Katzenkratzkrankheit Eine wichtige Differentialdiagnose der Lymphadenopathie

Zusammenfassung Wir berichten über 2 F?lle von Katzenkratzkrankheit. Diese Erkrankung z?hlt zu den seltenen Ursachen einer Lymphadenopathie. Die Verdachtsdiagnose stützt sich auf Katzenkratzer in der Anamnese und die typischen Befunde mit Lymphknotenschwellung im Bereich der Prim?rl?sion.      

Immunohistochemical examination of the INK4 and Cip inhibitors in the rat neonatal cerebellum: cellular localization and the impact of protein calorie malnutrition

Expression of the cyclin-dependent kinase inhibitors (CKIs) has been linked to the inhibition of cellular proliferation and the induction of differentiation. Based on structure function analysis, two distinct families of CDKIs, the INK4 and the Cip/Kip family have been identified. The INK4 family member p16(Ink4), and the Cip/Kip protein p27(Kip1) have been implicated in normal development of the CNS and cerebellum. Recent studies have suggested a functional inter-dependence between the CKI and the abundance of cyclin D1 in orchestrating growth factor-induced cellular proliferation. The neonatal rat cerebellum undergoes proliferative growth and differentiation, localized to distinct topographical regions and cell types. The cell type and the temporal profile of CKI expression during postnatal cerebellar development had not been described. The current studies determined the specific cerebellar cell types in which the CKIs were expressed during post natal development by co-staining for cell-type specific markers. p16(Ink4a) and p27(Kip1) immunostaining was identified in both neurons and glial cells, increasing progressively between postnatal days 6 to 13 into adulthood. By contrast, neuronal and glial cell p21(Cip1) staining was prominent at days 6-11 and decreased thereafter. Cyclin D1 was expressed in the proliferating external granular cells, with occassional staining in the molecular, and internal granular layers. Dual immunostaining demonstrated cyclin D1 within cells expressing CKI (p16(Ink4a), p21(Cip1),p27(Kip1)). Cerebellar cellular growth arrest, induced by protein-calorie malnutrition, inhibited cyclin D1 protein levels without affecting CKI immunostaining suggesting CKI do not mediate the developmental arrest. These results demonstrate that the CKIs are induced by differentiation cues in specific cell types with distinct kinetics in the developing cerebellum in vivo.     

Aufbau einer Referenzdatenband für nosokomiale Infektionen auf Intensivstationen Erste Ergebnisse des nationalen Krankenhaus-Infektions-Surveillance-Systems (KISS)

OBJECTIVES: To establish a surveillance system as an element of internal quality management, participating intensive care units (ICUs) report their ICU-associated infection surveillance data for aggregation into a national database. METHODS: In order to provide data on ICU-associated infections, a nosocomial surveillance system in German intensive care units (Krankenhaus-Infections-Surveillance-System (KISS)) started in 1997. The method of data collection is based on the (adult) ICU surveillance component from the National Nosocomial Infections Surveillance (NNIS)-System. Until now 113 German ICUs (most of them medical/surgical ICUs) were included in this system. We continuously collected and calculated the data from site-specific infections (device-associated pneumonias, blood stream infections and urinary tract infections). RESULTS: There are now a total of 393,177 patient-days (100,015 patients) among them 176,415 ventilator-days, 295,221 central line-days and 316,799 urinary catheter-days in the data base. The data analysis showed the following device-associated infection rates: 11.2 pneumonias/1000 ventilator-days, 1.8 primary bloodstream infections/1000 central line-days and 4.0 urinary tract infections/1000 urinary catheter-days. CONCLUSION: The project has reached high interest in Germany and animated more ICUs to take part or to apply the same method in order to use the reference data for comparison.     

Ergebnisse der Herzinfarktregister in Chemnitz 1974–1999

Myocardial infarction has great importance for the populations in industrial countries because of the high morbidity and mortality rates. For research of the epidemiological trends in the 1970s and especially in the 1980s, the World Health Organization (WHO) began registering myocardial infarction throughout the world. The most important aspect was the WHO Monitoring of Trends and Determinants of Cardiovascular Diseases (MONICA) project. From 1974 to 1994 and in 1999 in Chemnitz, Germany, data from patients with acute myocardial infarction were collected for the myocardial infarction register. Despite changes in the event rates from year to year, no decrease in the number of myocardial infarctions in the German population aged 25–64 years was detected, contrary to the trend in the Western industrial states in the period from 1984 to 1994. The event rates in men were significantly higher than in women. In 1999, a significant decrease in the event rates in men and women was found. This may be explained by an incomplete registration of patients with myocardial infarction in 1999 because of the change in the structure of the Public Health System. The highest 28-day fatality rates in men were detected in 1989 and 1990. In women with classic myocardial infarction, a decrease in the 28-day fatality rates after 1993 was recorded, reaching lower rates than those of men. Despite methodological problems, the myocardial infarction register can contribute to a comparison of the morbidity, mortality and case fatality rates of myocardial infarction for a longer period.     

Adenovirus-mediated genetic manipulation of the myocardial beta-adrenergic signaling system in transplanted hearts

OBJECTIVES: Ex vivo perfusion of the cardiac allograft during organ procurement is an ideal environment for adenoviral vectors with transgenes that target improving graft contractility. One such target is the beta-adrenergic receptor-signaling system, in which alterations in transgenic mice have elucidated novel means to improve the function of the heart in vivo. The purpose of the current study was to determine the functional consequences of beta-adrenergic receptor manipulation in a rabbit model of cardiac allograft transplantation. METHODS: New Zealand White rabbits weighing 3 kg served as recipients to 1-kg outbred donors. Donor hearts were arrested and harvested, and 1 of 3 adenoviral constructs was administered into the aortic root perfusing the graft. Transgenes delivered encoded either the human beta(2)-adrenergic receptor, a peptide inhibitor of beta-adrenergic receptor densensitization, or the marker transgene beta-galactosidase. RESULTS: Five days after cervical heterotopic transplantation, left ventricular performance was measured on a Langendorff apparatus. A moderate pattern of rejection was seen in all grafts. Biventricular myocyte expression of beta-galactosidase was observed, and beta(2)-adrenergic receptor density was elevated 10-fold in grafts that received adeno-beta(2)-adrenergic receptor. Left ventricular systolic and diastolic performance was significantly increased in grafts transfected with either adeno-beta(2)-adrenergic receptor or adeno-beta-adrenergic receptor densensitization compared with control grafts that received adeno-beta-galactosidase. CONCLUSIONS: Ex vivo adenovirus-mediated gene transfer is feasible in a rabbit allograft model and, more important, genetic manipulation of beta-adrenergic receptor signaling either by increasing beta(2)-adrenergic receptor density or blocking endogenous receptor desensitization improves graft function acutely in this allograft model.     

mGluR5 antagonist MPEP reduces ethanol-seeking and relapse behavior.

The glutamatergic system plays an important role in mediating neurobehavioral effects of ethanol. Metabotropic glutamate receptors subtype 5 (mGluR5) are modulators of glutamatergic neurotransmission and are abundant in brain regions known to be involved in ethanol self-administration. Here, we studied the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP), a highly potent, noncompetitive mGlu5 receptor antagonist, on voluntary ethanol consumption and relapse behavior. For this purpose, we used two models for the measurement of relapse behavior: (i) reinstatement of ethanol-seeking behavior by drug-associated cues and (ii) the alcohol deprivation effect in long-term ethanol-consuming rats. In the first set of experiments, rats were trained to lever press for ethanol in the presence of a distinct set of cues. After extinction, the animals were exposed to the respective cues that initiated reinstatement of responding. A response-contingent ethanol prime further enhanced responding compared to the conditioned cues alone. Under these conditions, MPEP (0, 1, 3, and 10 mg/kg) attenuated ethanol seeking significantly and in a dose-related manner. However, at the highest dose, MPEP also decreased the number of inactive lever responses. In the second set of experiments, rats with 1 year of ethanol experience and repeated deprivation phases were used. A subchronic treatment with MPEP (twice daily; 0, 3, and 10 mg/kg) resulted in a significant and dose-dependent reduction of the alcohol deprivation effect (ADE). Although the same MPEP treatment regimen decreased baseline drinking, this effect was not as pronounced as on the ADE. These results show in two commonly used models of relapse to ethanol that pharmacological targeting of mGlu5 receptors may be a promising approach for the treatment of alcoholism.