ABSTRACT
@#Crimean-Congo haemorrhagic fever (CCHF) is a severe human infection which can lead to fatal consequences. Acute CCHF patients were previously shown to exhibit frequencies of regulatory T-cell (Treg) but lower Treg-mediated suppressive activities than the healthy counterparts. This study aims is to investigate the phosphorylation levels of Foxp3 protein (master regulator of Treg cells) in CCHF patients. Blood samples collected from 18 CCHF patients and nine healthy volunteers were used to isolate peripheral blood mononuclear cells (PBMCs). Total and phosphorylated Foxp3 expression levels in the isolated PBMC samples were monitored by western blot and quantified using ImageJ software. Total Foxp3 expression levels in CCHF patients displayed decreasing trend, but not significantly. In contrast, significantly lower expression levels of phosphorylated Foxp3 were reported in CCHF patients. Our results suggest a possible association between Foxp3 dephosphorylation and CCHF pathogenesis. Nevertheless, more studies are required to evaluate the effect of Foxp3 dephosphorylation on Treg function, which would not only help to enlighten the CCHF pathogenesis but also contribute to the development of effective treatment strategies.
ABSTRACT
@#This study was conducted to investigate rickettsial seropositivity among hunters, a high-risk population for tick-borne diseases in northern Cyprus. Serum samples were collected from 300 hunters from different locations during the 2017-2018 hunting season (November 2017 - February 2018). The samples were analyzed by indirect immunofluorescence assay (IFA) using slides coated with Rickettsia slovaca, a species belonging to the spotted fever group (SFG). During the sample collection, a questionnaire was also applied to evaluate possible risk factors for rickettsial seropositivity. Of the 300 serum samples, six (2.0%) were found to be IgG-positive with a titer of 1:64. While all seropositive individuals were male, the statistical analysis revealed no significant association of gender with rickettsial seropositivity (p=1.000). Other factors including age (p=0.414), residential places of the participants (p=0.347), hunting years (p=0.694) or hunting abroad (p=1.000) did not significantly affect the IgG positivity. Also, no statistical correlation was found between a history of an arthropod (tick, louse, or flea) bite and rickettsial seropositivity (p=1.000). To our knowledge, this is the first study that demonstrates rickettsial seropositivity among human population in northern Cyprus. Our study suggests that awareness should be raised among the people especially involved in outdoor activities such as hunting, and control programs should be implemented to prevent possible rickettsiosis cases. Further serological studies using other Rickettsia spp. antigens, as well as molecular studies that search for Rickettsia spp. in humans, animals and arthropods are needed to obtain more comprehensive data on rickettsiosis in northern Cyprus.
ABSTRACT
In this study, an electrochemical DNA biosensor was developed using a straightforward methodology to investigate the interaction of indinavir with calf thymus double-stranded deoxyribonucleic acid (ct-dsDNA) for the first time. The decrease in the oxidation signals of deoxyguanosine (dGuo) and deoxy-adenosine (dAdo), measured by differential pulse voltammetry, upon incubation with different con-centrations of indinavir can be attributed to the binding mode of indinavir to ct-dsDNA. The currents of the dGuo and dAdo peaks decreased linearly with the concentration of indinavir in the range of 1.0-10.0μg/mL. The limit of detection and limit of quantification for indinavir were 0.29 and 0.98μg/mL, respectively, based on the dGuo signal, and 0.23 and 0.78μg/mL, respectively, based on the dAdo signal. To gain further insights into the interaction mechanism between indinavir and ct-dsDNA, spectroscopic measurements and molecular docking simulations were performed. The binding constant (Kb) between indinavir and ct-dsDNA was calculated to be 1.64 × 108 M-1, based on spectrofluorometric measure-ments. The obtained results can offer insights into the inhibitory activity of indinavir, which could help to broaden its applications. That is, indinavir can be used to inhibit other mechanisms and/or hallmarks of viral diseases.
ABSTRACT
The purpose of this experimental study was to evaluate the efficacy of hesperidin [HES] in protecting against methotrexate [MTX]-induced intestinal damage using histopathological and immunohistochemical techniques. Seventy-eight male Wistar albino rats were divided into 4 groups that received [a] saline only [control group], n = 19; [b] HES only, n = 19; [c] MTX only, n = 19, and [d] MTX plus HES, n = 21. On the first day of the study, a single dose of MTX [20 mg/kg] was administered intraperitoneally to group 3 and 4 rats. The HES [200 mg/kg] was administered by gavage for 5 days. For the MTX plus HES group, HES [200 mg/kg] was administered by gavage for 5 days after MTX treatment. Rats were sacrificed on the 2nd, 4th and 6th day of the study. Tissue samples from the jejunum were taken for histopathological and immunohistochemical analysis. On the 4th day, crypt injury in the MTX plus HES group [1.00 +/- 0.00] was less than that in the MTX group [2.00 +/- 0.89; p < 0.05]. The small intestinal damage score was lower in the MTX plus HES group [6.33 +/- 0.82] as compared to the MTX group [8.00 +/- 2.37]. Inducible nitric oxide synthase and interleukin-8 levels were lower in the MTX plus HES group [65 and 25%, respectively] as compared to the corresponding values of the MTX group [80 and 52.5%, respectively]. On the 6th day, the Ki-67 proliferation index in the MTX group [45%] was lower than that in the MTX plus HES group [76.67%] and the control group [p < 0.05]. The small intestinal damage score was high in the HES group on the 4th day due to increased cellular infiltration. On the 6th day, the Ki-67 proliferation index rose in parallel with the decrease in cellular infiltration and therefore histopathological scoring. The proliferation-enhancing effect of HES also appeared in healthy rats. HES seemed to have a protective effect against MTX-induced intestinal injury