 was found to be an efficient biocatalyst for the biotransformation of cycloalkylcarboxylic acids into hydroxy and oxo derivatives. When cultivated in submerged culture, the fungus grew in pellets. In comparison with malt extract-glucose-peptone-yeast extract medium (medium E), Czapek-Dox medium was found to reduce pellet size. Cycloalkylcarboxylic acids were protected against microbial degradation by chemical transformation into 2-cycloalkyl-1,3-benzoxazoles. The transformations of protected cyclopentyl-, cyclohexyl-, cycloheptyl-, and cyclooctylcarboxylic acids by C. blakesleeana were investigated. The biotransformations were performed in medium E by using an aerated, stirred-tank bioreactor. The transformation of 2-cyclopentyl-1,3-benzoxazole yielded (1S,3S)-3-(benz-1,3-oxazol-2-yl)cyclopentan-1-ol as the main product. The main by-product was (1R)-3-(benz-1,3-oxazol-2-yl)cyclopentan-1-one, and 2-(benz-1,3-oxazol-2-yl)cyclopentan-1-ol was also obtained in small amounts. During the experiment, the enantiomeric excess of the main product increased up to 64%. 2-Cyclohexyl-1,3-benzoxazole was hydroxylated to 4-(benz-1,3-oxazol-2-yl)cyclohexan-1-ol. 2-Cycloheptyl-1,3-benzoxazole and 2-cyclooctyl-1,3-benzoxazole were transformed into several alcohols and ketones, all in low yields (2 to 19%).

Journal Article↗
PubMed1996

Mesoderm and endoderm differentiation in animal cap explants: identification of the HNF4-binding site as an activin A responsive element in the Xenopus HNF1alpha promoter.

The gene encoding the tissue-specific transcription factor HNF1alpha (LFB1) is transcriptionally activated shortly after mid-blastula transition in Xenopus embryos. We have now shown that the HNF1alpha protein is localized in the nuclei of the liver, gall bladder, gut and pronephros of the developing larvae. In animal cap explants treated with activin A together with retinoic acid, we induced HNF1alpha in pronephric tubules and epithelial gut cells, i.e. in mesodermal as well as in endodermal tissues. HNF1alpha can also be induced by activin A, but not by retinoic acid alone. To define the promoter element responding to the activin A signal, we injected various HNF1alpha promoter luciferase constructs into fertilized eggs and cultured the isolated animal caps in the presence of activin A. From the activity profiles of the promoter mutants used, we identified the HNF4-binding site as an activin-A-responsive element. As HNF4 is a maternal protein in Xenopus and localized in an animal-to-vegetal gradient in the cleaving embryo, we speculate that the activin A signal emanating from the vegetal pole cooperates with the maternal transcription factor HNF4 to define the embryonic regions expressing HNF1alpha.

Activins↗