The Effects of Different Canopy Covers on the Herb Layer in the Forest-Steppes of the Grazer Bergland (Eastern Alps, Austria)

The submontane belt of the eastern Alps is dominated by beech forests. However, on rocky and steep south-facing slopes, small vegetation mosaics have developed, which, to a certain degree, are similar to the Pannonian forest-steppes. In spite of their unique conservation importance and threatened status, they have received relatively little scientific attention. In this study we analyzed the spatial pattern of such mosaics. More specifically, our objective was to find out how canopy cover value inf luences the species composition of the herb layer. According to our results, canopy cover of Pinus sylvestris has a rather limited effect on the herb layer composition and species richness. Thus, in the studied canopy cover range (ca. 5–75% canopy cover), most species occurred under all canopy cover gr ades. This is presumably a result of the canopy char- acteristics and branching pattern of P. s y l v e s t r i s : it can be assumed that the physical conditions of the canopy and intercanopy patches are somewhat similar. This is in sharp contrast with the Pannonian forest-steppes dominated by Quercus pubescens . We conclude that, even though the cessation of traditional land-use may not result in a rapid change of the composition in eastern Austrian forest-steppes, every effort must be made to conserve these valuable habitats

Meningotheliomatöses Meningeom in einem reifen zystischen Teratom des Ovars

Zusammenfassung: Reife Teratome des Ovars zählen zu den Keimzelltumoren. Sie machen 27-44% aller Neoplasien des Ovars und bis zu 58% der benignen Ovarialtumoren aus. In reifen und unreifen Teratomen können sich sekundäre Tumoren der 3Keimblätter entwickeln. Diese können sowohl benigne als auch maligne sein. Wir berichten über den Fall eines meningotheliomatösen Meningeoms als Anteil eines reifen zystischen Teratoms bei einer 32-jährigen Patientin. Die typische Histomorphologie und die immunhistochemisch nachweisbare Expression von epithelialem Membranantigen (EMA) und Desmoplakin sind diagnostisch wegweisen

Revisiting A Festival of Violence : Two Comments, A Response [Book Review]

When, more than thirty years ago, I was writing my second graduate research paper, I was strongly advised by the professor in the course, John Morton Blum, to stop trying to weigh the factors I hypothesized might have caused the phenomenon I was trying to explain. Just list all the causes for which there is any credible evidence, I was told; don’t even try to rank them, and certainly don’t waste your time attempting to reject any. It’s not the historian’s job, and it’s probably not possible, anyway. Tell a good story, with interesting characters and active verbs. If you must, explain, but above all, entertain-that was the Blumian credo. I largely ignored the adjuration, reinforcing the then-department chairman’s view of me as a rebel with too few causes

Primäres zerebelläres T-Zell-Lymphom

Zusammenfassung: Primäre T-Zell-Lymphome des zentralen Nervensystems (ZNS) sind selten. Sie müssen differenzialdiagnostisch von reaktiven Läsionen unterschieden werden. Die Diagnosestellung sollte integrativ unter Verwendung von immunhistochemischen, molekulargenetischen und/oder zytogenetischen Methoden erfolgen. Wir beschreiben den Fall eines 50-jährigen Mannes, bei welchem ein primäres zerebelläres T-Zell-Lymphom diagnostiziert und eine klonale T-Zell-Rezeptorgen-Umlagerung nachgewiesen wurde. Nach 2Zyklen Chemotherapie entwickelte der Patient eine Pneumozystis-carinii-Pneumonie und verstarb 10Wochen nach Diagnosestellung. Die Autopsie ergab keinen Residualtumor im ZN

The validity of clinical diagnoses of dementia in a group of consecutively autopsied memory clinic patients

Background: Epidemiological studies show that up to 10 % of individuals aged 65 years and older suffer from dementia, most commonly from dementia of the Alzheimer Type (DAT) [1]. Clinicopathological studies are critical to our understanding of this disease and improving the accuracy of clinical diagnoses.Objectives: Our objectives were to examine the validity of clinical diagnoses of DAT, to determine the prevalence of different forms of dementia in this sample, and to investigate the relationship between age at death and polymorbidity.Subjects and method: Clinical data were available from 221 patients who had been examined at the Basel Memory Clinic between 1986 and 1996. From this population, 34 % (75 patients) were autopsied in the Department of Pathology, University Hospital Basel, and neuropathological examinations were additionally performed on 62 (83 %) of these patients. Clinical and neuropathological data were retrospectively compared.Results: 67.8 % of the neuropathologically examined patients received a definitive diagnosis of AD (Alzheimer's disease), vascular dementia (VaD) or mixed dementia (AD and VaD). AD alone or with other histopathological hallmarks of dementia was the most prevalent neuropathological diagnosis (63 %). VaD was deemed the only cause of dementia in only 4.8 % of patients. The sensitivity for DAT was 75.9 %, the specificity 60.6 %. Increasing age was associated with an increasing number of clinical and neuropathological diagnoses.Conclusion: The sensitivity and specificity of the clinical diagnoses of DAT found in our study are similar to previous reports (2-5). Older patients had more etiologies of their dementia than younger patients. This study reaffirms the need for internationally accepted criteria for clinical and neuropathological diagnoses, as well as further clinical-neuropathological investigations to further refine the clinical diagnostic proces

Hereditary Systemic Angiopathy (HSA) with cerebral calcifications, retinopathy, progressive nephropathy, and hepatopathy

Several hereditary conditions affecting cerebral, retinal and systemic microvessels have recently been described. They include CADASIL, CRV, and HERNS. We here report on a variant form of a hereditary systemic angiopathy (HSA) affecting two generations of a Caucasian family. Clinical symptoms of HSA appear in the mid-forties and are characterized by visual impairment, migrainelike headache, skin rash, epileptic seizures, progressive motor paresis and cognitive decline. Late symptoms include hepatic and renal failure. Retinal capillary microaneurysms and arteriolar tortuosity are associated with marked optic disc atrophy. Radiological hallmarks consist of multiple cerebral calcifications and tumor-like subcortical white matter lesions. Brain, peripheral nerve, muscle, kidney and colon biopsies have revealed a multi organ small vessel involvement with partly altered endothelium, perivascular inflammation and thrombotic microangiopathy. No curative therapeutic options are known for hereditary cerebral vasculopathies. The use of cyclophosphamide, azathioprine and methotrexate was of no benefit in our cases of HSA. Early diagnosis of hereditary systemic angiopathies is important in order to prevent patients from repetitive invasive diagnostic measures and to avoid the use of inappropriate and potentially harmful drug

Determinants of diagnostic investigation sensitivities across the clinical spectrum of sporadic Creutzfeldt-Jakob disease

To validate the provisional findings of a number of smaller studies and explore additional determinants of characteristic diagnostic investigation results across the entire clinical spectrum of sporadic Creutzfeldt-Jakob disease (CJD), an international collaborative study was undertaken comprising 2451 pathologically confirmed (definite) patients. We assessed the influence of age at disease onset, illness duration, prion protein gene (PRNP) codon 129 polymorphism (either methionine or valine) and molecular sub-type on the diagnostic sensitivity of EEG, cerebral MRI and the CSF 14-3-3 immunoassay. For EEG and CSF 14-3-3 protein detection, we also assessed the influence of the time point in a patient's illness at which the investigation was performed on the likelihood of a typical or positive result. Analysis included a large subset of patients (n = 743) in whom molecular sub-typing had been performed using a combination of the PRNP codon 129 polymorphism and the form of protease resistant prion protein [type 1 or 2 according to Parchi et al. (Parchi P, Giese A, Capellari S, Brown P, Schulz-Schaeffer W, Windl O, Zerr I, Budka H, Kopp N, Piccardo P, Poser S, Rojiani A, Streichemberger N, Julien J, Vital C, Ghetti B, Gambetti P, Kretzschmar H. Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects. Ann Neurol 1999; 46: 224-233.)] present in the brain. Findings for the whole group paralleled the subset with molecular sub-typing data available, showing that age at disease onset and disease duration were independent determinants of typical changes on EEG, while illness duration significantly influenced positive CSF 14-3-3 protein detection; changes on brain MRI were not influenced by either of these clinical parameters, but overall, imaging data were less complete and consequently conclusions are more tentative. In addition to age at disease onset and illness duration, molecular sub-type was re-affirmed as an important independent determinant of investigation results. In multivariate analyses that included molecular sub-type, time point of the investigation during a patient's illness was found not to influence the occurrence of a typical or positive EEG or CSF 14-3-3 protein result. A typical EEG was most often seen in MM1 patients and was significantly less likely in the MV1, MV2 and VV2 sub-types, whereas VV2 patients had an increased likelihood of a typical brain MRI. Overall, the CSF 14-3-3 immunoassay was the most frequently positive investigation (88.1%) but performed significantly less well in the very uncommon MV2 and MM2 sub-types. Our findings confirm a number of determinants of principal investigation results in sporadic CJD and underscore the importance of recognizing these pre-test limitations before accepting the diagnosis excluded or confirmed. Combinations of investigations offer the best chance of detection, especially for the less common molecular sub-types such as MV2 and MM

Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons

Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in adult neurons remains unclear. Here we show that inducible Drp1 ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic Drp1 ablation. Collectively, our in vivo observations clarify the role of mitochondrial fission in neurons, demonstrating that Drp1 ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration