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C Hohmann

Publications and source records attributed to C Hohmann.

15 recordsLinked to original sources
PubMed2002

Overexpression of S100beta in transgenic mice does not protect from serotonergic denervation induced by 5,7-dihydroxytryptamine.

Transgenic mice overexpressing S100beta were used to examine whether the chronic elevation of this protein alters the response to selective partial serotonergic lesions produced by bilateral intracerebroventricular injections of 5,7-dihydroxytryptamine (5,7-DHT). Basal levels of S100beta mRNA examined by in situ hybridization were two- to threefold higher throughout the brain in transgenic than in control mice, whereas 5-HT levels in forebrain were similar in both. After the 5,7-DHT-induced lesions, no differences were found in the S100beta mRNA levels in either normal or transgenic mice. At 5 and 60 days after the lesion, forebrain 5-HT levels were reduced by 56% and 35%, respectively, in control mice and by 51% and 35%, respectively, in the transgenic mice. Analysis of the 5-HT immunostaining showed a marked decrease of the immunoreactivity in various brain regions, which was comparable at the two intervals postlesion. One exception was the medial hypothalamus, where an almost complete disappearance of 5-HT immunoreactivity was observed in the medial region at 5 days after lesion, followed by a marked reinnervation 60 days later. These hypothalamic changes were seen in both controls and S100beta-overexpressing transgenic mice. Quantitative analysis of the density of 5-HT transporter sites using [(3)H]citalopram binding, a marker of serotonergic terminals, showed a marked decrease in different brain regions at both 5 and 60 days after 5,7-DHT injections. No difference in basal and postlesion levels of [(3)H]citalopram binding was seen between transgenic and control mice. In conclusion, this study demonstrates that constitutive overexpression of S100beta in transgenic mice does not modify serotonin levels during development, nor does it protect the serotonergic neurons from selective neurotoxicity or modify the serotonergic sprouting induced by partial lesion.

5,7-Dihydroxytryptamine↗
PubMed2002

[Increased thrombocyte activation in dilated cardiomyopathy: a risk factor for development of ventricular thrombosis despite anticoagulant therapy?].

HISTORY AND CLINICAL FINDINGS: A 48-year-old patient with dilated cardiomyopathy complained of dyspnea at rest, severe sleeplessness and a slight pain in the stomach. The clinical examination was normal except for a murmur at the apex of the heart. There was no evidence of edema or congestion of the jugular veins. INVESTIGATION: The echocardiography demonstrated a dilated left ventricle with severely compromised function. No ventricular thrombi were present at this time. Coronary artery disease was excluded by coronary angiography. Endomyocardial biopsies were obtained from the right ventricular septum. The immunohistological analysis of the endomyocardial biopsy specimens revealed pathologically increased lymphocytic infiltrates and increased expression of interstitial and endothelial MHC I and II antigens. Flow cytometric analysis of platelets surface antigens (P-selectin, GP53, thrombospondin) was performed as a measure for intravasal platelet activation. Our patient compared to a healthy control group (> 4 SD) and to other patients with dilated cardiomyopathy (> 2 SD). A high grade increase of platelet activation was found. TREATMENT AND COURSE: ACE inhibitor, diuretics, spironolactone and digitalis were used to treat the heart insufficiency. Due to the severe left ventricular dysfunction phenprocoumone and aspirin were also prescribed. A follow-up echocardiography was performed 6 months later. Comparable to the first examination left ventricular contractility was found to be severely reduced. In addition, a marginal thrombus was now present in the left ventricle despite antithrombotic therapy. DISCUSSION: An increased platelet activation was found in the peripheral circulation of our patient with dilated cardiomyopathy. After 6 months, ventricular thrombi were found in the dilated ventricle, although aspirin and phenprocoumone had been administred. We speculate that an additional thrombotic treatment with clopidogrel is necessary in patients with dilated cardiomyopathy and increased platelet activation.

Anticoagulants↗
PubMed2000

An efficient synthesis of thioisomunchnones derived from uracils and uridine: novel type of mesoionic nucleosides

[reaction: see text] Synthetic approaches to a variety of thioisomunchnones derived from uracils and uridine are described, as well as their properties and cycloaddition tendencies. The anhydro-3-hydrocy-2-phenyl-6-(2',3',5'-tri-O-benzoyl-beta-D-ribofuranosyl)thiazolo[3,2-c]pyrimidine-5(6H)-on-4-ium hydroxide represents a novel class of mesoionic nucleosides.

Journal Article↗
PubMed1999

Risk factors for functional status decline in community-living elderly people: a systematic literature review.

To lay the groundwork for devising, improving and implementing strategies to prevent or delay the onset of disability in the elderly, we conducted a systematic literature review of longitudinal studies published between 1985 and 1997 that reported statistical associations between individual base-line risk factors and subsequent functional status in community-living older persons. Functional status decline was defined as disability or physical function limitation. We used MEDLINE, PSYCINFO, SOCA, EMBASE, bibliographies and expert consultation to select the articles, 78 of which met the selection criteria. Risk factors were categorized into 14 domains and coded by two independent abstractors. Based on the methodological quality of the statistical analyses between risk factors and functional outcomes (e.g. control for base-line functional status, control for confounding, attrition rate), the strength of evidence was derived for each risk factor. The association of functional decline with medical findings was also analyzed. The highest strength of evidence for an increased risk in functional status decline was found for (alphabetical order) cognitive impairment, depression, disease burden (comorbidity), increased and decreased body mass index, lower extremity functional limitation, low frequency of social contacts, low level of physical activity, no alcohol use compared to moderate use, poor self-perceived health, smoking and vision impairment. The review revealed that some risk factors (e.g. nutrition, physical environment) have been neglected in past research. This review will help investigators set priorities for future research of the Disablement Process, plan health and social services for elderly persons and develop more cost-effective programs for preventing disability among them.

Activities of Daily Living↗
PubMed1998

[Prospective study of the incidence, pathogenesis and therapy of spontaneous, by coronary angiography diagnosed coronary artery dissection].

Spontaneous coronary artery dissection is a rare cause of ischemic heart disease. Incidence, etiology and optimal treatment are ill-defined. Between July 1995 and December 1997, we prospectively identified 42 patients (36 men, six women, mean age 59 +/- 12 years) with spontaneous coronary artery dissection among 3803 consecutive angiographic examinations in which the diagnosis of coronary artery disease was established for the first time (incidence 1.1%). In comparison to the remaining study population with stable angina pectoris (8 cases of spontaneous coronary artery dissection among 2852 patients; incidence: 0.3%), the incidence of spontaneous coronary artery dissection was significantly higher in the patient subgroups with acute myocardial infarction (13/450; 2.9%) and with unstable angina pectoris or postinfarction angina (21/501; 4.2%). Dissection was most frequently located in the left anterior descending coronary artery (19 cases), followed by the right coronary artery (15 cases) and the left circumflex coronary artery (8 cases). Because of an ambiguous angiographic lesion appearance intravascular ultrasound imaging was performed in 13 patients to confirm the diagnosis. The presumed etiology of spontaneous coronary artery dissection was atherosclerotic plaque rupture in 35 cases, heavy physical exercise in four cases and hormonal influences related to pregnancy and contraception in one case. In two cases, no obvious risk factor could be identified. Therapy consisted of intracoronary stenting in 24 patients (including ten patients with acute myocardial infarction), coronary artery bypass grafting (CABG) in 8 patients and balloon angioplasty (PTCA) in seven patients. Three patients were treated conservatively. During a mean follow-up period of 13.5 +/- 9.9 months, two patients died and 31 patients remained entirely asymptomatic, including all patients who were treated with CABG. Restenosis developed in three patients after stent implantation (restenosis rate: 12.5%). Following primary PTCA, spontaneous coronary artery dissection recurred in two patients, one of whom subsequently died.

Adult↗
PubMed1996

Recurrent angina pectoris in patients with internal mammary artery to coronary artery bypass: treatment with coil embolization of unligated side branches.

PURPOSE: The purpose of the study was to evaluate the effect on the symptoms of transcatheter coil embolization of branches of the internal mammary artery. MATERIALS AND METHODS: In five patients with coronary steal syndrome that was caused by preferential flow in large unligated side branches of the internal mammary artery, coil embolization of the side branches was performed with use of a coaxial microcatheter. RESULTS: Anginal symptoms disappeared in three patients and were substantially reduced in one patient following the radiologic intervention. In the fifth patient, who had concomitant stenoses of other coronary vessels, only a moderate change in symptoms was noted. No complications occurred. CONCLUSION: In patients with internal mammary artery to coronary artery bypass who experience recurrent angina pectoris caused by preferential flow in large, unligated side branches of the internal mammary artery, repeat surgery may be circumvented or simplified by transcatheter coil embolization, which can help treat the angina.

Adult↗
PubMed1996

[Not Available].

Explore the source record for details and available documents.

Environmental Exposure↗
PubMed1995

Neurobiology of Rett syndrome.

From a neurobiologic perspective, Rett syndrome appears to disrupt the growth of axonodendritic connections among neurons. The cell packing density within the grey matter is increased but the total number of neurons is relatively normal, except for selected neuronal populations such as the nucleus basalis of Meynert (NBM) and the substantia nigra. Neurochemical assays of postmortem brain from patients with Rett syndrome patients demonstrate reductions in choline acetyltransferase (ChAT), the acetylcholine synthetic enzyme localized in NBM nerve terminals. In an animal model, early postnatal injury to the cholinergic pathways projected from the NBM causes permanent disruption of developing cholinergic neurons and a behavioral disorder on maze testing. The results suggest a mechanism by which early deficits in cholinergic and dopamine neurons projecting to the cerebral cortex from the brainstem and basal forebrain could disrupt axonodendritic development in the cerebral cortex. Studies in our laboratory are examining the mechanisms for these effects as well as the distribution and densities of neurotransmitter receptors in postmortem brains from Rett patients.

Acetylcholine↗
PubMed1992

In vivo clearance and elimination of nine marker substances during hemofiltration with different membranes.

The handling of low, middle and high molecular weight markers was examined in seven stable dialysis patients during hemofiltration with different membranes. Four membranes were examined in a randomized, crossover order (polysulfone, polyamide, AN69 polyacrylonitrile, Asahi polyacrylonitrile) by measuring plasma and dialysate concentrations of phosphate, creatinine, vitamin B12, beta 2-microglobulin, furanic acid, hippuric acid, retinol-binding protein, alpha-1-antitrypsin, and albumin. Sieving coefficients and plasma clearances of beta 2-microglobulin or retinol-binding protein were markedly or slightly lower during hemofiltration with the Asahi polyacrylonitrile membrane than with the other membranes (highest removal with polysulfone/AN69 polyacrylonitrile membranes). No differences of obvious clinical relevance could be seen between the four membranes. A high beta 2-microglobulin removal rate might be important to prevent dialysis-associated amyloidosis.

Aged↗
PubMed1990

Developmental expression of somatostatin in mouse brain. I. Immunocytochemical studies.

The postnatal development of the distribution of somatostatin immunoreactive (SOMLI) neurons and fibers in the forebrain of the Balb/C mouse and their relationship to cholinergic afferents have been examined. SOMLI was first discernable in the hypothalamus on postnatal day (PND) 3 and increased gradually to reach adult levels by PND 30. In the limbic system, SOMLI is detectable at birth. In all other structures of the forebrain, SOMLI could be observed by PND 3 but the distribution, density and morphology of the immunoreactive neurons evolved over the following 2-3 weeks. In general, SOMLI cells and fibers increased for 1-3 weeks after their initial appearance and subsequently declined to achieve adult levels. The distribution pattern of SOMLI elements in adult mouse brain was similar to previous reports in rat with a few notable differences in thalamus, olfactory structures and, to a lesser degree, cortex and hippocampus. The temporal pattern of SOMLI expression in extrahypothalamus forebrain regions, during development, suggests a role of this peptide in differentiation and synapse formation. Such an hypothesis receives further support from neonatal lesions of the basal forebrain which resulted in transient cortical cholinergic deafferentation, a delay of cortical differentiation and a transient increase in the number of SOMLI cells in cortex.

Aging↗
PubMed1990

Developmental expression of somatostatin in mouse brain. II. In situ hybridization.

The distribution and the levels of expression of preprosomatostatin (PPSOM) mRNA were examined during pre- and postnatal development of the mouse brain using the in situ hybridization technique. The signal obtained by in situ hybridization of embryonic tissues at day 14 and day 17 of gestation was highest over the neurons of the pyriform cortex, amygdala, and entopeduncular nucleus. The signal was very low over cells of the neocortex and the developing hippocampal formation. The density of grains overlying the neurons of the amygdala and pyriform cortex continued to be high during early postnatal life, but decreased as the animals became adults. A progressive increase of PPSOM mRNA expression was observed in postnatal animals in the stratum oriens and dentate gyrus of the hippocampal formation. In the cerebral cortex and striatum, the number of these neurons became maximal between postnatal weeks 1 and 3. In the diencephalon, the highest densities of grains were found over neurons in the nucleus reticularis thalami and zona incerta at postnatal day 21; these levels declined slightly thereafter. The cells of the periventricular nucleus of the hypothalamus had high densities of grains as early as postnatal week 1 and continued to have high densities of grains in adult animals. These patterns of hybridization density parallelled the distribution of SOM-like immunoreactivity in the mouse brain. When PPSOM mRNA expression was examined in the cerebral cortices of mice that received lesions of the nucleus basalis of Meynert as neonates, a transient increase in the number of cells expressing PPSOM mRNA was observed in the frontoparietal cortex ipsilateral to the lesion at postnatal day 10, but not at postnatal day 30. Importantly, the density of grains over the individual cells was not altered in lesioned animals at these two ages.

Aging↗
PubMed1989

Interaction between plasminogen activator inhibitor type 1 (PAI-1) bound to fibrin and either tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA). Binding of t-PA/PAI-1 complexes to fibrin mediated by both the finger and the kringle-2 domain of t-PA.

Plasminogen activation is catalyzed both by tissue-type-(t-PA) and by urokinase-type plasminogen activator (u-PA). This reaction is controlled by plasminogen activator inhibitor type 1 (PAI-1) that is either present in plasma or bound to fibrin, present in a thrombus. We studied the mechanism of in vitro inhibition of both t-PA and u-PA activity by PAI-1 bound to fibrin. It is shown that activation of latent PAI-1 unmasks a specific fibrin-binding site that is distinct from its reactive site. This reactive site of activated PAI-1 bound to fibrin is fully exposed to form complexes with t-PA and u-PA, that are unable to activate plasminogen. Upon complex formation with either one of the plasminogen activators, PAI-1 apparently undergoes a conformational change and loses its affinity for fibrin. Consequently, complexes of u-PA and PAI-1 dissociate from the fibrin matrix and are encountered in the fluid phase. In contrast, t-PA/PAI-1 complexes remain bound to fibrin. By employing recombinant t-PA deletion-mutant proteins, that precisely lack domains involved in fibrin binding, we demonstrate that binding of t-PA/PAI-1 complexes is mediated by both the "finger" (F) and the "kringle-2" (K2) domain of t-PA. A model is proposed that explains inhibition of the fibrinolytic process, at the level of plasminogen activation by t-PA, directed by PAI-1 bound to fibrin. An implication of the proposed model is that t-PA/PAI-1 complexes and free t-PA compete for the same binding sites on fibrin.

Animals↗