STAT1 inhibitor alleviates spinal cord injury by decreasing apoptosis.

Spinal cord injury (SCI) is typically caused by trauma or disease, and it severely affects patients' motor function. The relationship between signal transducers and activators of transcription-1 (STAT1) and neuronal death after cerebral focal ischemia has been comprehensively studied, but its role in SCI remains largely unknown. This study investigated the protective effect of an STAT1 inhibitor on SCI. Thirty SD rats were SCI-induced and were then randomly divided into two groups (N = 15 each), either receiving STAT1 or the STAT1 inhibitor S1491 by intraperitoneal injection. The motor dysfunction of the rats was evaluated by behavioral scores, followed by the examination of SCI by hematoxylin and eosin staining. Apoptosis was also detected by Western blot and terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling (TUNEL) assay. The motor functions of rats receiving STAT1 did not score as well as the STAT1 inhibitor group (P < 0.01). Further assays showed remarkable improvements in pathological damage to spinal code tissue in STAT1 inhibitor-treated rats, along with lower Bax and higher Bcl-2 expression. The STAT1 inhibitor also suppressed the occurrence of TUNEL-positive cells compared to the STAT1-treated group. In summary, we suggest that the STAT1 inhibitor alleviates SCI by decreasing apoptosis.

MiR-200c regulates ROS-induced apoptosis in murine BV-2 cells by targeting FAP-1.

OBJECTIVE: Reactive oxygen species (ROS) are significantly upregulated after spinal cord injury (SCI). MicroRNAs (miRNAs) are reported to be widely involved in regulating gene expression. This paper aims to explore the correlation between ROS-induced cell apoptosis and abnormal miRNA expression after SCI. METHODS: To profile the expression of miRNAs after SCI, miRNA microarray was applied and the result was verified by reverse transcription quantitative PCR (RT-qPCR). ROS production following H2O2 stimulation was examined using dihydroethidium staining and flow cytometry. The levels of miR-200c after H2O2 treatment were determined using RT-qPCR. Cell viability and apoptosis were examined in murine BV-2 cells transfected with miR-200c mimics, inhibitor or negative control. Immunofluorescence and western blot were used to further explore the effects of miR-200c on Fas-associated phosphatase-1 (FAP-1) expression. RESULTS: MiR-200c was showed to be significantly increased after SCI by miRNA microassay and RT-qPCR. ROS production enhanced miR-200c expression in a dose-dependent manner and induced significant apoptosis in BV-2 cells. The upregulation of miR-200c reduced cell viability and induced BV-2 cell apoptosis. MiR-200c negatively regulated the expression of FAP-1, thereby inducing FAS signaling-induced apoptosis. RT-qPCR analysis showed that the FAP-1-targeting small interfering RNA (siRNA) did not affect the level of miR-200c in murine BV-2 cells. In addition, suppression of FAP-1 by siRNA promoted apoptosis, even in cells that were co-transfected with the miR-200c inhibitor. CONCLUSIONS: The current data suggested that miR-200c contributes to apoptosis in murine BV-2 cells by regulating the expression of FAP-1. This proposes a therapeutic target for enhancing neural cell functional recovery after SCI.

[Progress of researches on global prevalence of Blastocystis hominis human infections and its subtypes].

Blastocystis hominis is a parasite that parasitizes in the intestines of humans and animals, and is closely related to a variety of gastrointestinal diseases such as abdominal pain and diarrhea. B. hominis is distributed worldwide, and the prevalence of B. hominis infections and dominant subgenotypes vary in countries and in regions from the same country. This paper reviews the global prevalence of B. hominis human infections, its subtypes and geographical distribution, so as to provide insights into the understanding of the global epidemiology of B. hominis and the management of B. hominis infections.

[Progress of researches on animal models of Blastocystis hominis infections].

Blastocystis hominis is a common parasitic protozoa in human and animal intestines; however, its pathogenicity remains controversial. Construction of animal models is of great significance to investigate the pathogenicity, pathogenic mechanisms and drug screening of B. hominis. Experimental animals, mode of infections, parasite strains and host immune status are important factors affecting the successful modeling of B. hominis infections in animals. Hereby, we review the progress of researches on animal models of B. hominis infections, and summarize the influencing factors and application of animal models of B. hominis infections, in order to provides insights into the selection of animals models of B. hominis infections.

Personality correlates of auditory augmenting response to clicks repeated around 2Hz.

Eighty-three subjects (47 women and 36 men) were submitted to Plutchik-van Praag's (PVP) depression inventory, Zuckerman's sensation seeking scales and Zuckerman-Kuhlman's personality inventory, and underwent auditory evoked potential studies using clicks at 4 different intensities of 70, 80, 90 and 100 dB. The clicks were delivered at an interstimulus interval varying randomly around 0.5s, which can elicit an obligatory subcomponent of N1. The P2 latency was significantly prolonged at the highest intensity. The intensity dependence of peak-to-peak N1-P2 and of baseline-to-peak N1 and P2 components was pronounced and the majority of subjects were augmenters. The N1 latency elicited at 70 dB was positively correlated with the thrill and adventure seeking, which then correlated the activity. The correlation suggests that a lower level of arousal, as indicated by prolonged N1 latency, would lead one to seek higher stimulation, such as the augmented response, the increased desire of physical thrill and adventure and elevated activity. This study, therefore, supports Zuckerman's theory that a sensation seeking personality is related to cortical arousal level.