Notes

Specialized medical application of polyfoliate anterolateral thigh perforator flap using single-perforator.
Drinking alcohol and using pornography more frequently were also associated with slutpage use behaviors. This study provides a new understanding of slutpages as a social form of image-based sexual abuse and informs researchers, educators, and policy makers to expand their inquiry into online sexual experiences and exploitation to include this phenomenon.Current cancer treatment regimens such as chemotherapy and traditional chemical drugs have adverse side effects including the appearance of drug-resistant tumor cells. For these reasons, it is imperative to find novel therapeutic agents that overcome these factors. To this end, we explored a cationic antimicrobial peptide derived from Litopenaeus vannamei hemocyanin (designated LvHemB1) that induces cancer cell death, but sparing normal cells. LvHemB1 inhibits the proliferation of human cervical (HeLa), esophageal (EC109), hepatocellular (HepG2), and bladder (EJ) cancer cell lines, but had no significant effect on normal liver cell lines (T-antigen-immortalized human liver epithelial (THLE-3) cells). In addition to its antiproliferative effects, LvHemB1 induced apoptosis, by permeating cells and targeting mitochondrial voltage-dependent anion channel 1 (VDAC1). Colocalization studies revealed the localization of LvHemB1 in mitochondria, while molecular docking and pull-down analyses confirmed LvHemB1-VDAC1 interaction. Moreover, LvHemB1 causes loss in mitochondrial membrane potential and increases levels of reactive oxygen species (ROS) and apoptotic proteins (caspase-9, caspase-3, and Bax (Bcl-2-associated X)), which results in mitochondrial-mediated apoptosis. Thus, peptide LvHemB1 has the potential of being used as an anticancer agent due to its antiproliferation effect and targeting to VDAC1 to cause mitochondrial dysfunction in cancer cells, as well as its ability to induce apoptosis by increasing ROS levels, and the expression of proapoptotic proteins.This study aims to investigate the role of miR-495 in neuronal cell apoptosis after acute spinal cord injury (ASCI). The ASCI rat model was established and the Basso, Beattie, and Bresnahan (BBB) score was assessed. miR-495, PR domain containing 5 (PRDM5), and Bcl-2 expressions were measured by qRT-PCR or western blotting. Neuronal cell line PC-12 was subjected to hypoxia condition to simulate the in vitro ASCI model. PC-12 cell apoptosis was measured by flow cytometry, and the interaction between miR-495 and PRDM5 was confirmed by dual luciferase reporter assay. Results showed that BBB score was significantly decreased in ASCI rats compared with sham rats. selleck chemicals miR-495 expression was down-regulated in spinal cord tissue of ASCI rats and hypoxia-induced PC-12 cells, and PRDM5 protein level was up-regulated in spinal cord tissue of ASCI rats and hypoxia-induced PC-12 cells. miR-495 overexpression could reduce apoptosis of PC-12 cells, and up-regulated anti-apoptosis protein Bcl-2 protein level. Moreover, PRDM5 was a target of miR-495, and mRNA and protein levels of PRDM5 were negatively regulated by miR-495. miR-495 overexpression could reduce the hypoxia-induced PC-12 cell apoptosis, while PRDM5 overexpression abolished this inhibiting effect. The agomir-495 was injected into ASCI rats, and Bcl-2 protein level and BBB score were increased, but the PRDM5 overexpression reversed these results. Overall, we concluded that miR-495 could inhibit neuronal cell apoptosis and relieve acute spinal cord injury through inhibiting PRDM5.This study aimed to explore the role of miR-363-3p in renal fibrosis (RF) in vitro. HK-2 cells were treated with transforming growth factor (TGF)-β1 for 72 h to establish an in vitro model of RF. Subsequently, western blot analysis and reverse transcription-quantitative PCR were used to detect the protein and mRNA expression levels of RF markers in TGF-β1-treated HK-2 cells, respectively. The results showed that the protein and mRNA expression levels of TGF-β2, α-smooth muscle actin (SMA), fibronectin, vimentin, collagen II and N-cadherin were increased, while the protein and mRNA expression levels of E-cadherin were decreased in TGF-β1-treated HK-2 cells. The level of miR-363-3p was significantly decreased in TGF-β1-treated HK-2 cells. TargetScan indicated that TGF-β2 was a direct target gene for miR-363-3p, which was further verified using dual luciferase reporter gene assays. Further analyses revealed that the increased protein and mRNA expression levels of TGF-β2, α-SMA, fibronectin, vimentin, collagen II, N-cadherin, increased phosphorylated-Smad3 protein level, and decreased E-cadherin protein and mRNA expression in TGF-β1-treated HK-2 cells were significantly reversed by miR-363-3p mimics. However, all the effects were suppressed by a TGF-β2-plasmid. The results suggested that miR-363-3p plays a protective role in RF by regulating the TGF-β2/Smad3 signaling pathway.Kawasaki disease is a kind of self-limited systemic vasculitis involving middle and small arteries, which usually occurs in children under 5 years old. Excessive inflammatory response caused by activation of monocytes is one of the important mechanisms of Kawasaki disease. Activated monocytes secrete large amounts of inflammatory mediators such as TNF-α and IL-1β. Activin A, a member of transforming growth factor-β superfamily, is a multifunctional growth and transforming factor. Several experimental evidences pinpoint that Activin A can regulate multiple biological function of the immune system. However, whether Activin A is involved in regulation of activation of monocytes in Kawasaki disease was not well characterized. Here, this study showed that the expression of Activin A in serum decreased in acute-phase Kawasaki disease. Furthermore, Activin A inhibits activin type IIA receptor, activin type IB receptor, CD86 and CD80 expression in over-activated monocytes. In addition, Activin A inhibited Smad3 expression and NF-κB signaling pathways. Specific function and mechanism of Activin A in acute-phase Kawasaki disease need further study.Depression is common among people living with HIV. Multiple studies demonstrate a link between depression and cognitive dysfunction in adults with HIV, but the association has been minimally investigated in children and adolescents with HIV in Africa. We conducted a cross-sectional analysis as part of the HIV-associated Neurocognitive Disorders in Zambia study, a prospective cohort study in Lusaka, Zambia. We included 208 perinatally-infected children with HIV ages 8-17 taking antiretroviral therapy and 208 HIV-exposed uninfected (HEU) controls. Cognition was assessed with a comprehensive neuropsychological battery. Depressive symptoms were evaluated using self-report and parent-report versions of the NIH Toolbox Sadness module and the Patient Health Questionnaire-9 (PHQ-9). Risk factors for depression and associations between depressive symptoms and cognition were evaluated in bivariable and multivariable regression models. Participants with HIV demonstrated higher levels of depressive symptoms than controls (mean NIH Toolbox Sadness T-Score 50 vs.
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