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Chen Chen,1 Linjing Wang,1 Li Wang,2 Qi Liu,1 Chunying Wang1 1Institute of Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin, 150040, People’s Republic of China; 2Harbin Traditional Chinese Medicine Hospital, Harbin, 150076, People’s Republic of ChinaCorrespondence: Chunying WangInstitute of Chinese Medicine, Heilongjiang University of Chinese Medicine, 24 Heping Road, Harbin, 150040, People’s Republic of ChinaTel/Fax +86-18644086608Email wcywyh7680@163.comPurpose: Acute ischemic stroke (AIS) is a leading health problem caused by cerebral ischemia/reperfusion (CI/R). This study aimed to unveil the potential clinical value and mechanism of lncRNA CASC15.Patients and Methods: The expression of CASC15, miR-338-3p was detected by quantitative real-time PCR (qRT-PCR). The correlations between CASC15 and national institutes of health stroke scale (NIHSS) scores or miR-338-3p were evaluated by Pearson correlation. A receiver operating characteristic (ROC) curve was performed to provide the diagnostic value of CASC15. Cell Counting Kit-8 (CCK-8) and flow cytometer were used to detect the condition of cell viability and apoptosis. The levels of interleukin-1beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) was detected by enzyme-linked immunosorbent assay (ELISA) assay.Results: The expression of CASC15 was increased and the levels of miR-338-3p were decreased in AIS patients. A positive association between CASC15 and NIHSS score and an inverse association between CASC15 and miR-338-3p were revealed by Pearson correlation. CASC15 might discriminate AIS patients from healthy people. Silenced CASC15 exerted neuroprotective roles on cell viability, apoptosis, and inflammation via the miR-338-3p/ETS1 axis.Conclusion: CASC15 might act as a potential diagnostic biomarker for AIS patients. CASC15/miR-338-3p/ETS1 axis played an essential role in cell viability, apoptosis, and neuroinflammation.Keywords: CASC15/miR-338-3p/ETS1, acute ischemic stroke, biomarker, inflammation

Objective. This review sought to evaluate the strength and validity of the existing evidence for the use of Chinese medicine for the treatment of polycystic ovary syndrome (PCOS). Methods. We retrieved systematic evaluations and meta-analyses of randomized controlled trials (RCTs) evaluating Chinese herbal interventions in polycystic ovaries, including the use of decoctions or Chinese patent medicines. The quality of these systematic evaluations was assessed using AMSTAR2 tools, and ovulation rate, pregnancy rate, effective rate, serum hormones (testosterone, luteinizing hormone, and follicle-stimulating hormone), and adverse reactions were recorded. Finally, the reliability of each result was evaluated according to the GRADE system. Data Sources. PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Data, CQVIP, and SINOMED databases were searched up to January 1, 2021. Outcomes. A total of 18 publications were included, all of which showed that PCOS symptoms were improved with Chinese medicine compared with control groups. However, most of the evaluations did not have good research designs and had issues with the analysis of their results. The reliability of most outcome measures was rated low or very low, and it is presumed that the reliability of the results was low due to the poor quality of the RCTs. Conclusions. At present, there is insufficient evidence to suggest that improved efficacy is achieved by the combined use of Chinese and Western medicine compared with Western medicine alone in treating PCOS. Therefore, it is recommended that multicenter, large-sample RCTs adopting standard designs and rigorous methods be carried out in the future while introducing standardized assessment plans for the systematic review of clinical trials so as to improve the quality of the resulting clinical evidence.

Huanglian-Houpo drug combination (HHDC) is a classical traditional Chinese medicine that has been effectively used to treat seasonal colds and flu. However, no systematic studies of the effects of HHDC on H1N1 influenza infection and the associated mechanisms have been reported. The aim of the present study was to determine the anti-H1N1 influenza effects of HHDC and explore the underlying mechanisms. A mouse model of H1N1-induced pneumonia was established and the mice were treated with HHDC (4, 8 and 16 g/kg) for 5 days after viral challenge. The antiviral effects of HHDC and the underlying mechanisms in the mice were investigated and evaluated with respect to inflammation, oxidative stress and Toll-like receptor (TLR)/myeloid differentiation factor (MyD88)/nuclear factor (NF)-κB signaling pathways. HHDC provided significant protection against weight loss and reduced the H1N1 viral load in the lungs. In addition, HHDC significantly decreased the lung index and increased the spleen and thymus indices of the H1N1-infected mice. HHDC also significantly ameliorated the histopathological changes of pneumonia, decreased serum levels of the cytokines interleukin (IL)-6, tumor necrosis factor-α and interferon-γ, and increased the serum level of IL-2. Moreover, HHDC significantly increased the levels of the antioxidant factors superoxide dismutase and glutathione, and reduced the serum level of nitric oxide. Furthermore, the mRNA and protein expression levels of TLR3, TLR7, MyD88, NF-κB p65 and tumor necrosis factor receptor-associated factor 3 in the lung tissues were significantly decreased by HHDC. These findings suggest that HHDC directly inhibited H1N1 infection in vivo and exerted a therapeutic effect on influenza-induced pneumonia in mice by modulating cytokines, antioxidant factors and TLR/MyD88/NF-κB signaling pathways.

Rats were divided into six groups: sham/control , Dl-3-n-butylphthalide, P1 (low phenytoin, 100 mg/kg), P2 (high phenytoin, 200 mg/kg), NP1 (Dl-3-n-butylphthalide 80 mg/kg, phenytoin 100 mg/kg), NP2 (Dl-3-n-butylphthalide 80 mg/kg, phenytoin 200 mg/kg). Hematoxylin/eosin and Nissl staining showed that, compared to the sham/control group, the Dl-3-n-butylphthalide group had no obvious hippocampal and cerebellar neuron loss, but there was a significant neuron loss in the P1 and P2 groups (P < 0.05), which was more obvious in the P2 group (P < 0.05). The positive expression of Bax and Bcl-2 proteins in hippocampal and cerebellar neurons was not significantly different between sham and Dl-3-n-butylphthalide groups; however, compared to sham, Bax expression was significantly increased and Bcl-2 was significantly decreased in the hippocampal and cerebellar neurons of rats in both P1 and P2 groups (P < 0.05), being more obvious in the P2 group (P < 0.05). Furthermore, the administration of Dl-3-n-butylphthalide attenuated the deleterious effects of phenytoin (P < 0.05). Our results indicate that phenytoin causes apoptosis of hippocampal and cerebellar neurons in rats in a dose-dependent manner, with the effect of a higher dose being more obvious, whereas, Dl-3-n-butylphthalide inhibits the phenytoin-induced apoptosis of neurons and has a neuroprotective role.

The effect of antibiotics on horizontal gene transfer (HGT) is controversial, and the underlying mechanism remains poorly understood. Here, using Escherichia coli SM10λπ as the donor strain, which carries a chromosomally integrated RP4 plasmid, we investigated the effect of antibiotics on conjugational transfer of a mobilizable gentamicin (Gm) resistance plasmid. The results showed that an exposure to gentamicin that restricted the survival of recipient cells significantly enhanced SM10λπ- Pseudomonas aeruginosa PAO1 conjugation, which was attenuated by a deficiency of lasI-rhlI , genes associated with the generation of the quorum sensing signals N -acyl homoserine lactones (AHLs) in PAO1, or the deletion of the AHL receptor SdiA in SM10λπ. Subsequent mechanistic investigations revealed that a treatment with Gm repressed the mRNA expression of lasI and rhlI in PAO1 and upregulated traI expression in SM10λπ. Moreover, PAO1 treated with other quorum sensing (QS)-inhibiting antibiotics such as azithromycin or chloramphenicol also showed a conjugation-promoting ability. On the other hand, when using non-AHL-producing E. coli strain EC600 as the recipient cells, the promoting effect of Gm on conjugation could not be observed. These data suggest that AHL-SdiA contributes to the effectiveness of antibiotics on plasmid conjugation. Collectively, our findings highlight the HGT-promoting effect of antibiotics and suggest quorum sensing as a promising target for controlling antibiotic resistance dissemination. These findings have implications for assessing the risks of antibiotic use and developing advisable antibiotic treatment protocols.

Artificial cochlear implant is a sort of device which is used to restore normal hearing to the profoundly deaf by electrical stimulation of the auditory nerve. This paper reviews the Continuous Interleaved Sampling (CIS) strategy for cochlear implant, and simulate it in PC using Matlab. The audible sound of cochlear implanter is synthesized, and preliminary analysis has also been done based on the simulation. Experimental results show that CIS strategy with 7~10 channels is sufficient to convey important sound signal to the cochlea and to simulate the auditory physiology of normal people.