Objective To investigate the status of clinical nursing teaching in the department of infection.Method To investigated the teachers and nursing students in the department of infection with a self-designed questionnaire.Results The evaluation from students to the teachers are:overall satisfaction score is(4?90±0?04),the lowest points are the advanced nursing of common diseases and the teaching attitude.While the evaluations from teachers are:overall satisfaction score is(4?45+0?04),the lowest are communication with patients and their families,conducting basic nursing operation and familiarity of common drugs.Conclusions To enhance teaching quality of clinical nursing teaching in the department of infection,it is efficient by improving the quality of teachers and their teaching methods,consolidating students’knowledge,and exercising their skills?

cells, the expression of PTEN was up-regulated while pAkt down-regulated. Conclusions AS-miR-221 and AS-miR-222 may enhance the radiosensitivity of MCF-7 breast cancer cells by up-regulating the expression of PTEN.

OBJECTIVETo study the radiation-sensitizing effect of up-regulating p27(kip1) expression by knocking down miR-221/222 in the U251 human glioblastoma cell line.

METHODSBy bioinformatic analysis, we searched the miRNA-221/222 sequence and found the relationship between p27(kip1) and miRNA-221/222. miRNA-221/222 antisense oligonucleotides were transfected into U251 human glioblastoma cells. Northern blot analysis was conducted to detect the expression of miR-221/222 in control, scrambled oligonucleotide (ODN) transfected and anti-mi-221/222ODNs transfected cell groups. The cell cycle kinetics was detected by flow cytometry. Clonogenic assay was used to measure the mitotic cell death and p27(kip1) expression was examined by Western blot analysis.

RESULTSBased on bioinformatic analysis, we found that the seed sequences of miR-221 and miR-222 coincide with each other, and p27(kip1) is a target for miRNA-221/222. The expression level of miR-221/222 was significantly knocked down in cells transfected with antimiR-221/222 as compared to the parental cells or cells transfected with scrambled ODN. Cell cycle was arrested in G0 or G1 phase in the anti-miR-221/222 group. When combined with irradiation, S phase fraction in the anti-miR-221/222 cell group is lower than that in the other two control groups. Anti-miR-221/222 combined with irradiation could synergistically enhance mitotic cell death. The expression of p27(kip1) was up regulated in the anti-miR-221/222 group revealed by Western blot analysis.

CONCLUSIONAnti-miR-221/222 may enhance the radiosensitivity of U251 human glioblastoma through upregulation of p27(kip1).

Base Sequence ; Cell Cycle ; radiation effects ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p27 ; genetics ; metabolism ; Glioblastoma ; genetics ; metabolism ; Humans ; MicroRNAs ; genetics ; metabolism ; Molecular Sequence Data ; Oligonucleotides, Antisense ; genetics ; metabolism ; Radiation Tolerance ; Sequence Alignment ; Up-Regulation ; radiation effects ; X-Rays

Objective To investigate the effect of Osthole on memory function of sleep deprivation(SD) mice. Methods Forty-eight male mice were randomly divided into 4 groups;normal control group(NC group ), large platform control group(TC group),sleep deprivation group(M group)and Osthole group(Ost group). The model of SD in mice was estabished by using improved multi platform method. The ability of learning and memory was tested by using Morris water maze test and pathological changes of hippocampal neurons in mice were observed by HE staining. The serum,hippcampus malondialdehyde(MDA)contents and superoxide dismutase(SOD)activity, so as the hippocampus No content,were detected. Results Compared with NC group and TC group,the escape la-tency of M group increased significiantly and the number of crossing platform decreased significantly. There were in-creased levels hippocampus tissue,serum MDA level,hippocampal SOD activity and NO content. After supplemen-tation of Osthole,the escape latency significantly shortened in mice. The number of crossing platform was increased while the contents of MDA both in hippocampus and serum were decreased,and the SOD activity in hippocampus re-turned to normal. However,the level of NO in hippocampus was not decreased. Conclusion Osthole can protect the memory function of SD mice by reducing the the damage of hippocampal neurons through antioxidant stress.

Objective:The study retrospectively identified the correlative factors of low back pain after single-level oblique lateral interbody fusion (OLIF).Methods:Records of 93 patients (55 males and 38 females) who underwent OLIF (oblique lateral interbody fusion) surgery for lumbar degenerative diseases from May 2016 to September 2019 were analyzed retrospectively and patients' age was 55.73±9.48 years (range 32-78 years). There were 18 patients underwent L 3, 4 segment (19.35%), 73 patients underwent L 4, 5 segment (78.50%), and 2 patients underwent L 5S 1 segment (2.15%). There were 43 patients underwent OLIF stand alone and 50 patients underwent OLIF combined with lateral or posterior internal fixation. The follow-up time was 22.86±5.90 months (range 12-32 months). According to whether the visual analog scale (VAS)≥3 at the last follow-up visit, the patients were divided into low back pain group and no low back pain group. The demographic characteristics (age, gender, body mass index and comorbidities), basic surgical data (surgical segments, surgical methods, surgical time, intraoperative bleeding, endplate injury or not during operation), imaging data (lumbar lordosis, segmental lordosis, intervertebral height and cage subside) and lumbar function were recorded. The potential related factors were analyzed by univariate analysis, and the factors with P<0.05 were selected in the multivariate logistic regression model. Then the risk factors of low back pain after OLIF were determined by multivariate logistic regression analysis. Results:Nineteen patients with VAS score equal or greater than 3 were included in low back pain group, and the remaining 74 patients were included in no low back pain group. There was no significant difference in baseline data such as age, gender, BMI, follow-up time and comorbidities between two groups. There was no significant difference in VAS score between the two groups before operation ( t=0.818, P=0.414), but there was significant difference in VAS score at last follow-up visit ( t=6.958, P<0.001). The incidence rate of osteoporosis in low back pain group (63.16%) was significantly higher than that in no low back pain group (25.68%) ( t=9.558, P=0.002). There was no significant difference in vertebral height between the two groups ( t=1.008, P=0.316), however, the vertebral height was higher in no low back pain group ( t=2.537, P=0.316) at the last follow-up. The incidence of cage subsidencewas 8.11% in no low back pain group and 36.84% in low back pain group and there was significant difference between the two groups ( t=10.381, P=0.001). Multivariate logistic regression analysis showed that osteoporosis ( P=0.009), intraoperative bone endplate injury ( P=0.031), decreased intervertebral space height ( P=0.029) and cage subsidence ( P=0.016) were associated with low back pain after single-level OLIF. Conclusion:Low back pain is one of the common complications after OLIF. Osteoporosis, intraoperative bony endplate injury, decreased intervertebral space height and cage subsidence were closely related to postoperative low back pain. In order to reduce the incidence of postoperative low back pain and improve the clinical outcomes, attention should be paid to the protection of the bony endplate, rational use of internal fixation and active anti-osteoporosis treatment after operation.

Objective:To investigate risk factors for early mortality (EM) in patients with newly diagnosed multiple myeloma (NDMM) and to build an EM-predictive model.Methods:In a cohort of 275 patients with NDMM, risk factors for EM at 6, 12, and 24 months after diagnosis (EM6, EM12, and EM24, respectively) were determined to establish a model to predict EM.Results:The rates of EM6, EM12, and EM24 were 5.5% , 12.7% , and 30.2% , respectively. The most common cause for EM was disease progression/relapse, accounting for 60.0% , 77.1% , and 84.3% of EM6, EM12, and EM24, respectively. EM6 was associated with corrected serum calcium >2.75 mmol/L and platelet count <100×10 9/L, whereas risk factors for EM12 included age >75 years, ISS Ⅲ, R-ISS Ⅲ, corrected serum calcium >2.75 mmol/L, serum creatinine >177 μmol/L, platelet count <100×10 9/L, and bone marrow plasma cell ratio ≥ 60% . In addition to the risk factors for EM12, EM24 was also associated with male sex and 1q21 gain. By multivariate analysis, age >75 years, platelet count <100×10 9/L, and 1q21 gain were independent risk factors for EM24 but there were no independent risk factors significantly associated with EM6 and EM12. Using a scoring system including these three risk factors, a Cox model for EM24 was generated to distinguish patients with low (score<3) and high (score ≥ 3) risk. The sensitivity and specificity of the model were 20.7% and 99.2% , respectively. Further, an internal validation performed in a cohort of 183 patients with NDMM revealed that the probability of EM24 in high-risk patients was 26 times higher than that in low-risk patients. Moreover, this model was also able to predict overall survival. The median overall survival of patients with scores of 0, 1, 2, 3, 4, and 5 were 59, 41, 22, 17.5, and 16 months, respectively. Conclusion:In the study cohort, the EM6, EM12, and EM24 rates were 5.5% , 12.7% , and 30.2% , respectively, and disease progression or relapse were main causes of EM. An EM24-predictive model built on three independent risk factors for EM24 (age>75 years, platelet count<100×10 9/L, and 1q21 gain) might predict EM risk and overall survival.

Objective:To investigate the effect of tofacitinib,a pan-Janus kinase(JAK)inhibitor,on transforming growth factor-beta 1(TGF-β1)-induced fibroblast to myofibroblast transition(FMT)and to explore its mechanism.To provide a theoretical basis for the clinical treatment of connective tissue disease-related interstitial lung disease(CTD-ILD).Methods:(1)Human fetal lung fibroblast 1(HFL-1)were cultured in vitro,and 6 groups were established:DMSO blank control group,TGF-β1 in-duction group,and TGF-β1 with different concentrations of tofacitinib(0.5,1.0,2.0,5.0 μmol/L)drug intervention experimental groups.CCK-8 was used to measure the cell viability,and wound-healing assay was performed to measure cell migration ability.After 48 h of combined treatment,quantitative real-time PCR(RT-PCR)and Western blotting were used to detect the gene and protein expression levels of α-smooth muscle actin(α-SMA),fibronectin(FN),and collagen type Ⅰ(COL1).(2)RT-PCR and enzyme-linked immunosorbnent assay(ELISA)were used to detect the interleukin-6(IL-6)gene and protein expression changes,respectively.(3)DMSO carrier controls,1.0 μmol/L and 5.0 μmol/L tofacitinib were added to the cell culture media of different groups for pre-incubation for 30 min,and then TGF-β1 was added to treat for 1 h,6 h and 24 h.The phosphorylation levels of Smad2/3 and signal transducer and activator of transcription 3(STAT3)protein were detected by Western blotting.Results:(1)Tofacitinib inhibited the viability and migration ability of HFL-1 cells after TGF-β1 induction.(2)The expression of α-SMA,COL1A1 and FN1 genes of HFL-1 in the TGF-β1-induced groups was signifi-cantly up-regulated compared with the blank control group(P＜0.05).Compared with the TGF-β1 in-duction group,α-SMA expression in the 5.0 μmol/L tofacitinib intervention group was significantly inhi-bited(P＜0.05).Compared with the TGF-β1-induced group,FN1 gene was significantly inhibited in each intervention group at a concentration of 0.5-5.0 μmol/L(P＜0.05).Compared with the TGF-β1-induced group,the COL1A1 gene expression in each intervention group did not change significantly.(3)Western blotting results showed that the protein levels of α-SMA and FN1 in the TGF-β1-induced group were significantly higher than those in the control group(P＜0.05),and there was no significant difference in the expression of COL1A1.Compared with the TGF-β1-induced group,the α-SMA protein level in the intervention groups with different concentrations decreased.And the differences between the TGF-β1-induced group and 2.0 μmol/L or 5.0 μmol/L intervention groups were statistically significant(P＜0.05).Compared with the TGF-β1-induced group,the FN1 protein levels in the intervention groups with different concentrations showed a downward trend,but the difference was not statistically sig-nificant.There was no difference in COL1A1 protein expression between the intervention groups com-pared with the TGF-β1-induced group.(4)After TGF-β1 acted on HFL-1 cells for 48 h,the gene ex-pression of the IL-6 was up-regulated and IL-6 in culture supernatant was increased,the intervention with tofacitinib partly inhibited the TGF-β1-induced IL-6 gene expression and IL-6 in culture supernatant.TGF-β1 induced the increase of Smad2/3 protein phosphorylation in HFL-1 cells for 1 h and 6 h,STAT3 protein phosphorylation increased at 1 h,6 h and 24 h,the pre-intervention with tofacitinib inhibited the TGF-β1-induced Smad2/3 phosphorylation at 6 h and inhibited TGF-β1-induced STAT3 phosphorylation at 1 h,6 h and 24 h.Conclusion:Tofacitinib can inhibit the transformation of HFL-1 cells into myofi-broblasts induced by TGF-β1,and the mechanism may be through inhibiting the classic Smad2/3 path-way as well as the phosphorylation of STAT3 induced by TGF-β1,thereby protecting the disease progres-sion of pulmonary fibrosis.