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Introduction and objective: Two-thirds of patients with hepatitis C virus (HCV) infection are unaware of their infection in the European Union. The WHO aims to reduce the number of new cases of chronic hepatitis by 90% by 2030. The proportion of people infected with HCV in prisons can be up to ten times higher compared to the general population. This article is a summary of the results of the HCV screening carried out in the Hungarian prisons between 2007 and 2017. Method: Screening of anti-HCV antibodies has been performed on a voluntary basis followed by HCV PCR and genotyping in positive cases. After obtaining written informed consent from the patients, treatment was started. Treatments were performed under the guidance of hepatologists in collaboration with prison medical staff. Results: HCV screening programs and treatments are in place in 84% of Hungarian prisons. A total of 25 384 patients underwent anti-HCV screening. Anti-HCV positive result was detected in 6.6% and HCV PCR positivity was confirmed in 3.8% of the screened inmates. 55.2% patients from the HCV PCR positive population were put on treatment. Only 143 patients received full treatment, while 162 (42.6%) treatments were terminated prematurely, and the duration of treatment was unknown in 75 patients. Based on the results available on the 24th week after the end of treatment, sustained virologic response rate was 88%. Discussion: Education of patients and collaboration between hepatologists and prison medical staff play an important role in the successful result of treatment. Conclusion: Our experience demonstrates that the test and treat principle is feasible and effective at microeliminating HCV in prisons.

Melanin-concentrating hormone (MCH), the neuropeptide produced mainly in the hypothalamus, plays an operative role in regulating food intake and the sleep/wake cycle. Considering that these physiological functions pursue diurnal variations, we checked whether the total hypothalamic MCH level depends on the time of the day. The aggregated MCH peptide content of the whole MCH neuron population was significantly higher at the end of the sleeping period (lights on), than at the end of the active period (lights off). This result, together with earlier observations, indicates that in contrast to the MCH gene expression, the level of MCH peptide is object of circadian variation in the hypothalamus.

Introduction: During 2011 and 2013, 155 Hungarian hepatitis C genotype 1 infected patients, mostly with advanced liver fibrosis, who did not respond to prior peginterferon + ribavirin dual therapy, started boceprevir based triple therapy in an early access program., Aim and Method: Efficacy and safety of the therapy was retrospectively assessed based on sustained virologic responses, as well as on frequency and type of serious adverse events and of those leading to therapy discontinuation., Results: In an intent-to-treat analysis 39.4% patients (61/155) reached sustained virologic response. Amongst pervious relapsers, partial responders and null-responders 59.5%, 41.4 % and 22.9% (p<0.05 compared to the other two categories) reached sustained virologic response, respectively, while amongst non-cirrhotics and cirrhotics 52.5% and 31.3% (p<0.05 compared to the non-cirrhotics) achieved sutained virologic response, respectively. Six out of the 33 most difficult to cure patients (previous null responder and cirrhotic) have reached sustained virologic response (18.2%). Frequency of early discontinuations due to insufficient virologic response was 31.1%, while due to adverse event 10.3%. Reported frequency of serious adverse event was 9.8%. These events represented anemia, diarrhoea, depression, agranulocytosis, elevated aminotransferases, generalized dermatitis and severe gingivitis with loss of teeth, prolonged QT interval on ECG, generalized oedema and severe dyspnoea, uroinfection, exacerbation of Crohn's disease, Campylobacter pylori infection and unacceptable weakness and fatigue. Eight patients received transfusion, 4 patients erythropoietin and 1 granulocyte colony stimulating factor during therapy. No death has been reported., Conclusions: With boceprevir based triple therapy, one of the bests available in 2011-2013 in Hungary, a relevant proportion of hepatitis C infected patients with advanced liver fibrosis achieved sustained viral response. In this cohort, side-effects resembled those reported in registration studies, and resulted in therapy discontinuation with consequent treatment failure in a relevant number of patients. Efficacy and tolerability of boceprevir-based triple therapy are suboptimal, particularly in the most difficult to cure patient population. Orv. Hetil., 2016, 157(34), 1366-1374.

It has previously been demonstrated that Dp71, the most abundant dystrophin protein in the brain, is mainly localized in the postsynaptic densities. Here we show the localization of Dp71f, one of the splice variants of this protein, within the CA3 region of the hippocampus. Immunopositivity occurs in the postsynaptic density of small asymmetrical axospinous and axodendritic synapses, while it is absent in the postsynaptic densities of the axospinous synapses of the large mossy fiber terminals. Dp71f immunoreactivity was found to be attached to the membranes of the mossy fibers in the stratum lucidum of the CA3 area. In a certain population of thin myelinated axons the protein seems to be present within the axon proper. These data support the notion of a physiological role of Dp71f distinct from other dystrophin isoforms present in the central nervous system.

The dystrophin glycoprotein complex (DGC) is a membrane-associated protein complex binding extracellular matrix (ECM) molecules, such as laminin and forming a bridge towards the cytoskeleton. The molecular composition of the DGC is cell type dependent and it is involved in cell adhesion and motility. Here we present immunocytochemical localization of beta-dystroglycan, the central member of the DGC, utrophin and Dp71f, the spliced 71 kDa dystrophin protein product of the DMD gene, in cultured retinal Muller glial cells. It is shown that beta-dystroglycan and utrophin are colocalized in clusters in all parts of Muller cells including the lamellipodium and leading edge of migrating cells. As a contrast, Dp71f labels are distinct from beta-dystroglycan and confined to the perinuclear cytoplasm of Muller cells indicating that Dp71f is not a member of the DGC in cultured Muller cells.

Vimentin contributes to the cytoskeleton of different cell-types, among them glial cells. We report here that different forms of this protein, distinguishable by the monoclonal antibodies Vim3B4 and V9, are species-specifically expressed in cultures of glial fibrillary acidic protein (GFAP) positive, primary astrocytes of the chicken and rat. Most cells in the cultures co-expressed GFAP and one of the two vimentin epitopes. The Vim3B4 positive epitope was present in chicken astrocytes, while the V9 positive was not. Inverse situation was found in the astrocytes of rat. In vitro age of the cells did not influence the hierarchy of vimentin epitope expression with respect to species-specificity. Our result shows that the different vimentin expression program of cultured astrocytes of the chicken and rat is preserved under in vitro conditions. The presented data support the concept of the species-specific regulation of vimentin forms in glial cells of the central nervous system.

Remote astroglial response was evoked in the adult rat visual cortex by unilateral destruction of the corpus geniculatum laterale. Homogenates of ipsi- and contralateral (operated and control) visual cortices were analysed by immunoblotting. A peak increase in glial fibrillary acidic protein (GFAP) was observed 2 weeks after lesion which then declined but did not return to normal showing a time course similar to that of previously observed immunohistochemical changes. Findings prove that the mechanism underlying the enhanced immunoreactivity during remote astroglial response is an up-regulation of GFAP synthesis in the astroglial processes surrounding degenerating synapses.

Microtubule-associated tau proteins are likely candidates to interfere with axonal transport of membranous organelles. We studied that tau proteins influenced the enzyme activity of kinesin, known to drive anterograd transport along microtubules. An in vitro reconstituted system was applied; microtubules were assembled from purified tubulin with or without tau proteins. Both types of reconstituted microtubules stimulated MgATPase activity of purified kinesin in a concentration dependent, saturable manner. The extent of maximal stimulation by tau-coated microtubules was lower than that of microtubules without tau proteins. Analysis of kinetic data, on the other hand, suggests that tau-coated microtubules apparently bind kinesin with higher affinity then microtubules not associated with tau proteins. Tau proteins, similarly to tubulin dimers, seem to bind to the heavy chain of kinesin. These data support the notion that tau proteins could act as regulators of kinesin-driven processes.

Two monoclonal antibodies directed against vimentin, Vim 3B4 and V9 could distinguish between vimentins originating from certain species, when tested on cell lines (Bohn et al, 1992). Our comparative immunohistochemical studies in the rat and chicken brain with the same antibodies suggest the coexistence of two vimentin forms in the glial cells of both species. One of these forms bearing the epitope present in the respective non-glial cell lines is present in astrocytes and Bergmann glia independently of the ontogenic state of the animal. The other epitope appeared also mutually in both species, albeit its expression was more restricted. These patterns suggest that in these two species, the expression of the different vimentin forms might be differently regulated.

Clinical data of 70 patients, treated and observed with myelodysplastic syndrome between 1977 and 1989 were analysed. Two-thirds of the patients belonged to the elder age-group and a mild female predominance was registered. With the application of complex cytochemical-histological and cytogenetical methods, correct diagnosis could be established. The clinical material included patients from different morphologic subtypes: 19 with refractory anaemia (with a longer course of the illness). 20 with sideroblastic anaemia, 26 with chronic myelomonocytic leukaemia and the remaining 5 with refractory anaemia with excess of blasts (a more progressive type of the myelodysplastic syndrome, with a short duration). The mean survival of all patients were 42 months. 45 (69%) died during this period and 12 (18.5%) among them in acute myelogenous leukaemia (mean survival: 16 month). Megakaryoblastic leukaemic transformation was observed in three patients with sideroblastic refractory anaemia. Haemorrhage and infection-sepsis, due to thrombocytopenia and/or granulocytopenia, was fatal in 30 cases. In the treatment of the myelodysplastic syndrome an appropriate supportive therapy (blood transfusion, antibiotics) has a decisive importance. A more aggressive treatment with cytostatic drugs is suggested in the progressive form of the disease of younger patients and in patients with overt acute leukaemia.