The severity of ischemic brain injury was closely associated with the mortality and disability of stroke. How to limit ischemic brain injm-y to the greatest extent and promote the recovery of neurological function is one of the most concerned hotspots at present in the field of neuroscience. A large number of studies have shown that a variety of factors involve in the pathological process of ischemic brain injury, in which, the role of T lymphocyte-mediated immune inflammatory response in ischemic brain injury has received increasing attention. This article mainly reviews the role of T cells in ischemic brain injury.

Objective To explore and build a real, objective, comprehensive clinical nursing individual performance indicators architecture model,and check the rationality and validity for prize distribution by clinical application. Methods The methods included that discuss new ideas of nursing performance management by multi- disciplinary experts,developed clinical personal nursing staff performance evaluation program,worded out indicators and methods for the clinical assessment of individual nurses and nurse managers respectively,then applied research in the pilot departments and hospital step by step. Results A personal performance evaluation framework model was constructed, which include clinical nurses and nursing managers. Experimental results show that the nursing staff in this regard performance program have a high degree of recognition, 98.82% (1 741/1 762) nursing staff understanding of the purpose and significance, 97.15%(1 712/1 762) nurses think the performance model structure is reasonable. After the implementation of the performance program, the outstanding rate of personal performance appraisal of nurses was 93% (1 639/1 762). Conclusions The application of scientific performance appraisal programs can play a positive role in helping improve the quality of clinical care, and promote the stable development of the care team.

Objective To assess the clinical value of systemic vascular resistance index (SVRI) combined with serum procalcitonin (PCT) and sequential organ failure assessment (SOFA) score in the early diagnosis of sepsis. Methods A retrospective study was conducted. The data of critical patients admitted to Department of Critical Care Medicine of the Third People's Hospital of Hechi from November 2013 to April 2016 were enrolled. The clinical data were recorded as follows: gender, age, infection site, SOFA score, serum PCT level (enzyme linked fluorescence analysis) within 1 hour after intensive care unit (ICU) admission, hemodynamics parameters, including mean arterial pressure (MAP), central venous pressure (CVP), cardiac index (CI), SVRI, global end diastolic volume index (GEDVI), extravascular lung water index (EVLWI), which were monitored by pulse indicator continuous cardiac output (PiCCO) after ICU admission. The patients were divided into sepsis and non-sepsis groups according to the diagnostic criteria of sepsis. Septic patients were divided into low SVRI group, normal SVRI group, and high SVRI group according to SVRI normal value (170-240 kPa·s·L-1·m-2), and the differences in parameters among the three groups were compared. The correlations between SVRI and various parameters were analyzed by using Pearson correlation analysis. The receiver operating characteristic curve (ROC) was plotted to evaluate the diagnostic efficiency of each parameter. Results Totally 103 critical patients were enrolled, 55 in sepsis group, and 48 in non-sepsis group. Compared with non-sepsis group, SVRI in septic group was significantly lowered (kPa·s·L-1·m-2: 146.56±45.17 vs. 188.04±56.27), and serum PCT was significantly increased (μg/L: 10.43±6.17比0.32±0.11) with statistically significant differences (both P < 0.05). In 55 sepsis patients, there were 21 in low SVRI group, 19 in normal SVRI group, and 15 in high SVRI group. There were no statistically significant differences in gender, age and infection site among the three groups, indicating that the baseline data among all groups was balanced with comparability. SOFA score, PCT, and CI in the low SVRI group were significantly higher than those of normal SVRI and high SVRI groups [SOFA: 10.57±2.89 vs. 5.73±2.28, 5.73±2.15, PCT (μg/L): 24.15±12.43 vs. 7.18±5.05, 7.39±4.38, CI (mL·s-1·m-2): 71.01±9.67 vs. 62.01±8.34, 62.51±8.67, all P < 0.05], but no significant difference was found between the normal SVRI group and high SVRI group. There was no statistically significant difference in MAP, CVP, EVLWI, and GEDVI among the three groups. It was shown by Pearson correlation analysis that SVRI was negatively correlated with PCT, SOFA score, and CI (r value was -0.622, -0.598, -0.398, all P = 0.000). It was shown by ROC curve that area under ROC curve (AUC) of PCT combined with SVRI for diagnosis of sepsis was higher than that of PCT or SVRI alone (0.943 vs. 0.911, 0.884). When the cut-off value of PCT was 3.79 μg/L, and cut-off value of SVRI was 156.81 kPa·s·L-1·m-2, the sensitivity and specificity were 94.6% and 92.3% respectively. Conclusions For sepsis patients, SVRI is related to PCT and SOFA score. Combined monitoring of PCT, SVRI, SOFA score can accurately reflect the severity of sepsis patients, guide diagnosis and treatment, and estimate prognosis. The efficacy of PCT combined with SVRI in the early diagnosis of sepsis is better than that of the two alone.

The aim of this study was to synthesize 1-(5-(hydroxymethyl)-4-methyl-3-oxo-3,4-dihydro-pyrazin-2-yl) guanidine (mucunaguanide),a pyrazinone alkaloid compound extracted from the seed of Stizotobium cochinchinensis.Starting from benzyloxy acetaldehyde,following four steps in reaction including condensation,cyclization,substitution and hydrogenation reaction,mucunaguanide was synthesized with total yield of 27.9％,and purity of more than 97.5％.Structures of all the intermediates and target compound were confirmed by IR,1H NMR and MS.This synthetic process was characterized with raw materials available,simple in operation with much milder reaction conditions,and was an ideal method of synthesis of this compound.

To establish a gene regulation system compatible with biopharmaceutical industry and gene therapy, we constructed a fusion protein of biotin ligase from Bacillus subtilis (BS-BirA) and the trans-activation domain, and used its expression vector as the regulatory vector. Meanwhile, BS-BirA-specific operators were ligated upstream of attenuated CMV promoter to obtain the response vector. In this way, a novel eukaryotic gene regulation system responsive to biotin was established and named BS-Biotin-On system. BS-Biotin-On system was further investigated with the enhancing green fluorescent protein (EGFP) as the reporter gene. The results showed that our system was superior to the current similar regulation system in its higher induction ratio, and that the expression of interest gene could be tuned in a rapid and efficient manner by changing the biotin concentrations in the cultures, Our results show that the established system may provide a new alternative for the exogenous gene modulation.
Bacillus subtilis ; Biotin ; chemistry ; Eukaryotic Cells ; metabolism ; Gene Expression Regulation ; Genetic Vectors ; Promoter Regions, Genetic ; Trans-Activators

BACKGROUND:Islet beta cell replacement therapy is one of the most promising approaches for treating type 1 diabetes mellitus. However, its large scale application is hampered by a shortage of islet beta cells for transplantation. Pluripotent stem cells are one of ideal seed cells for islet beta cell replacement therapy, but pancreatic beta-cell differentiation is time-consuming and labor-intensive. OBJECTIVE:To construct a high efficient pancreatic and duodenal homeobox 1 (Pdx1)/insulin dual-reporter vector and to monitor the key genes expression during pancreatic beta-cell differentiation from pluripotent stem cells. METHODS:In order to construct a high efficient Pdx1/insulin dual-reporter vector, puromycin resistance gene was firstly introduced into pTiger vector, and then the original 410 bp mouse Ins1 promoter of the vector was replaced by 646 bp mouse Ins1 promoter. Finally, the dual-reporter vector was transduced into INS-1 and human induced pluripotent stem cells to testify its function. RESULTS AND CONCLUSION:The high efficient Pdx1/insulin dual-reporter vector was constructed successfully. The vector successfully acquired puromycin resistance gene and high gene expression efficacy of insulin in INS-1 cells. The specific gene expression pattern of Pdx1/insulin was first found in INS-1 cells. To conclude, the real-time monitoring function of Pdx1/insulin expression is preliminarily confirmed during pancreatic beta-cell differentiation.

Objective. To study the effects of XW630 on bone formation in overiectomized(OVX) rats and in human osteoblast-like cell line TE85.Method. Bone histomorphometric analysis was performed with undecalcified bone sections and tetracycline intraperitoneally labeling.Results. Compared with that of OVX rats, the static data of trabecular bone volume(TBV)/ total tissue volume(TTV), TBV/sponge bone volume(SBV) and mean trabecular plate density (MTPD) were enhanced while mean trabecular plate spacing(MTPS) decreased after treated with XW630 for 13w. The dynamic data of single-labeled surface [Sfract(s)], double-labeled surface[Sfract(d)],Sfract(d+1/2s),trabecular osteoid surface(TOS), and bone formation rate in tissue level (Svf) were increased and osteoid maturation period (OMP) shortened in XW630 group. In osteoblast-like cells, both 3H-thymidine incorporation and cell count increased after treated with XW630 for 48. Treated with XW630 for 12～18h,inducible nitric oxide synthase(iNOS) activity and cGMP content increased in time-dependent manners.Conclusions. XW630 enhanced bone activation frequency and increased trabecular connectivity, stability, and strength. The cellular mechanism related to effects of XW630 on bone formation in ovariectomized rats.

Perinatal depression is a psychological disorder that occurs during pregnancy and within one year of delivery, which can seriously affect the physical and mental health of pregnant and postpartum women, as well as the cognitive and behavioral abilities of offspring, with potential multigenerational effects. Therefore, it is important to identify its potential modifiable risk factors. Phthalic acid esters (PAEs), as common environmental endocrine disruptors, can affect maternal estrogen through multiple mechanisms and are important potential modifiable risk factors for developing maternal perinatal depression. At present, studies on the correlation between PAEs and perinatal depression are still very limited, and the mechanisms by which PAEs affect perinatal depression have not been clarified. Based on existing epidemiological and toxicological studies at home and abroad, the article briefly introduced the characteristics of multiple pathways, high doses, and long-term exposure to maternal PAEs, focused on reviewing the current status of epidemiological studies, pointed out the possible associations between some specific PAEs exposure and elevated risk of perinatal depression. It also summarized the potential roles of hormone-neurotransmitter pathway, inflammation mediation, gene regulation, and other possible mechanisms in the association between exposure to PAEs and perinatal depression. The article concluded with a look at how future research on the association between exposure to PAEs and perinatal depression can be scientifically validated, with a view to providing more high-quality evidence for the scientific prevention of the onset and progression of maternal depressive symptoms.

OBJECTIVETo study the effect of emodin on the proliferation, cell cycle distribution, apoptosis and expression of hematopoietic growth factors in bone marrow mesenchymal stem cells (BMSCs).

METHODSThe proliferation of rat BMSCs exposed to emodin was analyzed using MTT assay, and flow cytometry was used to detect the apoptosis and cell cycle changes of the exposed cells. Real-time quantitative PCR was used to determine the mRNA expression of the hematopoietic growth factors.

RESULTSExposure to 0.1 and 1 µg/ml emodin for 48 and 72 h significantly enhanced the proliferation of BMSCs (P<0.01). The cells exposed to 0.1 µg/ml emodin showed significantly increased percentage of cells in G2/M phase (P<0.05), and 1 µg/ml emodin exposure caused increased cells in S phase (P<0.01) and decreased cells in G1/G0 phase (P<0.05). Emodin exposure for 48 h resulted in significantly decreased cell apoptosis (P<0.05). BMSCs treated with 0.1 µg/ml emodin showed a significant increase in the expression of thrombopoietin mRNA (P<0.05).

CONCLUSIONEmodin can promote the proliferation of BMSCs in vitro possibly by regulating the cell cycle distribution, cell apoptosis and thrombopoietin expression.

Animals ; Apoptosis ; Cell Cycle ; Cell Proliferation ; drug effects ; Emodin ; pharmacology ; Hematopoietic Cell Growth Factors ; metabolism ; Mesenchymal Stromal Cells ; cytology ; drug effects ; RNA, Messenger ; Rats

Objective To observe the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) and to investigate the epigenetic regulation of EZH2 inhibitor DZNeP on osteogenic differentiation of hPDLSCs. Methods The hPDLSCs were isolated and cultured, and their proliferation under different concentrations of DZNeP (0, 1, 2, 5 and 10 μmol/L) was detected by MTT. The effects of DZNeP on osteogenic differentiation of hPDLSCs were observed by alkaline phosphatase (ALP) staining and alizarin red staining. The effect of DZNeP on the trimethylation of histone H3K27 in hPDLSCs was detected by immunofluorescence staining. Results Compared with the control group, the proliferation of hPDLSCs after 1, 2, 5 and 10 μmol/L DZNeP treatment for 48 h was significantly decreased, respectively (all P<0.05), and it was concentration-dependent. The result of ALP staining and alizarin red staining showed that DZNeP could promote the expression of early osteogenic markers ALP and the formation of advanced calcified nodules of hPDLSCs. The immunofluorescence staining result showed that the trimethylation fluorescence intensity of histone H3K27 was significantly decreased in the DZNeP group compared with the control group. Conclusions As an EZH2 inhibitor, DZNeP can inhibit the proliferation of hPDLSCs and promote the differentiation of hPDLSCs into osteoblasts in vitro, suggesting that DZNeP can be used as a potential small molecule drug for the treatment of periodontitis.