Helical edge states in silicene and germanene nanorings in perpendicular magnetic field

Due to nonzero intrinsic spin-orbit interaction in buckled honeycomb crystal structures, silicene and germanene exhibit interesting topological properties, and are therefore candidates for the realization of the quantum spin Hall effect. We employ the Kane-Mele model to investigate the electron states in hexagonal silicene and germanene nanorings having either zigzag or armchair edges in the presence of a perpendicular magnetic field. We present results for the energy spectra as function of magnetic field, the electron density of the spin-up and spin-down states in the ring plane, and the calculation of the probability current density. The quantum spin Hall phase is found at the edges between the nontrivial topological phase in silicene and germanene and vacuum. We demonstrate that the helical edge states in zigzag silicene and germanene nanorings can be qualitatively well understood by means of classical magnetic moments. However, this is not the case for comparable-sized armchair nanorings, where the eigenfunctions spread throughout the ring. Finally, we note that the energy spectra of silicene and germanene nanorings are similar and that the differences between the two are mainly related to the difference in magnitude of the spin-orbit coupling.Comment: 17 pages, 10 figure

The effects of valsartan on cardiac function and pro-oxidative parameters in the streptozotocin-induced diabetic rat heart

© 2020, University of Kragujevac, Faculty of Science. All rights reserved. Diabetes mellitus is a major risk factor for cardiovascular diseases, while cardiovascular diseases are a leading cause of morbidity and mortality worldwide. The renin–angiotensin– aldosterone system controls renal, cardiovascular, adrenal function and regulates fluid and electrolyte balance as well as blood pressure. Because of his role, inhibition of renin-angiotensin-aldosteron system is another therapy approach that reduces the risk of diabetes and cardiovascular disease. In this study, our goal was to evaluate effect of valsartan,as inhibitor of angiotensin II receptor type 1, on cardiac tissue and function, with focus on cardiodynamic and oxidative stress. The present study was carried out on 20 adult male Wistar albino rats (8 week old and with body masses of 180-200 g). Rats were divided randomly into 2 groups (10 animals per group). Healthy animals treated with 1 μM of valsartan and streptozotocin-induced diabetic animals perfused with 1 μM of valsartan 4 weeks after the induction of diabetes. Our results demonstrated that acute application of valsartan has different effect on cardiodynamics in rat heart of diabetic and healthy animals but did not improve cardiac function in hy-perglycemia-induced changes. A challenge for further investi-gations are studies with chronic or acute administration, alone or in combination with other angiotensin-converting-enzyme inhibitor in various models of diabetes

Blocked Elements in 1-D and 2-D Arrays—Part I: Detection and Basic Compensation on Simulated and <italic>In Vivo</italic> Targets

During a transcostal ultrasound scan, ribs and other highly attenuating and/or reflective tissue structures can block parts of the array. Blocked elements tend to limit the acoustic window and impede visualization of structures of interest. Here, we demonstrate a method to detect blocked elements and we measure the loss of image quality they introduce in simulation and in vivo. We utilize a fullwave simulation tool and a clinical ultrasound scanner to obtain element signals from fully sampled matrix arrays during simulated and in vivo transcostal liver scans, respectively. The elements that were blocked by a rib showed lower average signal amplitude and lower average nearest-neighbor cross correlation than the elements in the remainder of the 2-D aperture. The growing receive-aperture B-mode images created from the element data indicate that the signals on blocked elements are dominated by noise and that turning them OFF has a potential to improve visibility of liver vasculature. Adding blocked elements to the growing receive apertures for five in vivo transcostal acquisitions resulted in average decrease in vessel contrast and contrast to noise ratio of 19% and 10%, respectively

Alcohol consumption among the elderly citizens in Hungary and Serbia: comparative assessment

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The Encapsulation of Lycopene in Nanoliposomes Enhances Its Protective Potential in Methotrexate-Induced Kidney Injury Model

Methotrexate is an antimetabolic drug with a myriad of serious side effects including nephrotoxicity, which presumably occurs due to oxidative tissue damage. Here, we evaluated the potential protective effect of lycopene, a potent antioxidant carotenoid, given in two different pharmaceutical forms in methotrexate-induced kidney damage in rats. Serum biochemical (urea and creatinine) and tissue oxidative damage markers and histopathological kidney changes were evaluated after systemic administration of both lycopene dissolved in corn oil and lycopene encapsulated in nanoliposomes. Similar to previous studies, single dose of methotrexate induced severe functional and morphological alterations of kidneys with cell desquamation, tubular vacuolation, and focal necrosis, which were followed by serum urea and creatinine increase and disturbances of tissue antioxidant status. Application of both forms of lycopene concomitantly with methotrexate ameliorated changes in serum urea and creatinine and oxidative damage markers and markedly reversed structural changes of kidney tissue. Moreover, animals that received lycopene in nanoliposome-encapsulated form showed higher degree of recovery than those treated with free lycopene form. The findings of this study indicate that treatment with nanoliposome-encapsulated lycopene comparing to lycopene in standard vehicle has an advantage as it more efficiently reduces methotrexate-induced kidney dysfunction

ASSOCIATION OF NEUROPEPTIDE S RECEPTOR 1 AND GLUTAMATE DECARBOXYLASE 1 GENE POLYMORPHISMS WITH POSTTRAUMATIC STRESS DISORDER

Background: Posttraumatic stress disorder (PTSD) is an anxiety disorder caused by highly traumatic experiences. The aim of this study was to investigate the influence of single nucleotide polymorphisms (SNPs) in the neuropeptide S receptor 1 (NPSR1) and the glutamate decarboxylase 1(GAD1) gene on PTSD and its psychopathological aspects among individuals affected by the Balkan wars during the 90s. Subjects and methods: This study was conducted as part of the South Eastern Europe (SEE) study on molecular mechanisms of PTSD. It comprised 719 participants (539 males), including those with current PTSD, remitted PTSD and healthy volunteers. Psychometric evaluation was performed using the Mini International Neuropsychiatric Interview (M.I.N.I.), the Clinician Administrated PTSD Scale (CAPS) andthe Brief Symptom Inventory (BSI). We examined NPSR1 single nucleotide polymorphism (SNP) rs324981 and GAD1 variant rs3749034 genotypes. Case-control analyses were carried out using logistical regression to determine genotype differences between all patients that had either current or remitted PTSD and control individuals. To analyse the influence of the analysed SNPs on PTSD severity, we performed linear regression analyses with CAPS and BSI within each of the two patient groups separately. All of the calculations were performed for additive allelic, recessive, dominant and genotypic models. Results: We observed a nominally significant association for the major allele (G) of GAD1 rs3749034 with an increased risk to develop PTSD in a case control analysis in the recessive model (P=0.0315, odds ratio=0.47, SE=0.35). In contrast, a nominally significant association of the minor allele (A) with higher CAPS scores was identified within the patient group with lifetime PTSD in the dominant model (P=0.0372, ????=6.29, SE=2.99). None of these results did withstand correction for multiple tests. No nominal significant results of GAD1 rs3749034 were found with regard to the intensity of psychological BSI symptoms. Case control analyses of NPSR1 rs324981 revealed a nominally significant higher risk for homozygous T allele carriers to develop PTSD (P=0.0452) in the recessive model. On the other hand, the T allele showed a nominally significant association with higher BSI scores in patients suffering from lifetime PTSD in the recessive model (P=0.0434). Again, these results were not significant anymore after correction for multiple tests. No associations of NPSR1 rs324981 and CAPS score was identified. Conclusion: The findings of this study provide some evidence that the NPSR1 and GAD1 polymorphisms might play a role in the development of war-related PTSD and its related psychological expressions. Further research is needed to elucidate the interactions of specific gene variants and environmental factors in the development of PTSD

ROLE OF THE ALLELIC VARIATION IN THE 5-HYDROXYTRYPTAMINE RECEPTOR 1A (HTR1A) AND THE TRYPTOPHAN HYDROXYLASE 2 (TPH2) GENES IN THE DEVELOPMENT OF PTSD

Background: Post-traumatic stress disorder (PTSD) is a stress related disorder which can occur in an individual after exposure to a traumatic event. It most commonly co-occurs with depression. The two disorders share not only overlapping symptoms, but also genetic diathesis. The aim of this study was to investigate the potential role of single nucleotide polymorphisms (SNPs) of the two serotonergic candidate genes 5-hydroxytryptamine receptor 1A (HTR1A) and tryptophan hydroxylase 2 (TPH2) in the pathogenesis of PTSD and comorbid psychopathology. Subjects and methods: 719 (487 males, 232 females) participants who had experienced war-related trauma between 1991 and 1999 in Bosnia and Herzegovina, Kosovo and Croatia were included in the study. The Sociodemographic questionnaire, Mini International Neuropsychiatric Interview (M.I.N.I.), Clinician Administered PTSD Scale (CAPS) and Brief Symptom Inventory (BSI) were used to collect clinical data. The SNPs rs6295 (HTR1A), rs11178997 and rs1386494 (TPH2) were investigated for their association with PTSD and comorbid psychopathology. Results: A nominal significant association was found between the BSI total score in Lifetime PTSD with the SNP rs6295 of the HTR1A gene. The best result was seen in the dominant model (P=0.018), with the minor allele (C) being the risk allele. Several BSI subscores were also associated with the minor (C) allele in Lifetime PTSD. No association was found for the TPH2 SNPs rs11178997 and rs1386494 in relation to PTSD or comorbid psychopathology. Conclusions: Our findings suggest that rs6295 in the HTR1A gene may contribute to the psychopathology of PTSD