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The expression of microRNA-181b (miR-181b) has been investigated in various human cancers. However, the expression and functions of miR-181b in non-small cell lung cancer (NSCLC) are yet to be studied. In the present study, miR-181b expression in NSCLC tissues and cell lines was analyzed by quantitative polymerase chain reaction, and was shown to be recurrently downregulated. Following transfection of the H23 and H522 NSCLC cells lines with miR-181b, cell migration and cell invasion assays were performed to evaluate the effect of miR-181b overexpression on the cell motility. It was demonstrated that overexpression of miR-181b inhibited the migration and invasion of NSCLC cells. Subsequently, bioinformatics analysis, western blotting and luciferase reporter assays were conducted to investigate the mechanism underlying the miR-181b-mediated inhibition of NSCLC cell motility. It was found that miR-181b directly targeted high-mobility group box-1 (HMGB1) in NSCLC cells. These results reveal a novel therapeutic target, the miR-181b/HMGB1 axis, in NSCLC. Treatment approaches targeting this axis will be beneficial to prevent NSCLC from becoming invasive. [ABSTRACT FROM AUTHOR]

Arteriovenous malformations (AVMs) associated with aneurysm have rarely been reported in the literature. The present study reports the case of a 21-year-old pregnant female patient who presented with a subarachnoid hemorrhage and an intracranial hematoma located in the anterior end of the corpus callosum. Furthermore, an anterior cerebral aneurysm and an AVM were identified by digital subtraction angiography and magnetic resonance angiography. The aneurysm was clipped and the AVM was successfully removed by microsurgery. The diagnosis of AVM associated with an aneurysm was confirmed via intraoperative and postoperative pathological examinations. By performing a review of the current literature, issues and surgical considerations associated with AVM associated with aneurysm were analyzed. [ABSTRACT FROM AUTHOR]

An increase in the morbidity of upper respiratory tract infections and the attack and exacerbation of autoimmune diseases has been observed to occur in the few days following sudden environmental temperature decreases, but the mechanisms for these phenomena are not well understood. To determine the effect of a sudden ambient temperature drop on the levels of stress hormones and T-lymphocyte cytokines in the plasma, the Toll-like receptor 4 (TLR4) expression of immunocompetent cells in rat spleens and the levels of regulatory T (Treg) cells in the peripheral blood, Sprague Dawley rats were divided into three groups of different ambient temperatures (20, 4 and -12˚C). In each group, there were four observation time-points (1, 12, 24 and 48 h). Each ambient temperature group was subdivided into non-stimulation, lipopolysaccharide-stimulation and concanavalin A-stimulation groups. The levels of adrenocorticotropin (ACTH), epinephrine (EPI), angiotensin-II (ANG-II), interleukin-2 (IL-2), interferon-γ (IFN-γ), IL-4 and IL-10 in the plasma were determined using ELISA. The cellular expression levels of TLR4 and the presence of cluster of differentiation (CD)4+CD25+ and CD4+CD25+Forkhead box P3 (Foxp3)+ cells were determined using flow cytometry. The experiments demonstrated that the ACTH, EPI, ANG-II and IL-10 levels in the plasma were significantly increased at 4 and -12˚C compared with those at 20˚C, while the plasma levels of IFN-γ, IL-2 and IL-4, the TLR4 expression rates of immunocompetent cells in the rat spleen and the percentage of CD4+CD25+Foxp3+ Treg cells among the CD4+CD25+ Treg cells in the peripheral blood were decreased at 4 and -12˚C compared with those at 20˚C. These data indicate that cold stress affects the stress hormones and the innate and adaptive immunity functions in rats. [ABSTRACT FROM AUTHOR]

Rhizoma Dioscoreae polysaccharides (RDPS) are the primary active ingredient of Rhizoma Dioscoreae, which is a traditional Chinese medicine. RDPS have previously been shown to scavenge reactive oxygen species, and protect against D-galactose-induced mimetic aging. The present study aimed to investigate the neuroprotective effects of RDPS against hypoxia-induced neuronal cell apoptosis. Neuronal cells harvested from pregnant Sprague-Dawley rats were divided into groups, as follows: i) Normal control group; ii) hypoxia-induced apoptosis neuronal cell model; iii) 0.025 g/l RDPS-treated group; iv) 0.05 g/l RDPS-treated group; v) 0.1 g/l RDPS-treated group; and vi) 0.25 g/l RDPS treated group. Neuronal cell viability was investigated using an MTT assay, and neuronal cell apoptosis was analyzed using Annexin V-fluorescein isothiocyanate/propidium iodide double-staining, Hoechst 33342 fluorescent staining, Rhodamine 123 staining, polymerase chain reaction and immunocytochemical staining. The RDPS-treated neuronal cells exhibited improved viability, and decreased hypoxia-induced mitochondrial injury and apoptosis. In addition, the mRNA and protein expression levels of caspase-3 and B-cell lymphoma (Bcl)-2-associated X protein (Bax) were significantly downregulated, whereas the mRNA and protein expression levels of Bcl-2 were significantly upregulated, in the RDPS-treated hypoxic neurons, as compared with the apoptosis model (P<0.05). Furthermore, the ratio of Bcl-2 expression:Bax expression significantly increased following RDPS treatment, as compared with the apoptosis model (P<0.05). The results of the present study suggested that RDPS may attenuate hypoxia-induced neuronal cell apoptosis by altering the expression levels of key apoptosis-regulating proteins in hypoxic neurons. [ABSTRACT FROM AUTHOR]