Objective To evaluate the role of spinal extracellular signal-regulated kinase (ERK) signaling pathway in reduction of remifentanil-induced hyperalgesia by electro-acupuncture (EA) at Zusanli in rats with incisional pain.Methods Fifty male adult Sprague-Dawley rats, weighing 250-280 g, in which the intrathecal catheter was successfully placed without complications, were randomly divided into 5 groups (n=10 each) using a random number table: control group (group C), remifentanil + incisional pain group (group RI), EA at acupoint group (group E) , EA at non-acupoint group (group NE), and 1/2 ERK inhibitor U0126 + EA at acupoint group (group UE).Normal saline 0.1 ml · kg-1 · min-1 was infused intravenously for 60 min in group C.In RI, E, NE and UE groups, after the model of incisional pain was established, remifentanil 1.0 μg · kg-1 · min-1 was infused for 60 min, and in addition, EA (intensity 10 mA, frequency 4 Hz) of Zusanli lasting for 60 min was performed at the same time in E and UE groups, and EA was performed at the points 5 mm lateral to the acupoints of Zusanli on the operated side simultaneously in group NE.ERK1/2 inhibitor U0126 5 μg (in 5％ dimethyl sulfoxide 10 μl) was injected intrathecally in group UE, and 5％ dimethyl sulfoxide 10 μl was injected intrathecally in the other groups.The mechanical paw withdrawal threshold (MWT) was measured before remifentanil or normal saline infusion (T1) , and at 2 h, 1, and 2 days after the end of infusion (T2-4).After MWT was measured at T4, the expression of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2) in spinal cord dorsal horns was measured by Western blot.Results Compared with group C, the MWT was significantly decreased at T2-4 in RI, E, NE and UE groups, and the expression of p-ERK1/2 was up-regulated in RI, E and NE groups (P＜0.05).Compared with group RI, the MWT was significantly increased at T2-4 , and the expression of p-ERK1/2 was down-regulated in E and UE groups (P＜0.05);and no significant change was found in the parameters mentioned above in group NE (P＞0.05).Compared with group E, the MWT was significantly increased at T2-4, and the expression of p-ERK 1/2 was down-regulated in group UE (P＜0.05).Conclusion The mechaism by which EA at Zusanli reduces hyperalgesia induced by remifentanil in rats with incisional pain is related to inhibited activation of ERK signaling pathway in the spinal cord.

Objective To observe the efficacy and prognosis of recombinant human brain natriuretic peptide ( rhBNP) and conventional treatment in acute myocardial infarction patients undergoing percutaneous coronary intervention therapy complicated by acute of left heart failure. Methods Retrospective analysis of 229 cases of hospitalized patients with acute myocardial infarction undergoing percutaneous coronary intervention therapy in 24 hours after admission, complicating with acute left ventricular failure in Shenyang Military General Hospital from June 2012 to January 2014 were enrolled and devided into: the conventional heart failure therapy group (the control group, n=122) and the rhBNP plus conventional treatment group ( the treatment group, n =107 ) , according to the patient's economic conditions and wishes. Observed improvement in heart failure symptoms before and after treatment during hospitalization and follow-up and also the 30 days and 12 months mortality. Results After 72 hrs of treatment of heart failure, both groups had decrease in heart rates, systolic blood pressure and NT-proBNP levels as compared to pre-treatment levels ( all P ﹤ 0. 05 ) . The NT-proBNP levels and heart rate of the treatment group decreased more significantly compared to the control group (both P﹤0. 05). Compared with the control group, rhBNP which to be used 72 hrs, can improve the cardiac function of AMI patients with the ratio of KillipⅡ-Ⅲ(72. 9%vs. 54. 9%, P=0. 005). There was no significant differences between two groups in in-hospital mortality and early follow-up period ( 30 days ) ( P ﹥0. 05 ) . After 12 months of follow-up, the mortality of the treatment group was lower than the control group ( 6. 5% vs. 13. 9%, P = 0. 068 ) . Through logistic regression analysis, the value of NT-proBNP and whether patients were treated with rhBNP on the basis of the routine drug were independent influencing factors for mortality of 12 months. Conclusions Additional to standard conventional therapy for acute left heart failure in patients with acute myocardial infarction undergoing PCI, rhBNP can lower the 12 months mortality and improve prognosis.

BACKGROUND:Chinese medicineTangbikang can improve nerve conduction velocity in diabetic rats, and has anti-inflammatory and antioxidant effects. Insulin like growth factor-I is a key target in the treatment of diabetic peripheral neuropathy. OBJECTIVE:To observe the effect ofTangbikangon the expression of insulin-like growth factor-I and its receptor protein and mRNA in the sciatic nerve of diabetic rat model. METHODS:The experimental diabetes melitus rat models were induced by feeding high fat forage and injection with streptozotocin. After model establishment, rats were givenTangbikang 4.18, 8.35, 16.7 mg/kg per day. This study set positive control methycobal, model and normal control groups. Intragastric administration was performed for 16 weeks. RESULTS AND CONCLUSION: Compared with the model group, blood glucose levels were similar in the methycobal group, but decreased in the high-doseTangbikang group (P < 0.01). Immunohistochemical staining and real-time fluorescence quantitative PCR detection revealed that body mass, motor nerve conduction velocity, insulin like growth factor-I and its receptor protein and mRNA expressions were increased in the methycobal and high-dose Tangbikang groups (P< 0.05 orP < 0.01). Results indicated that Tangbikang can prevent and treat diabetic peripheral neuropathy by promoting insulin like growth factor-I and its receptor. Cite this article:Mu XH, Sun W, Qin LL, Wu LL, Li WL, Guo X, Zhang L, Liu TH.Effects of Tangbikang on insulin like growth factor-I and its receptor expression in sciatic nerves of diabetic rats. Zhongguo Zuzhi

Objective Neonatal sepsis (NS) is one of the main causes of neonatal death.Immune therapy is an important way in the comprehensive treatment of NS.This study investigated several databases in order to find the clinical evidence for the immunological treatment of neonatal sepsis (NS),and to explore its clinical application value.Methods Systematic reviews and randomized (or quasi-randomized) controlled trials (RCT) for immunological treatment of NS in newborn infants were searched from the databases of MEDLINE,EMBASE and Cochrane Library.The relevant literatures were statistically analyzed.Results Six systematic reviews (including 37 RCTs) were found to be involved in the therapy,and the drugs included intravenous immunoglobulin (containing high level of IgM),antistaphylococcal immunoglobulins,neutrophile granulocyte,granulocyte colony-stimulating factor,granulocyte-macrophage colony-stimulating factor,pentoxifylline and glutamine.Pentoxifylline could decrease the mortality (Z =2.71,P =0.006 8),shorten the hospitalization (Z =2.01,P =0.044),and reduce the incidence rate of necrotizing enterocolitis (NEC) (Z =1.67,P =0.095) of the NS infants.No therapeutic effect was found for other drugs in the treatment of NS.Conclusions Current clinical evidence for the immunological treatment of NS indicates that only Pentoxifylline could decrease the mortality,reduce the incidence rate of NEC and shorten the hospitalization of infants with NS.However,current evidence is only a small scale sampling and lacks multicenter studies.Researchers are encouraged to undertake large scale and well-designed multicenter trials to confirm the effectiveness of the immunological treatment of NS.

Objective To systematically analyze and assess the overall value of transrectal shear wave elastograpy in diagnosis of prostate cancer (PCa) using Meta-analysis.Methods Relevant Chinese and foreign papers diagnosing PCa with transrectal shear wave elastograpy published before December 2016 were searched.The references were evaluated and screened according to the criteria of diagnostic research.The selected references were analyzed by Meta-Disc 1.4 and Stata 12.0 statistical software.Results Eight articles were included in the present Meta-analysis.Five of these literatures were about transrectal shear wave elastograpy in diagnosis of PCa,the summarized sensitivity (SEN) and summarized specificity (SPE) in diagnosis of PCa were 0.80 (95％CI [0.75,0.84]) and 0.75 (95％CI [0.71,0.79]),respectively;the positive likelihood ratios (PLR) and negative likelihood ratios (NLR) were 3.60 (95 ％ CI [2.57,5.05]) and 0.17 (95 ％ CI[0.08,0.37]),respectively;the area under SROC curves was 0.895.Five of these literatures were about transrectal shear wave elastograpy supplemental prostatic biopsy in diagnosis of PCa,the summarized SEN and SPE were 0.86 (95％ CI [0.83,0.88]) and 0.84 (95％CI [0.82,0.85]) respectively;the PLR and NLR were 5.81 (95％CI [3.07,10.99]) and 0.14 (95％CI [0.04,0.49]) respectively;the area under SROC curves were 0.924.Conclusion Transrectal shear wave elastograpy has better clinical value in detection of PCa and can be used to supplemental prostatic biopsy.

Objective:To observe the effects of All-trans retinoic acid (ATRA) on the immune functions of AChR-specific lymphcytes via in vitro assays,and investigate the possibility of ATRA in the clinical treatment of myasthenia gravis (MG).Methods:CFA control group and EAMG experimental rats were established to obtain single lymphocytes suspension and cells were followed by AChR97-116 peptide with or without ATRA stimulation for 72 h,and then viable cell population,cell apoptosis,cell cycle and the distribution of Th cells were determined by flow cytometry.CCK-8 assay was selected to evaluate the effects of ATRA on proliferatory ability of lymphocytes.ELISA was used to detect the antibody secretion of B cells affected by ATRA.Results:Compared with CFA group,lymphocytes obtained from EAMG rats had higher ratios of living cells,and this ratio was obviously decreased after ATRA treatment,P＜0.001.Different concentrations of ATRA promoted the apoptosis of AChR-specific cells (P＜0.001),and the promoted effects were ATRA dose-dependent,however,cell cycles were not changed.ATRA markedly inhibited the proliferation of cells from both CFA and EAMG groups,moreover,AChR-specific cells were more sensitive to ATRA treatment (P＜0.01) than that of cells from CFA rats (P＜0.05).The ratio of AChR-specific CD4+T cells was reduced by ATRA (P＜0.01),and ATRA incubation significantly promoted the percentages of Th2,(PCD4+-4IL-4+＜0.001),Treg (PCD4+-Foxp3+＜0.001) cell types,but markedly inhibited the percentages ofThl7 (PCD4+-IL-17+＜0.05),Thl (PCD4+-IFN-γ+＜0.001) cells.ELISA data showed us that ATRA obviously down regulated the antibody secretion of AChR-specific B cells,P＜0.01.Conclusions:ATRA not only inhibited the functions of AChR-specific T cells,but also suppressed the roles of AChR-specific B cells,predicating a therapeutic effect of ATRA on myasthenia gravis therapy.

Objective:To explore the effect of continuous nursing on the psychology and quality of life of patients with mild traumatic brain injury.Methods:A review of 120 patients with mild traumatic brain injury who were hospitalized in the Second Affiliated Hospital of Wenzhou Medical University from January 2016 to December 2019 were selected. According to the order of admission, sample numbers were drawn from the random number list and entered into groups. There were 60 cases in the control group and the intervention group. The control group received routine general nursing, and the intervention group received continuous nursing. The Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD), and Quality of Life Scale (SF-36) were used to evaluate the psychology and quality of life of patients on the day of discharge and one week, one month, and three months after discharge.Results:There was no significant difference in the scores of HAMA, HAMD and SF-36 between the two groups on the day of discharge ( P>0.05). The HAMA scores at 1 week, 1 month and 3 months after the intervention of the intervention group were (18.2±8.6), (13.7±5.8) and (5.6±2.3), which were significantly lower than those of the control group (24.2±11.2), (20.4±8.2), (8.9±3.6), the differences were statistically significant ( t values were 2.32, 3.67, 4.13, P<0.05). The HAMD scores at 1 week, 1 month and 3 months after the intervention of the intervention group were (24.3±7.1), (10.9±4.2), (6.8±2.9), which were significantly lower than those of the control group (28.6±8.5), (15.3±8.3), (14.8±4.6), the differences were statistically significant ( t values were 2.11, 2.57, 7.99, P<0.05). The SF-36 scores at 1 week, 1 month and 3 months after the intervention of the intervention group were (77.2±8.9), (85.2±9.7), (87.8±12.9), which were significantly higher than those of the control group (72.3±8.2), (79.4±10.9), (81.0±11.5), the differences were statistically significant ( t values were -2.23, -2.14, -2.13, P<0.05). Conclusions:Continuing care can be extended to the patient's family, so that the health problems faced by the patient after discharge from the hospital can be effectively solved, relieve psychological pressure and improve the quality of life, and it is worthy of clinical application.

Objective To investigate the possible function of integrin-linked kinase (ILK)/protein kinase B (PKB/Akt) signaling in repair of neonatal rat hypoxia-ischemia brain damage (HIBD). Methods Postnatal day 10 SD rats were randomly divided into hypoxia ischemia (HI) group and sham control group. Rat brains were collected at 0 h, 4 h, 6 h, 12 h, 24 h, 48 h and 72 h after hypoxia ischemia damage. Immunolfuorescence staining was used to observe the distribution and expression of ILK. Western blot was used to detect the expression of ILK, Akt, phosphorylated Akt (p-Akt) and vascular endothelial growth factor (VEGF). Lentiviral vectors expressing ILK shRNA were constructed to inhibit the expression of ILK in neonatal rats. After intracerebroventricular injections of LV-ILK shRNA lentivirus and LV-control respectively, HIBD model was established. Rat brains were collected at 4 h and 24 h after HIBD. Western blot was used to detect the expression of ILK, p-Akt, and VEGF. TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining was used to detect cell apoptosis. Results Immunolfuorescence staining showed that ILK was widely distributed in cortex and hippocampus both in HI group and sham control group. ILK located at cell membrane and cytoplasm. Western blot results demonstrated that ILK protein increased after HI, with a peak at 24 h, and maintained higher level than those in sham control group. The p-Akt protein signiifcantly increased at 4 h after HI, and signiifcantly decreased in the following 24 h, and then increased again, with a peak at 48 h, but the level of p-Akt protein was higher than that of sham control group. The VEGF protein increased at 4 h after HI, with a peak at 12 h, higher than that of sham control group. The expression of Akt protein showed no signiifcant difference between HI group and sham control group. Lentiviral vectors containing RNAi targeting ILK was applied successfully in vivo. At 4 h and 24 h after HIBD model, the expression of ILK, p-Akt, and VEGF proteins in right side brain received LV-ILK shRNA signiifcantly decreased compared with those of right side brain received LV-control at the same time point. And cell apoptosis signiifcantly increased in LV-ILK shRNA group. Conclusions The expression of ILK, p-Akt, VEGF proteins increased after HI. By inhibiting the expression of ILK, the expression of p-Akt and VEGF proteins can be reduced, and cell apoptosis could increase in newborn rats after HIBD. The results suggest that ILK may induce the expression of VEGF through activating the PI3K/Akt signaling pathway, and promote cell survival and angiogenesis after HIBD.

This study was aimed to explore the effect of Tang-Nai-Kang (TNK) on trans-differentiation of renal tubular epithelial cell in KKAy mice in order to discuss the possible mechanism. Fifty 12-week-old male KKAy mice were randomly divided into the model group, valsartan group, TNK high-dose, middle-dose and low-dose group, with 10 rats in each group. Ten C57BL/6J mice were used in the normal group. Rats in the model group and normal group were given 0.9% sodium chloride solution. Rats in other groups were given the corresponding drugs. After 8 weeks of gavage administration, kidneys of all mice were sampled and given Mosson and PAS dyeing. Expression distribution of α-smooth muscle actin (α-SMA) and E-cadherin in kidney tissues were observed under immunohistochemical staining. Expression of transforming growth factor-β1 (TGF-β1) was measured by western blot. The results showed that compared with the normal group, the area of renal fibrosis in the model group was significantly increased (P < 0.01); the expression of α-SMA was stronger; and the expression of E-cadherin was weaker. Compared with the model group, the area of renal fibrosis in the valsartan group, TNK high-dose, middle-dose and low-dose groups were significantly decreased (P< 0.01); the expression of α-SMA was weaker (P< 0.01);and the expression of E-cadherin was obviously increased (P < 0.05). The TGF-β1 expression in the model group was significantly higher than that in the normal group (P < 0.01). Compared with the model group, the TGF-β1 expression in the valsartan group, TNK low-dose, middle-dose and high-dose groups were significantly lowered (P<0.01). And the TGF-β1 expression in the TNK high-dose group was even lower than that in the valsartan group. It was concluded that TNK was able to suppress the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cell, and lessen the renal tubule interstitial fibrosis, in order to protect the kidney.