PubMed Health⌕ Search

Biomedical subjects

B Baumann

Publications and source records attributed to B Baumann.

At least 19 recordsLinked to original sources

Anterior cruciate ligament constructs fabricated from human mesenchymal stem cells in a collagen type I hydrogel.

BACKGROUND: Disruptions of the anterior cruciate ligament (ACL) of the knee joint are common and are currently treated using ligament or tendon grafts. In this study, we tested the hypothesis that it is possible to fabricate an ACL construct in vitro using mesenchymal stem cells (MSC) in combination with an optimized collagen type I hydrogel, which is in clinical use for autologous chondrocyte transplantation (ACT). METHODS: ACL constructs were molded using a collagen type I hydrogel containing 5 x 10(5) MSC/mL and non-demineralized bone cylinders at each end of the constructs. The constructs were kept in a horizontal position for 10 days to allow the cells and the gel to remodel and attach to the bone cylinders. Thereafter, cyclic stretching with 1 Hz was performed for 14 days (continuously for 8 h/day) in a specially designed bioreactor. RESULTS: Histochemical analysis for H and E, Masson-Goldner and Azan and immunohistochemical analysis for collagen types I and III, fibronectin and elastin showed elongated fibroblast-like cells embedded in a wavy orientated collagenous tissue, together with a ligament-like extracellular matrix in the cyclic stretched constructs. No orientation of collagen fibers and cells, and no formation of a ligament-like matrix, could be seen in the non-stretched control group cultured in a horizontal position without tension. RT-PCR analysis revealed an increased gene expression of collagen types I and III, fibronectin and elastin in the stretched constructs compared with the non-stretched controls. DISCUSSION: In conclusion, ACL-like constructs from a collagen type I hydrogel, optimized for the reconstruction of ligaments, and MSC have been fabricated. As shown by other investigators, who analyzed the influence of cyclic stretching on the differentiation of MSC, our results indicate a ligament-specific increased protein and gene expression and the formation of a ligament-like extracellular matrix. The fabricated constructs are still too weak for animal experiments or clinical application and current investigations are focusing on the development of a construct with an internal augmentation using biodegradable fibers.

Animals↗

A functional-structural model to understand cardiac autonomic nervous system (ANS) dysregulation in affective illness and to elucidate the ANS effects of antidepressive treatment.

Numerous studies provide evidence that major depression (MD) is associated with certain disorders of cardiac autonomic nervous system (ANS) function, in particular, with an autonomic neurocardiac imbalance characterized by a low cardiovagal modulation, a raised sympathetic nerve activity and a high resting heart rate. We assume that such MD-associated cardiac ANS disorders are mainly caused by functional-structural abnormalities within the central autonomic network (CAN), in particular, by well-defined abnormalities of hypothalamic structures in MD. In view of the well-known association between an autonomic neurocardiac imbalance and the risk for cardiac arrhythmias, we assume that MD-associated cardiac ANS disorders are at least partly responsible for the high cardiovascular mortality risk in MD. It is, however, still unclear whether antidepressive treatment will lower the risk for cardiovascular complications in MD. There is convincing evidence that a successful antidepressive treatment with electroconvulsive therapy, cognitive behavioral therapy, or pharmacotherapy with primarily non-antimuscarinergic antidepressants can improve an initially disturbed cardiac ANS function in MD. These studies correspond well to our findings that treatment with both, nefazodone or reboxetine, can induce a reduction of central sympathetic nerve activity and an increase of the initially lowered cardiovagal modulation depending on the improvement of depressive symptoms after treatment. Since both effects occured obviously independent from the primarily serotonergic or noradrenergic action of the antidepressants, our findings suggest the existence of a generally supraordinate and uniform mechanism underlying the ANS effects of antidepressive treatment with drugs inhibiting serotonin- or noradrenaline reuptake.

Antidepressive Agents↗

Mechanisms of action in the prevention of recurrent mood disorders.

BACKGROUND: Since long-term treatment is a need in many patients with mood disorders, knowledge on mechanisms of action in the prevention of recurrence is of major relevance. METHODS: Follow-up studies, which are best suited to prove the linkage of causal factors and mechanisms with the clinical course of the disorders, are rare. Another approach to search for preventive mechanisms is to address actions of pharmacological agents, which are effective in prophylactic treatment of mood disorders. Studies over the past several years have indicated that intracellular signaling cascades mediate long-term pharmacological effects via modulation of transcription factors and gene expression of neurotrophic and neuroprotective factors which may interfere with recurrence of affective illness. RESULTS: The impact of treatment on stress responsive systems varies with different therapeutic strategies and the relevance of a treatment-related modification of stress reliability for the course of the disease is not clear. Functional and structural actions of mood stabilizers and of antidepressants on mood-relevant anatomical circuits and modulation of chronobiological alterations also appear to be involved in preventive mechanisms in mood disorders. Moreover, cognitive mediators of prophylactic effects have been described. CONCLUSION: Combined clinical and biological studies should assess the relevance of those modes of action for the long-term course of mood disorders.

Antidepressive Agents↗

[Neurobiological principles of bipolar affective disorders].

The neurobiology of bipolar affective illness can be described in a model with structural and functional components, which also address the role of stressors, coping mechanisms, and psychophysical disposition. More data exist on depressive than on manic patients or on patients switching from one clinical pole to the other. Structural and functional chronobiological alterations appear to play a major role in the pathophysiology of bipolar illness. From an anatomical view, neurobiological abnormalities are primarily confined to limbic-striatal-pallidal-thalamocortical circuits. The whole cascade of neural signaling is changed starting from neurotransmitters and neuromodulators to receptor-mediated intracellular signal transduction targeting nuclear gene expression. Transnosological factors such as suicidal tendency appear to essentially modulate those changes. Replicated data on decisive neurobiological differences between bipolar and unipolar affective disorders are currently not yet available.

Bipolar Disorder↗

[Evaluation of capacity for informed consent in psychiatric and neurological patients--proposal of a stepwise decisional procedure].

Evaluation of capacity for informed consent in psychiatric and neurological patients is assuming increasing importance in clinical practice. After a brief description of legal aspects, a procedural algorithm is presented for evaluation of capacity concerning consent of patients in medical treatment and procedures. This evaluation is based on the investigation and documentation of understanding, voluntariness, and decisional capacity. Relevant deficits of only one of these components in the evaluative procedure exclude capacity for informed consent. The outlined approach is compared with international proposals and discussed with regard to its application in clinical practice.

Decision Making↗

Therapeutic drug monitoring of clozapine and relapse--a retrospective study of routine clinical data.

OBJECTIVE: Therapeutic drug monitoring (TDM) of the atypical antipsychotic drug clozapine is recommended. Clinical studies have indicated a therapeutic window for clozapine serum levels in schizophrenic and schizo-affective patients during acute treatment, i.e. for patients who do not respond to treatment with typical antipsychotics. However, despite the frequent use of clozapine also in maintenance treatment, very few data are available showing the relationship between serum levels of clozapine and the prevention of relapse. Thus, the primary objective of the study was to investigate the relationship between serum levels ofclozapine and relapse during maintenance treatment. METHODS: A retrospective study of routine TDM-data was conducted. Samples obtained on an acute treatment ward from patients with < 4 days hospitalization (recent admissions) were regarded as samples associated with relapse. Samples which can be attributed to an intoxication were identified as described in the TDM-form. The serum level of clozapine, as well as age, gender, smoking habits, concurrent drugs, psychiatric diagnosis and dose of clozapine were evaluated. Data analysis was performed on individual samples and, alternatively, on multiple samples from a single patient which are summarized according to a typical clinical situation. RESULTS: 404 serum levels were measured in 86 patients. After exclusion of patients receiving acute treatment, 65 relevant clinical situations were identified in 50 patients: 12 relapses, 8 intoxications (a total of 20 situations with poor outcome) and 45 situations involving patients with good maintenance outcome. Samples involving relapse had serum levels of 198 +/- 211 ng/ml (10-624), intoxications had serum levels of 1,969 +/- 705 ng/ml (900-2,900) and those with good outcome had serum levels of 384 +/- 255 ng/ml (56-1,028) (mean +/- SD (range)). By means of sensitivity of receiver operating characteristic curves (ROC) a lower limit of the therapeutic window can be estimated at about 50-250 ng/ml and an upper limit at about 745-1,050 ng/ml. The frequencies of good and poor outcome were significantly different within and outside these ranges, e.g. chi2 = 11.8 and p < 0.001 for 250 to 745 ng/ml. Comparison of only good outcome and relapse provided a significant difference in the serum level of clozapine (Student's t-test p = 0.024). However, 67% of relapses were predicted in a model of logistic regression only if the variables serum level and concurrent treatment with other psychotropic drugs were included simultaneously as independent variables. Neither variable was able to predict relapse if used as a single variable in separate models. Finally, it was found that serum levels of clozapine were increased in women, in aged patients and in nonsmokers. CONCLUSIONS: It is tentatively concluded that serum levels of clozapine < 50 ng/ml are related to relapse irrespective of concurrent psychotropic drugs. In cases where there are no concurrent psychotropic drugs, serum levels of clozapine < 250 ng/ml are associated with relapse. The risk of relapse is low for serum levels of clozapine > 250 ng/ml irrespective of concurrent psychotropic drugs. The risk of intoxication is increased with serum levels > 750 ng/ml. The TDM of clozapine is recommended during maintenance treatment.

Adult↗

IgM-enriched immunoglobulin preparation for immunoprophylaxis in cardiac surgery.

OBJECTIVE: Evaluating the effects of prophylactic administration of IgM-enriched immunoglobulins (IVIG) on immunological- and clinical parameters in cardiac surgical patients. PATIENTS AND METHODS: 41 patients were randomized to receive either an IgM-enriched immunoglobulin (Pentaglobin(R)) preparation (1,300 ml immunoglobulin, equivalent to 65 g protein) combined with routine antibiotic prophylaxis (Group A; n = 20, 1 drop-out), or routine antibiotic prophylaxis plus placebo (Group B; n = 20). Patients were comparable with respect to their APACHE II score, comorbidity, coronary risk, operating time, clamp, and ischemic time. Endotoxin and endotoxin neutralizing capacity (ENC) were determined by a kinetic turbidimetric Limulus amebocyte lysate (LAL) assay with internal standardization. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF)-alpha, soluble TNF-Receptor I (sTNF-R1), and interleukin-10 (IL-10) were determined by ELISA. Data analysis was performed by area under the curve (AUC) calculation and ANOVA for endotoxin neutralizing capacity and by ANOVA for all other cases. RESULTS: All patients survived. Endotoxin plasma levels were generally but not significantly higher in group A than in controls, while the difference in endotoxin neutralizing capacity (ENC) reached significance. IL-6, TNF-alpha, IL-10 and TNF-R1 were not different between both groups, however. There were significantly less patients with signs of inflammation (fever, leukocytosis, hypotension) in group A (group A n = 2; group B n = 9; p<0.05). This was paralleled by a slightly reduced hospitalization period in group A patients compared to group B patients (A:12.05 +/- 3.66 vs. B:13.45 +/- 3.72 days; n.s.). All data are given as mean +/- standard deviation (SD). CONCLUSION: The results of this study support that IgM-enriched IVIG preparation are effective when used prophylactically in patients undergoing procedures with cardiopulmonary bypass. The mechanisms of endotoxin neutralization and the effect of the host immune status on the efficacy of IVIG treatment remain to be elucidated.

Adult↗

Circumscribed numerical deficit of dorsal raphe neurons in mood disorders.

BACKGROUND: Neurocircuits comprising limbic, striato-pallidal and thalamo cortical brain areas are assumed to be involved in the pathophysiology of mood disorders. All these brain regions receive serotonergic afferents arising from the rostral raphe, mainly the dorsal raphe. Although serotonergic systems appear to be involved in the pathology of mood disorders, there is uncertainty as to whether structural alterations in raphe nuclei exist alongside a functional dysregulation of the serotonergic system. METHODS: In the brains of 12 patients with mood disorders (major depressive disorder N= 6, bipolar disorder N = 6) and 12 normal subjects we performed a morphometric post-mortem study on neuronal morphology in all subnuclei of the dorsal raphe nucleus using Nissl stained 20 microm axial serial sections of the brainstem. RESULTS: The number of neurones of the ventrolateral subnucleus of the dorsal raphe was reduced by 31 % in patients with mood disorders compared with non-psychiatric control subjects. Ventrally located subnuclei of the rostral dorsal raphe (ventrolateral, ventral, interfascicular) taken together also showed a smaller number of neurones. Neurone numbers of the dorsal and the caudal subnucleus and volumes of all single subnuclei appeared to be unchanged. Analysis of morphological neuronal types revealed a smaller number of triangular neurones in the ventrolateral subnucleus. Numbers of ovoid and round neurones in the ventrolateral subnucleus also showed a trend to reduction. No correlation was found between neurone numbers in any subnucleus of the dorsal raphe and duration of illness. Neurone numbers did not differ in any subnucleus between patients with unipolar and those with bipolar affective disorder. CONCLUSIONS: Results indicate that patients with primary mood disorders have a circumscribed numerical neuronal deficiency in the dorsal raphe. This structural deviation may contribute to impaired serotonergic innervation of brain regions which are involved in the pathology of mood disorders.

Adult↗

Detection of differentially expressed genes in particle disease using array-filter analysis.

UNLABELLED: The precise cellular mechanism of osteolysis in particle disease is still unknown. The aim of the study was to screen for new gene products in macrophages during particle contact. METHOD: In an established macrophage model THP1-cells (human monocytic cells) were differentiated under the influence of vitamin D3 and GM-CSF into macrophage-like cells (MLC). MLCs were incubated each with different concentrations of polyethylene particles, Lipopolysaccharids (LPS) and controls. Isolated RNA was transcribed into complementary radioactive 32P labeled cDNA. This probe was hybridised on an human cDNA expression array and analysed by autoradiography. To obtain a more reliable method quantifying mRNA, the reverse transcriptase polymerase chain reaction (RT-PCR) was used. RESULTS: The arrays showed an upregulation of the following genes by particles: TNF-Rezeptor 2, IL-1 Receptor Antagonist, Bone Morphogenic Protein 4 and HM 145. This was proven three times using RT-PCR and statistically significant in comparison to the controls. LPS induced the same upregulation except for HM145 whereas particles caused downregulation of this mRNA expression. CONCLUSION: Our results prove that the model of differentiated THP-1 cells treated with PE particles is a suitable system to analyse differential gene expression patterns, since the induction of the major positive control genes TNF alpha and IL1 beta were detected by this approach. BMP 4 is known as signal protein which mediates ectopic bone formation and can also be interpreted as a contra regulatory gene. HM 145 belongs to the leukocyte chemotactic peptide receptor family. HM 145 seems to be one of the first genes that is enhanced along the septical pathway but less expressed by contact with particles. Analysis of HM 145 expression might help to diagnose septic versus aseptic loosening of prosthesis.

Bone Morphogenetic Protein 4↗

Emergency-culling and mortality in growing/fattening pigs in a large Hungarian "farrow-to-finish" production unit.

The trial was carried out in a large Hungarian 2000 sow "farrow-to-finish" production unit. Out of a total number of 15,841 evaluated growing/finishing pigs, 1319 pigs died or were emergency-culled and were post-mortem routinely examined. For the purpose of this study the emergency-culling and mortality were recorded into the same category. The average annual emergency-culling/mortality rate was unusual high (8.62%). Five body condition related categories were registered. The majority of the mortality comprised animals of body condition "below average", representing 891 pigs (67.56%) and "average" (407 pigs = 30.85%). The rest of the examined animals comprised 17 pigs (1.29%) "emitted", 2 pigs "kachexia" (stunted pig) or "fat" (0.15% each). The overall study showed that gastrointestinal tract disorders (395 animals = 29.95%) were the most frequently recorded cause of emergency-culling or mortality. Both inflammatory disorders (7.66%) and rectal stricture (7.51%) were in this category the most frequent diagnosis followed by rectal prolapse (5.92%). Gastric ulcers comprised 4.55% of the necropsied animals. Torsion of abdominal organs and miscellaneous cases represented slightly more than 2% of the post-mortem examined pigs. Lesions which involved the respiratory system, comprised 14.85% of the necropsied pigs. Bronchopneumonia due to Mycoplasma hyopneumoniae occurred in 5.61%, embolic suppurative or necrotic pneumonia in 4.78% and pleuropneumonia due to Actinobacillus pleuropneumoniae in 3.1% of the cases. Diseases involving the urinary system were diagnosed in 21 cases (1.59%). Five cases of skin disorders were registered (0.38%). Cardiovascular disorders were represented by congestive heart failure (31 pigs = 2.35%), pericarditis (22 animals = 1.66%) or endocarditis (21 pigs = 1.60%). Cardiomyopathy was found in 15 (1.2%) animals. Lesions involved the locomotor system ranked second of all cases (15.92%). Claw lesions accounted 13.72%, arthritis 2.13% of the animals and luxation or fracture was diagnosed only in one case (0.07%). Systemic infections were reported in 96 cases (7.28%) including polyserositis (4.09%), erysipelas, edema disease or miscellaneous causes (each category slightly more than 1%). Genetic problems were involved in 8.19% of the fatal cases and social stress or cannibalism related culling or mortality comprised 37 animals (2.81%). In 161 cases (12.20%) of the mortality the causes of death were not established. Two or more lesions related to culling or mortality were found in 320 pigs (24.26%, p < 0.001). The most common diagnosed pathologic changes in association with other lesions were Mycoplasma hyopneumoniae caused bronchopneumonia (4.09%), embolic suppurative or necrotic pneumonia (4.55%), followed by inflammatory gastrointestinal problems (3.10%), gastric ulcer (2.35%), claw lesions (2.19%) and arthritis (1.14%). It appears from the presented study that a routine post-mortem examination of all emergency-culled or dead pigs over a long period of time gives a clear picture of causes of mortality enabling the management to plan management strategies as vaccination programs, genetic improvements and optimising environmental conditions.

Animals↗

Fewer beta-endorphin expressing arcuate nucleus neurons and reduced beta-endorphinergic innervation of paraventricular neurons in schizophrenics and patients with depression.

In order to elucidate whether the hypothalamic expression of beta-endorphin is altered in patients with mental disorders we studied the cellular localization of the peptide in arcuate nucleus neurons as well as the beta-endorphinergic innervation of paraventricular neurons in nine schizophrenics, six subjects with depression, and nine controls. A polyclonal antiserum against beta-endorphin was employed for the immunohistochemical detection of the peptide in sections of postmortem human brains. Quantitative analysis revealed that the number of beta-endorphin-containing arcuate neurons was statistically reduced in schizophrenics and depressives in comparison to controls. Moreover, the number of endorphinoceptive (i.e. beta-endorphin-innervated) paraventricular nerve cells was also lower in psychiatric patients than in control cases. Our results showing an altered endorphinergic system in human hypothalami of schizophrenics and depressives might contribute to a renewal of interest in this peptide as a possible factor of importance in psychiatric disorders.

Adult↗

Activity of a novel bcl-2/bcl-xL-bispecific antisense oligonucleotide against tumors of diverse histologic origins.

BACKGROUND: Increased expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL is involved in the development and progression of many tumors. We recently reported that the bcl-2/bcl-xL-bispecific antisense oligonucleotide 4625 induces apoptosis in lung carcinoma cells. To further assess the therapeutic potential of oligonucleotide 4625, we investigated its effect on a series of human tumor cell lines of diverse histologic origins in vitro and in vivo. METHODS: Oligonucleotide 4625-mediated inhibition of bcl-2 and bcl-xL expression in vitro was measured in breast carcinoma cells with the use of reverse transcription-polymerase chain reaction (PCR), real-time PCR, and western blotting. Cytotoxicity was assessed in several different cell lines by measurement of tumor cell growth, propidium iodide uptake, and nuclear apoptosis. The in vivo activity of oligonucleotide 4625 was determined by the inhibition of growth of established tumor xenografts in nude mice, immunohistochemical staining of Bcl-2 and Bcl-x proteins in the tumors, and western blotting of tumor lysates. Apoptosis in tumor xenografts was detected with the use of in situ TUNEL (i.e., terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-digoxigenin nick end labeling) staining. All statistical tests are two-sided. RESULTS: In breast carcinoma cells, oligonucleotide 4625 treatment reduced bcl-2 and bcl-xL messenger RNA levels in a dose-dependent manner. At 600 nM:, oligonucleotide 4625 reduced Bcl-2 and Bcl-xL protein levels to 25% (95% confidence interval [CI] = 16% to 34%) and 20% (95% CI = 14% to 26%), respectively, of the levels in untreated cells and it decreased viability in all cell lines mainly by inducing apoptosis. In vivo, oligonucleotide 4625 statistically significantly inhibited the growth of breast and colorectal carcinoma xenografts by 51% (95% CI = 28% to 74%) and 59% (95% CI = 44% to 74%), respectively, relative to those treated with control oligonucleotide 4626; it also reduced Bcl-2 and Bcl-xL protein levels and induced tumor cell apoptosis. CONCLUSION: The bcl-2/bcl-xL-bispecific antisense oligonucleotide 4625 merits further study as a novel compound for cancer therapy.

Animals↗

Validation of the sterilization procedure of allogeneic avital bone transplants using peracetic acid-ethanol.

Different procedures are available to inactivate bacteria and fungi, including their spores, as well as viruses in human bone transplants. The most efficient methods are considered to be gamma irradiation and thermal inactivation as well as chemical sterilization methods like the peracetic acid-ethanol treatment (PES). Following national and international standards or draft standards, the antimicrobial effectiveness of this procedure was evaluated. Due to the standardizable size as well as the clinical relevance, defatted human spongiosa cuboids (15x15x15 mm) served as model system. After treatment with PES for 2 and 4 hours, respectively, the titre of living micro-organisms was determined in the supernatant and the cuboid. A reduction in the titre of viable micro-organisms below the detection level (reduction factor >5 log10) was already achieved after an incubation time of 2 hours (Staphylococcus aureus, Enterococcus faecium, Pseudomonas aeruginosa, Bacillus subtilis, Clostridium sporogenes, Mycobacterium terrae, Candida albicans as well as spores of Bacillus subtilis). No viable micro-organisms could be detected in any of the PES-treated test cuboids. Spores of Aspergillus niger were also completely inactivated. The PES procedure proved to be a reliable method for the sterilization of human bone transplants derived from spongiosa.

Bacteria↗

Standardized tests of heart rate variability: normal ranges obtained from 309 healthy humans, and effects of age, gender, and heart rate.

The authors undertook this study to determine the effects of age, gender, and heart rate (HR) on the results of cardiac autonomic function tests for measuring heart rate variability (HRV) in a large sample of healthy subjects (n = 309). Conventional tests (deep breathing, maximum/minimum 30:15 ratio), and a standardized 5-minute resting study, including spectral analysis of HR, were used. The main findings included (1) the indices of all tests, except for the ratio of the low- (LF) to high-frequency (HF) spectral power (LF/HF ratio) and HR itself, are inversely related to age in both sexes; (2) the 5-minute spectral bands (except for the LF/HF ratio), the variation coefficient, expiratory-inspiratory ratio during deep breathing, and the maximum/minimum 30:15 ratio are independent of HR; (3) women up to the age of 55 years have a higher resting HR compared with men; (4) young and middle-aged women show a significantly lower LF power and LF/HF ratio compared with age-matched men, whereas no significant gender differences are observed in the absolute HF power. The authors computed age- and gender-dependent normal values for each of the HRV indices studied here and discuss the clinical consequences arising from gender differences in HRV.

Adolescent↗

Increased number of nitric oxide synthase immunoreactive Purkinje cells and dentate nucleus neurons in schizophrenia.

There is growing interest in the cerebellum as a site of neuropathological changes in schizophrenia. Reports showing that schizophrenics have higher nitric oxide synthase (NOS) activity and MAPKinase levels in the vermis, point to possible aberrations in the cerebellar signal transduction of schizophrenics. It has been speculated that Ca(2+)-dependent extracellular to intracellular signal transduction may be disrupted in the cerebellum of schizophrenics. We decided to test this hypothesis by studying the nitrergic system and markers of the Ca(2+)-triggered signal cascade in the cerebellum of schizophrenics, depressives and controls. The cellular distribution of two calcium sensor proteins (VILIP-1 and VILIP-3) and of neuronal NOS immunoreactivity was studied morphometrically in the flocculonodulus, the inferior vermis and the dentate nucleus of 9 schizophrenics, 7 depressive patients and 9 matched controls. In comparison to controls and depressed patients there were fewer Nissl-stained neurons in the dentate nucleus of schizophrenics. The number of NOS-expressing Purkinje neurons was however strongly increased. In the flocculonodulus and the vermis no differences between the groups were found with regard to the density of Nissl-stained Purkinje cells. The number of NOS-expressing Purkinje neurons was increased in schizophrenics, however. No differences between schizophrenics, depressives and controls were found in the number of VILIP-1 immunoreactive dentate nucleus neurons and VILIP-3 immunoreactive vermal and flocculonodular Purkinje cells. Our data provide further histochemical evidence in favor of structural abnormalities in discrete cerebellar regions of schizophrenics. They confirm and extend earlier reports of increased cerebellar NOS immunoreactivity in schizophrenia and point to possible neurodevelopmental disturbances. Our failure to show an altered expression of two calcium sensor proteins possibly points to a less important role of calcium signaling in cerebellar pathology of the disease.

Adult↗