Comparative study of Navicula hasta Pantocsek and Navicula rakowskae Lange-Bertalot morphology and distribution

Despite numerous reports of Navicula hasta in the literature its distribution still remains unknown. More detailed studies of Navicula hasta and related taxa resulted recently in the separation of several new species. One of these, Navicula rakowskae Lange-Bertalot, was described from a karstic spring in Poland. The holotype of N. hasta, a portion of the type material from the Natural History Museum in Budapest and the material collected from Poland (Krakowsko-Częstochowska Upland) were examined with LM and SEM. Based on the protologue and the material examined the morphological characters of both species are described. Their distribution is briefly discussed on the basis of the material collected and the reliable records in the literature

A májfibrosis nem invazív jellemzésének lehetőségei a klinikai adatok tükrében

Liver cirrhosis is one of the leading causes of death worldwide. Liver biopsy is considered as the gold standard for the diagnosis of chronic liver diseases. Studies have focused on non-invasive markers for liver fibrosis because of the dangers and complications of liver biopsy. The authors review the non-invasive direct as well as indirect methods for liver fibrosis assessment and present the positive and negative predictive value, sensitivity and specificity of those. Clinical utilities of transient elastography (Fibrsocan) is also reviewed. Non-invasive methods are useful in the assessment of liver fibrosis, monitoring disease progression and therapeutic response. Their accuracy can be increased by the combined or sequential use of non-invasive markers

The past, present, and future of the accounting profession and its digitalization: Where is accounting going next?

The technological development of the past decade has brought about revolutionary changes in our everyday life. We communicate and find information differently than ten years ago. In comparison to this, the changes brought about by networked devices are understated, even in the short term this technological step can be the one which fundamentally changes the lives of individual users and organizations, the production structure, and also business models. It can be said that Industry 4.0 has transformed the global industrial environment, not sparing accountancy either. The accounting profession can be considered to be traditional, in which the rules and principles have not radically changed in the last decade(s). Globalization, increasing regulations, new technological solutions, and innovations have also made an impact on the profession. Therefore, accountants have a significant opportunity to expand their digitized skills and knowledge, but at the same time, the changes also pose a threat to them if they do not understand how they affect the organization. The challenges facing the individual accountant are manifested in the rapid adaptation and necessity of business practices and business processes without sacrificing the basic accounting rules and principles. In our research, on the one hand, the opportunities and risks related to the digitization of the accounting profession are examined, on the other hand, the challenges faced against digitalization are overviewed, and, thirdly, the results of a questionnaire study administered amongst people working in the field and students are reported. Our results highlight that digitization represents both significant opportunities and risks for the future. The most important challenges to digitization can be outlined as follows: the use of big data in accounting and reporting, cloud-based and continuous accounting, artificial intelligence and blockchain technology. In conclusion, it can be said that technological advances and digitization will have a significant impact on the industry in the future as well, which will introduce changes in the education system, and the needs of the users of accounting information will change. These changes will affect the work of accountants, the acquisition and adaptation of new knowledge, and ultimately the quality of accounting reports

Mode of action of the positive modulator PNU-120596 on alpha7 nicotinic acetylcholine receptors.

We investigated the mode of action of PNU-120596, a type II positive allosteric modulator of the rat alpha7 nicotinic acetylcholine receptor expressed by GH4C1 cells, using patch-clamp and fast solution exchange. We made two important observations: first, while PNU-120596 rapidly associated to desensitized receptors, it had at least hundredfold lower affinity to resting conformation, therefore at 10 muM concentration it dissociated from resting receptors; and second, binding of PNU-120596 slowed down dissociation of choline molecules from the receptor radically. We propose that when agonist concentration is transiently elevated in the continuous presence of the modulator (as upon the neuronal release of acetylcholine in a modulator-treated animal) these two elements together cause occurrence of a cycle of events: Binding of the modulator is limited in the absence of the agonist. When the agonist is released, it binds to the receptor, and induces desensitization, thereby enabling modulator binding. Modulator binding in turn traps the agonist within its binding site for a prolonged period of time. Once the agonist finally dissociated, the modulator can also dissociate without re-binding, and the receptor assumes its original resting conformation. In kinetic simulations this "trapped agonist cycle" mechanism did not require that the orthosteric and allosteric ligands symmetrically modify each other's affinity, only the modulator must decrease agonist accessibility, and the agonist must induce a conformation that is accessible to the modulator. This mechanism effectively prolongs and amplifies the effect of the agonist

A Los Angeles és Duarte galaktóz-1-foszfát-uridil-transzferáz-variánsok allélgyakorisága a magyar populációban

Classical galactosaemia is an autosomal recessively inherited disorder caused by deficient activity of the enzyme galactose-1-phosphate uridyltransferase (GALT), which can be detected by newborn screening. The p.N314D mutation defines two variant forms of the GALT enzyme, the Los Angeles and Duarte, depending on the presence of additional base changes. Aim: The aim of our study was to analyze a healthy Hungarian population for the frequencies of the Los Angeles and Duarte galactose-1-phosphate uridyltransferase variant alleles. Methods: DNA samples from 100 subjects were analyzed by polymerase chain reaction, followed by digestion with restriction endonucleases. Results: The frequencies of the p.N314D, the Los Angeles and the Duarte variants were 11.5%, 2.5% and 9%, respectively. Conclusions: The allele frequencies of the Los Angeles and Duarte variant alleles in the Hungarian population correlate well with the allele frequencies in other healthy Caucasian populations

Juvenile Huntington’s disease skin fibroblasts respond with elevated parkin level and increased proteasome activity as a potential mechanism to counterbalance the pathological consequences of mutant Huntingtin protein

Huntington’s disease (HD) is an inherited neurodegenerative disorder, caused by an abnormal polyglutamine (polyQ) expansion in the huntingtin protein (Htt). Mitochondrial dysfunction and impairment of the ubiquitin-proteasome system (UPS) are hallmarks of HD neurons. The extraneural manifestations of HD are still unclear. We investigated the crosstalk between mitochondria and proteolytic function in skin fibroblasts from juvenile HD patients. We found reduced mitosis, increased cell size, elevated ROS and increased mitochondrial membrane potential in juvenile HD fibroblasts, while cellular viability was maintained. Mitochondrial OXPHOS analysis did not reveal significant differences compared to control. However, the level of mitochondrial fusion and fission proteins was significantly lower and branching in the mitochondria network was reduced. We hypothesized that juvenile HD fibroblasts counterbalance cellular damage and mitochondrial network deficit with altered proteasome activity to promote cell survival. Our data reveal that juvenile HD fibroblasts exhibit higher proteasome activity, which was associated with elevated gene and protein expression of parkin. Moreover, we demonstrate elevated proteasomal degradation of the mitochondrial fusion protein Mfn1 in diseased cells compared to control cells. Our data suggest that juvenile HD fibroblasts respond to mutant polyQ expansion of Htt with enhanced proteasome activity and faster turnover of specific UPS substrates to protect cells

Go-6976 reverses hyperglycemia-induced insulin resistance independently of cPKC inhibition in adipocytes.

This paper was originally published in PLOS ONE (Robinson KA, Hegyi K, Hannun YA, Buse MG, Sethi JK, PLoS ONE 2014, 9(10): e108963. doi:10.1371/journal.pone.0108963).Chronic hyperglycemia induces insulin resistance by mechanisms that are incompletely understood. One model of hyperglycemia-induced insulin resistance involves chronic preincubation of adipocytes in the presence of high glucose and low insulin concentrations. We have previously shown that the mTOR complex 1 (mTORC1) plays a partial role in the development of insulin resistance in this model. Here, we demonstrate that treatment with Go-6976, a widely used "specific" inhibitor of cPKCs, alleviates hyperglycemia-induced insulin resistance. However, the effects of mTOR inhibitor, rapamycin and Go-6976 were not additive and only rapamycin restored impaired insulin-stimulated AKT activation. Although, PKCα, (but not -β) was abundantly expressed in these adipocytes, our studies indicate cPKCs do not play a major role in causing insulin-resistance in this model. There was no evidence of changes in the expression or phosphorylation of PKCα, and PKCα knock-down did not prevent the reduction of insulin-stimulated glucose transport. This was also consistent with lack of IRS-1 phosphorylation on Ser-24 in hyperglycemia-induced insulin-resistant adipocytes. Treatment with Go-6976 did inhibit a component of the mTORC1 pathway, as evidenced by decreased phosphorylation of S6 ribosomal protein. Raptor knock-down enhanced the effect of insulin on glucose transport in insulin resistant adipocytes. Go-6976 had the same effect in control cells, but was ineffective in cells with Raptor knock-down. Taken together these findings suggest that Go-6976 exerts its effect in alleviating hyperglycemia-induced insulin-resistance independently of cPKC inhibition and may target components of the mTORC1 signaling pathway.This work was supported by grants from the Biotechnology and Biological Sciences Research Council (David Phillips Fellowship, JF16994), Diabetes UK (BDA:RD06/0003237) and British Heart Foundation (PG/10/38/28359) to J.K. Sethi and also from National Institute of Diabetes and Digestive and Kidney Diseases (DK-02001) to M.G. Buse