40 research outputs found

    Analyza Y-specifickych sekvenci u pacientek s Turnerovym syndromem.

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    Turner syndrome (TS) is caused by gonosomal aberrations. There is an incidence of TS 1 in 2000 - 2500 of live born girls in general population. Typical TS karyotype is identified as 45,X in 50%. The remaining cases are different mosaics or structural abnormalities of the chromosome X or Y. The frequency of Y sequences in TS patients is relatively high. Y-positive cell lines can promote development of gonadoblastoma in undifferentiated gonads of TS patients. The risk of tumour genesis is about 30%. The region responsible for the tumour is localised near to the centromere. Testis-specific protein Y-encoded (TSPY) gene is considered to be responsible for tumorogenesis due to confirmed TSPY expression in gonadoblastoma. The aim of this work is the molecular and molecular-cytogenetic analysis of Y-specific sequences in 130 samples from TS patients, from paraffin embedded pathological gonadal tissues and from fresh gonadal tissues. PCR, QF PCR, sequencing and cDNA analysis are components of the molecular investigation, FISH method was used for the molecular-cytogenetic testing. The results serve for a more exact diagnostic technique constructing. Preventive gonadectomy is the clinical consequence of the work.Available from STL Prague, CZ / NTK - National Technical LibrarySIGLECZCzech Republi

    The effects of 5-aminoimidazole-4-carboxamide riboside on the pancreas in neonatal streptozotocin-diabetic rats

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    In this study, we aimed to determine the alterations of beta-cell ultrastructure, insulin mRNA and protein products of the same gene on the pancreas of rats following long-term treatment of 5-aminoimidazole-4-carboxamide riboside (AICAR). A single dose of streptozotocin (STZ) 100 mg/kg was injected intraperitoneally (i.p.) to 2-day-old newborn (n2) rats. The rats were divided into three groups. The first group was the n2 STZ-diabetic rats. The second group consisted of n2 STZ-diabetic rats treated with AICAR 10 mg/kg/day for one month. The third group was non-diabetic control rats. Our findings demonstrate that AICAR treatment decreases the blood glucose level but increases the body weight in n2 STZ-diabetic rats. In the AICAR-treated group, numerous beta cells showed increased insulin gene expression. We also observed increased exocytosis in this group, in an ultrastructural manner. As a result, it is suggested that AICAR may induce insulin synthesis and betacell regeneration in n2 STZ-diabetic rats

    PENETRATION OF CIPROFLOXACIN INTO PLEURAL FLUID

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    The penetration of oral 1000 mg/day ciprofloxacin into pleural fluid is investigated in 15 patients with exudative pleural effusion. After 4 days of ciprofloxacin therapy ciprofloxacin concentrations were measured in plasma and pleural exudate simultaneously by high-performance liquid chromatography (HPLC). Mean serum ciprofloxacin level was 1.58 +/- 0.91 mg/L and mean pleural exudate concentration was 1.00 +/- 0.59 mg/L. The concentrations achieved were all above the MIC90 of the majority of Gram-positive and Gram-negative pathogens. It is concluded that ciprofloxacin penetrates well into the pleural fluid

    Effects of propofol on conditioned place preference in male rats: Involvement of nitrergic system

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    Background: Drug-induced conditioned place preference (CPP) is linked to the addictive properties of the drug used. The number of studies that have investigated the effects of propofol on CPP is limited. Research findings suggest that nitric oxide (NO) might play an important role in substance use disorders. Objectives: The present study sought to investigate the role of the nitrergic system on the rewarding effects of propofol by using the CPP protocol in rats. Methods: The experiment followed habituation, pre-conditioning, conditioning, and post conditioning sessions. Male Wistar albino rats weighing 240-290 g were divided into eight groups: control (saline), propofol (10, 20, and 40 mg/kg), the NO synthase (NOS) inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) alone (30 and 60 mg/kg), and in combination with propofol (30 and 60 mg/kg L-NAME plus 40 mg/kg propofol) (n = 8 for each group). The CPP effects of propofol, L-NAME, saline, and their combinations were evaluated. All the drug and saline administrations were performed by intraperitoneal (ip) injections. Results: Propofol (10-40 mg/kg) produced CPP that was statistically significant relative to saline. Propofol-induced CPP was significantly reversed by pretreatment with L-NAME. When administered alone, L-NAME did not produce CPP and also did not produce any significant change on locomotor activity of naive rats. Conclusion: Our results suggest that propofol produces CPP effects in rats and that NO-related mechanisms may be responsible for propofol-induced CPP. Thus, propofol might have the potential to be addictive, and this possibility should be considered during clinical applications of this drug
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