Objective To discuss the application effect of new physical therapy technique in the rehabilitation of patients with hand injury afte operation. Methods Patients with hand injury after operation (150 cases) were divided into the observation group (87 cases) and the control group (63 cases) randomly. The control group received routine treatment and nursing. The observation group was given irradiation by He-Ne laser therapeutic instrument, vinegar therapy and static electromagnetic field therapy. The rehabilitative effect after operation was compared between the two groups. Results The time for disappearance of pain and swelling in the obsevation group was shorter than that of the control group (P<0.05). Conclusions Application of new physical therapy technique in patients with hand injury afte operation could shorten time of rehabilitation and improve rehabilitative quality.

Objective To examine the association of serum 25-hydroxyvitamin D levels with arterial stiffness and left ventricular hypertrophy (LVH) in elderly hypertension patients.Methods We recruited 166 elderly patients [mean age,(80.8 ± 6.2) years] with primary hypertension.Arterial stiffness was assessed by carotid femoral pulse wave velocity (cfPWV).Left ventricular mass index (LVMI) was determined according to the Devereux formula.Based on serum 25-hydroxyvitamin D levels,the patients were divided into two groups,the low 25-hydroxyvitamin D group (＜20 μg/L)and the high 25-hydroxyvitamin D group (≥20 μg/L).Results Faster cfPWV and larger LVMI values were observed in the low 25-hydroxyvitamin D group as compared with the high 25-hydroxyvitamin Dgroup [(15.00±3.04) m/s vs.(11.26±3.09) m/s;(120.14±25.82) g/m2 vs.(96.74±23.10) g/m2 ; t=-6.79,-5.16,respectively; both P=0.000].Multiple liner regression analysis showed that the 25-hydroxyvitamin D level was independently associated with LVMI (β=0.215,P=0.001) and cfPWV (β=-0.469,P＜0.001).Conclusions Serum 25-hyroxyvitamin D is independently associated with arterial stiffness,LVH Vitamin D may play an important role in the pathogenesis of arterial stiffness and LVH in elderly hypertension patients.

Objective To explore the relationship between the polymophisms of interleukin?17 (IL?17)?197A/G and the outcomes of hepatitis B virus (HBV) infections. Methods The polymorphism of genotypes and al?leles of IL?17?197A/G in 222 chronic HBV infected patients and 88 HBV infected ones as controls. The contains of serum HBV DNA were detected using PCR combined with DNA amplification in vitro, serum IL?17 expression was detected with ELISA and genotype and allele frequency of IL?17?197A/G locus was detected by Beckman SNP kit. Results There was a significant difference in the serum IL?17 expression (F=158.1, r2=0.61, P<0.000 1) among all the groups. For IL?17?197A/G, there were significant differences for the comparison between the two groups, and the frequency of AA genotype was 47.72%in liver cirrhosis group. Moreover, the highest frequency of GG was in HBV clear?ance group (74.81%);and the lowest group was in chronic HBV liver cirrohosis group (19.05%). Conclusion IL?17?197A/G AA genotype and allele might be associated with susceptibility of HBV infection in Han population in Hei?bei Province.

Objective: To explore the potential biological mechanism of chronic obstructive pulmonary disease (COPD) qi deficiency syndrome, we used the integrated pharmacology network computing platform and carried out experimental verification.Methods: Using an integrated pharmacology strategy to analyze the potential biological targets of COPD qi deficiency syndrome. Based on the established qi deficiency syndrome rat model of COPD, the bio-logical targets of lung and skeletal muscle were detected by electron microscopy, adenosine triphosphate (ATP) content assays, and western blotting. Results: According to the integrated pharmacological results, it was found that the locations of cell components related to COPD qi deficiency syndrome were mainly mitochondria. Electron microscopy results using lung tissue showed that mitochondria in the lipopolysaccharide (LPS group) and pulmonary instillation of LPS combined with cigarette smoke (LPS+CS group) were swollen, deformed, and frag-mented, with disappearing or broken crista. Results also showed that the total content of ATP in the lung and skeletal muscle of both groups was significantly lower than that in the control group at the 12th week (P<.05). At the 12th week, the expression of dynamin-related protein 1 (DRP1) and mitofusin 1 (MFN1) protein was significantly difference than that of the control group (P<.05). At the 10th and 14th weeks, changes in fission and fusion proteins in mitochondria of the lung and skeletal muscle were further detected. There was also a significant difference in the expression between the two groups compared to that in the control group at the 10th week and 14th week (P<.05). Conclusion: These findings suggest that the changes in mitochondrial morphology and ATP content and the unbalanced expression of DRP1 and MFN1 might be the key mechanisms underlying qi deficiency syndrome in rats with COPD.

Objective To investigate value of peripheral NLR and PLR for the survival of patients with neuroblastoma.Methods The clinical data of 41 neuroblastoma patients were analyzed by the Kaplan-Meier,Log-rank test,and multivariate COX regression.Results NLR,PLR levels of neuroblastoma patients were significantly higher than that in the healthy control group (1.81 ±0.29 vs.1.07 ±0.29,P ＜ 0.01) (169 ± 23 vs.76 ± 3,P ＜ 0.01);The elder the age,the higher the clinical stages,the higher the serum levels of NSE,and urine VMA were,the higher was the NLR (x2 =3.93,6.286,7.676,6.689,all P＜0.05) and PLR (x2 =4.111,5.707,8.019,8.922,all P ＜0.05).The higher the serum level of LDH,the higher was the NLR (x2 =7.769,P =0.02).3-year overall survival in low NLR group was 84％ and that in high NLR group was 73％ (x2 =4.002,P =0.045);3-year progression-free survival in low NLR group was 74％ and that in high NLR group was 50％ (x2 =4.082,P =0.043);3-year progression-free survival of low PLR group was 85％ and high PLR group was 38％ (x2 =9.388,P =0.002).The clinical stages,MYCN genetic expression,NLR levels were independent factors for the overall survial in patients with neuroblastoma (P ＜ 0.05).Conclusion Pretreatment NLR level can effectively predict the prognosis of neuroblastoma.

Objective To investigate the inhibitory effect of salinomycin on human breast cancer cells in vitro, and to explore the related molecular mechanism.Methods Human breast cancer MDA-MB-231 cells were treated with salinomycin at different concentrations and at various time points.The effect of salinomycin on MDA-MB-231 cells proliferation was studied by CCK-8 method.The cell cycle status was examined by flow cytometry.RT-PCR and Western blot were used to detect the expression of Shh, Smo and Gli1 in the Hedgehog pathway at mRNA and protein levels.Results Proliferation of MDA-MB-231 cells treated with salinomycin was markedly inhibited in a concentration and time dependent manner.Salinomycin at concentrations of 0,0.4,0.8 and 1.6 μmol/L inhibited the growth at the rates of 11.18%,25.88%, 50.03%, 92.65%, respectively.Salinomycin prevented MDA-MB-231 cells from G1 into S phase.Salinomycin at concentrations of 0,0.8 and 1.6μmol/L resulted in S-phase percentage of 25.03%,11.85%and 35.21%, respectively ( P <0.05 ).RT-PCR and Western blot showed that the expression of key elements Shh, Smo and Gli1 in the Hedgehog pathway was inhibited by salinomycin in a concentration dependent manner( P<0.05) .Conclusion Salinomycin prevents breast cancer cell transition from G1 to S phase through downregulation of the target genes of Hedgehog signaling pathway, leading to an effective inhibition of MDA-MB-231 cells.

OBJECTIVETo investigate the inhibitory effect of salinomycin on human breast cancer cells in vitro, and to explore the related molecular mechanism.

METHODSHuman breast cancer MDA-MB-231 cells were treated with salinomycin at different concentrations and at various time points. The effect of salinomycin on MDA-MB-231 cells proliferation was studied by CCK-8 method. The cell cycle status was examined by flow cytometry. RT-PCR and Western blot were used to detect the expression of Shh, Smo and Gli1 in the Hedgehog pathway at mRNA and protein levels.

RESULTSProliferation of MDA-MB-231 cells treated with salinomycin was markedly inhibited in a concentration and time dependent manner. Salinomycin at concentrations of 0, 0.4, 0.8 and 1.6 µmol/L inhibited the growth at the rates of 11.18%, 25.88%, 50.03%, 92.65%, respectively. Salinomycin prevented MDA-MB-231 cells from G1 into S phase. Salinomycin at concentrations of 0, 0.8 and 1.6 µmol/L resulted in S-phase percentage of 25.03%, 11.85% and 35.21%, respectively (P < 0.05). RT-PCR and Western blot showed that the expression of key elements Shh, Smo and Gli1 in the Hedgehog pathway was inhibited by salinomycin in a concentration dependent manner (P < 0.05).

CONCLUSIONSalinomycin prevents breast cancer cell transition from G1 to S phase through downregulation of the target genes of Hedgehog signaling pathway, leading to an effective inhibition of MDA-MB-231 cells.

The discovery of immune checkpoint inhibitors, such as PD-1/PD-L1 and CTLA-4, has played an important role in the development of cancer immunotherapy. However, immune-related adverse events often occur because of the enhanced immune response enabled by these agents. Antibiotics are widely applied in clinical treatment, and they are inevitably used in combination with immune checkpoint inhibitors. Clinical practice has revealed that antibiotics can weaken the therapeutic response to immune checkpoint inhibitors. Studies have shown that the gut microbiota is essential for the interaction between immune checkpoint inhibitors and antibiotics, although the exact mechanisms remain unclear. This review focuses on the interactions between immune checkpoint inhibitors and antibiotics, with an in-depth discussion about the mechanisms and therapeutic potential of modulating gut microbiota, as well as other new combination strategies.
Anti-Bacterial Agents/therapeutic use* ; Humans ; Immune Checkpoint Inhibitors/therapeutic use* ; Immunotherapy ; Neoplasms/drug therapy* ; Programmed Cell Death 1 Receptor