Biomedical subjects
Publications and source records attributed to A Batra.
Data in this study indicate that both adipocytes and preadipocytes express abroad set of TLRs and they also respond to specific stimulation by cytokine production. The may be of relevance to Crohn's disease and a suggests a closer link between adipose tissue and innate immunity.
INTRODUCTION: The high morbidity and mortality caused by smoking highlights the importance of investigating new strategies for smoking cessation or reduction. Galantamine is an acetylcholinesterase inhibitor that increases the effect of acetylcholine (ACh). The nicotinic ACh receptor is activated via positive allosteric modulation (APL). METHODS: We investigated whether galantamine reduces smoking by performing a 24-week randomized, placebo-controlled, multicentric clinical trial in recently detoxified alcohol-dependent patients. We included all study subjects irrespective of an intention or motivation to abstain from nicotine. Specific treatment for cessation or reduction of smoking was not provided. Smoking behavior was assessed by means of patients' diaries. The nicotine metabolite cotinine was measured to verify the number of smoked cigarettes as documented in the patient's diary. RESULTS: 114 randomized smokers received galantamine (n = 56) or placebo (n = 58) for 12 weeks. Follow-up examinations were terminated after an additional 12 weeks without treatment. Smoking behavior did not differ between both groups at baseline. After treatment, the intention-to-treat analysis revealed significant differences with a 20% lower cumulative number of smoked cigarettes and a 15% lower number of smoking days in the galantamine group compared to placebo. The average number of smoked cigarettes per smoking day as well as the cotinine values decreased about 10%. Cotinine values showed a positive correlation with the number of documented cigarettes, validating the patients' diaries. CONCLUSION: Our tentative data indicate that galantamine reduces smoking behavior even without any additional specific intervention. We suggest introducing the term "substitution therapy" into the treatment of smoking. This result could open up a new treatment approach for groups of patients which usually have a low motivation for change.
Leukostasis is a fatal complication in granulocytic leukaemia. Brain and lung are most commonly involved organs in leukostasis. In the lung, the clinical presentation simulates infections and haemorrhagic complications of acute leukaemia. Being a medical emergency, early recognition of leukostasis and initiation of therapy prevents mortality.
As the enzyme dopamine-beta-hydroxylase (DbetaH) converts dopamine to norepinephrine and both transmitters seem to be involved in the pathology of alcoholism and severe alcohol withdrawal symptoms, the gene encoding DbetaH (DBH) was applied to explore the genetic background of alcoholism and severe withdrawal symptoms. 102 healthy control subjects and 208 alcoholics, including 97 patients with a history of mild withdrawal symptoms, 57 with a history of alcohol withdrawal seizure (AWS) and 82 with a history of delirium tremens (DT) were genotyped for the DBH*444G/A polymorphism revealing a significantly elevated frequency of genotypes carrying the A-allele (p = 0.02; after Bonferroni adjustment for multiple tests) in alcoholics compared to healthy controls. Frequencies of alleles and genotypes of individuals with mild withdrawal symptoms did not differ significantly from those of patients with DT or AWS.
BACKGROUND: Infertility may considerably reduce quality-of-life. Many of the existing generic quality-of-life measures, which often focus on physical impairments, do not represent the specific complaints of infertile patients. In this article, we report on the development and validation of the TLMK (Tübinger Lebensqualitätsfragebogen für Männer mit Kinderwunsch), an instrument for measuring quality-of-life in male patients with involuntary childlessness. METHODS: The first version of the questionnaire, which consisted of 91 items, was administered to 275 men who attended andrology and gynaecology clinics for fertility evaluations. After the questionnaires were scored, item analysis and reduction, principal component analysis and internal consistency analyses were conducted. RESULTS: The final version of the TLMK consists of 35 items in four scales and provides an internally consistent quality-of-life profile for men experiencing involuntary childlessness. Convergent and discriminant validity was supported through the correlation of the TLMK scales with established questionnaires on life satisfaction (FLZ) and partnership (PFB). CONCLUSION: The TLMK provides information about the quality-of-life in men experiencing involuntary childlessness and was found to be easy to administer and acceptable to patients. It may be used to assess patients' baseline and ongoing quality-of-life during fertility treatment and as an outcome variable in the evaluation of integrated psychological counselling.
Leptin is primarily known as a hormone regulating food intake and the adjustment to a distinct state of nutrition. In the present work a new function of leptin will be described, namely the role of leptin in the immune system. Structural characteristics of leptin and the leptin receptor already suggest an immune modulatory function. The effect of leptin on the various populations of immune cells in vitro will be described. These data are supported by findings obtained in in vivo animal models as well as descriptive and functional data from leptin-deficient humans which will be outlined in detail. In conclusion, the chimeric function of leptin as hormone and a cytokine/adipokine represents a unique link between the immune and the endocrine system thus opening a new field of research and therapeutic options.
Cerebral inflammation as well as systemic immunological alterations have been reported in Alzheimer's disease (AD). We examined the production of the proinflammatory cytokines interleukin-6, interleukin-12, interferon-gamma, and tumor necrosis factor-alpha in whole blood cell cultures of AD patients and age-matched controls. The production of all measured cytokines after mitogen stimulation is significantly decreased in the AD group compared to controls. The results reflect an attenuated secretory activity of monocytes/macrophages, but also of T-helper cells. The data sustain the assumption that a systemic, possibly age-related alteration of immune mechanisms may play a pathogenetic role in the development of AD.
The role of leptin in the immune system has been well established. While adipocytes represent the major source, leptin production by lymphocytes, infiltrating at the site of inflammation, was recently demonstrated. However, the significance of this locally released leptin remains unresolved. In the present study, two models in which absence of leptin-signalling is associated with protection were employed: the model of ConA-induced hepatitis and the CD4(+)CD45Rb(high) transfer model of colitis. For the ConA model, scid mice were reconstituted with either WT or leptin-deficient (ob/ob) CD4(+) T cells. Eight weeks post transfer, ConA was injected and serum ALT, TNFalpha, leptin as well as liver mononuclear cell activation and histological signs of inflammation were evaluated. No difference between recipients of WT or ob/ob cells was observed for any of the parameters evaluated. In the second model, either WT or ob/ob CD4(+)CD45Rb(high) cells were transferred into scid mice. No histological differences were detected, although recipients of ob/ob cells showed higher weight loss compared to recipients of WT cells. Spontaneous production of IL-6 from colon cultures obtained from recipients of ob/ob cells was reduced compared to recipients of WT cells, whereas stimulation of lamina propria lymphocytes with leptin resulted in a higher IFNgamma release in recipients of ob/ob cells compared to recipients of WT cells. In conclusion, the present study provides evidence that T cell-derived leptin does not play a major role in the regulation of the inflammatory process, indicating that the adipose tissue is the critical player in the immune-modulating effects of leptin.
Acute disseminated encephalomyelitis(ADEM) is an uncommon inflammatory demyelinating disease involving central nervous system white matter. A series of seven cases seen over a period of one year have been described. The patients presented with acute onset of focal neurological deficit (3 patients), alteration of sensorium(3) and ataxia(1). CT scan showed non specific hypodensity in 4 cases and was normal in 3 patients . MRI showed characteristic radiological changes. Complete recovery was seen in 3 patients , one died and 3 were left with sequelae.
PURPOSE: To review magnetic resonance (MR) diffusion-weighted imaging (DWI) and spectroscopy findings in patients with focal cerebral tuberculosis and to assess whether these techniques can adequately characterize focal cerebral tubercular lesions. MATERIAL AND METHODS: Sixteen patients with single or multiple lesions were evaluated on a 1.5T MR system. DWI was performed with three 'b' values of 50, 500, and 1000 s/mm2 and the apparent diffusion coefficient maps were calculated. MR spectroscopy was performed using the point-resolved single-voxel technique with 2 echo time values of 135 ms and 270 ms. The signal intensities of the tubercular lesions on diffusion images and the apparent diffusion coefficients (ADCs) of their centers, along with MR spectroscopy findings, were analyzed in relation to their T2-weighted MR appearances. RESULTS: DWI identified 17 of the 20 lesions evaluated. Increased signal intensity was seen in 9 of the 17 lesions. The ADCs of the lesions ranged from 0.406 to 2.64 x 10(-3) mm2/s (mean +/- SD: 1.038 +/- 0.609 mm2/s). Most of the lesions with hyperintense centers on T2-weighted images were of increased intensity on diffusion images, while those with hypointense centers on T2-weighted images were of decreased signal intensity on diffusion images. However, no statistical difference in the ADCs was found between lesions with increased and those with decreased signal intensity centers on T2-weighted images. MR spectroscopy revealed a lipid peak at 0.9-1.3 ppm in all of the 14 lesions evaluated. An increase in normalized choline:creatine ratio was found in all the lesions in which the spectra were obtained with the voxel, including a variable portion of the lesion wall. CONCLUSION: DWI and MR spectroscopy help in determining the nature of cerebral tubercular lesions; however, since the findings are varied, they do not help in specific characterization.
PURPOSE: To evaluate and delineate the characteristics of cerebral toxoplasmosis lesions using a combination of magnetic resonance (MR) spectroscopy, diffusion, and perfusion studies. MATERIAL AND METHODS: A total of 8 patients with 23 lesions were evaluated on a 1.5-T MR system. Diffusion-weighted imaging (DWI) was performed with three 'b' values of 50, 500, and 1000 s/mm2, and the apparent diffusion coefficient maps were calculated. The diffusion-weighted appearances and the T2-weighted MR appearances of the lesions were compared. MR spectroscopy was performed using the point-resolved single-voxel technique with two TE values of 135 ms and 270 ms. Perfusion studies were carried out using the dynamic contrast-enhanced technique, and the relative cerebral blood volume maps were qualitatively and quantitatively analyzed. RESULTS: DWI revealed the majority of the lesions as having increased diffusion within their necrotic centers, with the ADC ranging from 0.5 to 3.01 (mean +/- SD: 1.49 +/- 0.7). All the lesions revealed a predominant lipid peak on MR spectroscopy and were extremely hypovascular on perfusion MR studies. CONCLUSION: MR diffusion, spectroscopy, and perfusion studies help in characterizing toxoplasmosis lesions and, in most cases, can be used in combination to help establish the diagnosis of toxoplasmosis.
The purpose of the present paper was to evaluate the utility of perfusion MRI in cerebral gliomas showing imperceptible contrast enhancement on conventional MRI, and to evaluate the relationships of perfusion MRI and magnetic resonance (MR) spectroscopic results in these tumours. Twenty-two patients with histopathologically proven cerebral gliomas and showing insignificant contrast enhancement on conventional MR were included in the present study. All patients underwent perfusion MRI and MR spectroscopy on a 1.5-T MR system. Significant differences of the relative cerebral blood volume (rCBV) values and the choline : creatine ratios were noted between low-grade and anaplastic gliomas (P < 0.01). Good correlation was found between the rCBV values and the choline : creatine values (y = 0. 532x + 1.5643; r = 0.67). Perfusion MRI can be a useful tool in assessing the histopathological grade of non-contrast-enhancing cerebral gliomas. Along with MR spectroscopic imaging it can serve as an important technique for preoperative characterization of such gliomas, so that accurate targeting by stereotactic biopsies is possible.
The present report describes two patients with glioblastoma multiforme with the tumour demonstrating low central apparent diffusion coefficient values similar to those found in cerebral abscesses. Although conventional MR images were fairly specific for tumour, the cases illustrate the need for exercising caution when using diffusion-weighted (DW) MR images for the differentiation of necrotic brain tumours from abscesses. The DW MR imaging information should always be integrated with the conventional spin-echo MR images.
BACKGROUND: Leptin regulates appetite through the long isoform of its receptor in the hypothalamus. Although leptin regulates immune responses, it is still unknown whether a direct effect of leptin on lymphocytes is required. AIMS: To clarify whether expression of leptin receptors on T lymphocytes modulates intestinal inflammation in mice. METHODS: The model of colitis induced by transfer of CD4(+)CD45RB(high) (RB(high)) cells into scid mice was used. Wild-type (WT) or leptin receptor deficient (db/db) RB(high) cells were transferred into scid mice and development of colitis evaluated. RESULTS: Leptin receptors were expressed on both RB(high) and RB(low) cells. Intestinal lymphocytes of mice with colitis expressed high leptin levels compared with healthy controls whereas the opposite was true for serum leptin levels. Transfer of RB(high) cells from db/db mice induced delayed disease compared with transfer of WT cells. A high rate of apoptosis in lamina propria lymphocytes and reduced cytokine production were observed early on in scid mice receiving db/db RB(high) cells. These effects were not due to the high levels of glucocorticoids present in db/db mice as administration of corticosterone to WT mice failed to reproduce this phenomenon. High expression of peroxisome proliferator activated receptor gamma was observed in the colon of recipients of db/db compared with WT cells. Freshly isolated db/db RB(high) cells produced low levels of interferon gamma. Despite delayed onset of colitis, as disease progressed differences between mice receiving WT or db/db cells were no longer apparent. CONCLUSIONS: These results suggest that leptin affects the immune response, partly by acting on the long isoform of its receptor expressed on T lymphocytes.
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Data on liver enzyme elevations were collected in a retrospective study of 7,263 treatment courses with haloperidol, clozapine, perphenazine, and perazine. Charts of 233 patients hospitalized between 1980 and 1992 at Tübingen University Psychiatric Clinic were selected because clinically relevant increases of liver enzymes had been detected during monotherapy with one of the four examined neuroleptics. At least one hepatic enzyme (mostly alanine aminotransferase [ALAT]) exceeded the established reference range of 3-fold elevations of ALAT, aspartate aminotransferase, gamma-glutamyl transpeptidase, and glutamate dehydrogenase and 2-fold elevations of alkaline phosphatase (AP) during monotherapy with clozapine in 15%, perazine in 7.6%, perphenazine in 4%, and haloperidol in 2.4% of the cases. If all liver enzyme abnormalities with any elevation greater than the conventional upper limits are considered, incidences were as follows: clozapine, 78%; perphenazine, 62%; perazine, 59%; and haloperidol, 50%. Testing for overall differences within the four neuroleptics resulted in significantly different incidences of liver enzyme elevations (chi2 test,p < 0.0001). Threefold increases of AP (>540 U/L) were seen in three patients receiving haloperidol (0.3%) only. Twofold increases of AP (>360 U/L) were distributed as follows: clozapine, 1%; haloperidol, 0.8%; perazine, 0.3%; and perphenazine, 0.1%. Only in the group with 1-fold elevations of AP (>180 U/L) were the differences within the drug regimens significant (clozapine, 40.3%; haloperidol, 33.2%; perphenazine, 23.4%; and perazine, 23.1%; chi2 test, p < 0.0001). In the period under study, no instance of icterus occurred.
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