Objective To explore the clinical effect of Tuina therapy for knee osteoarthritis (KOA) patients and their musculus quadriceps fexoris strength. Methods The 114 patients with KOA who met the inclusion criteria were randomly divided into the observation group and the control group (57 in each group). The patients in observation group were treated with Tuina therapy, and the control group were treated with Meloxicam. All the patients were treated for 30 days. The Isokinetic muscle strength test was used to evaluate the strength of the four biceps femoris muscle, and HSS score and pain score were observed before and after treatment. Results The total effective rate of the observation group was 91.2% (52/57), and the control group was 71.9% (41/57). The difference between 2 groups was statistically significant (χ2=3.971, P=0.018). After treatment, the HSS scores (79.0 ± 2.0 vs. 66.3 ± 1.4; t=3.121, P<0.01) in observation group were significantly higher than that in control group, and the pain scores (1.7 ± 1.1 vs. 3.2 ± 1.1; t=2.953, P<0.01) in observation group were significantly lower than that in control group. The PT (59.91 ± 25.90 Kgm vs. 55.17 ± 25.88 Kgm, t=2.652), AP (30.04 ± 12.59 W vs. 28.02 ± 17.03 W, t=3.618), TW (496.47 ± 257.26 Nm vs. 466.19 ± 225.70 Nm, t=3.227) of 60/s isokinetic muscle strength test and PT (37.22 ± 18.73 Kgm vs. 32.54 ± 15.22 Kgm, t=2.511), AP (39.43 ± 18.02 W vs. 36.14 ± 23.88 W, t=2.183), TW (326.03 ± 159.38 Nm vs. 267.66 ± 156.93 Nm, t=2.073) of 180/s isokinetic muscle strength test in observation group were significantly higher than those in control group (P<0.05). Conclusions Tuina therapy could improve KOA patients' musculus quadriceps fexoris strength, which curative effect were better than oral treatment of Meloxicam.

Objective:To establish the determination of paeoniflorin in Gubenyichang Tablet.Methods:RP-HPLC method was used for determination of paeoniflorin in Gubenyichang Tablet on C 18 column. The mobile phase was consisted of methanol-water (32∶68) and detection wavelength was at 230nm.Results:The average recovery was 98.9% and RSD was 1.22%. Conclusion:The method is simple, accurate and with good speciality.

Objective To evaluate the effects of dexmedetomidine pretreatment on extracellular sig?nal?regulated kinase ( ERK) pathway during acute lung injury in a rat model of liver transplantation. Meth?ods Sixty male Sprague?Dawley rats, weighing 235-250 g, were divided into 4 groups ( n=15 each) u?sing a random number table: sham operation group (group S), liver transplantation group (group LT), low?dose dexmedetomidine pretreatment group ( group LD ) and high?dose dexmedetomidine pretreatment group ( group HD) . In LT, LD and HD groups, the model of orthotopic liver transplantation was estab?lished, and the operation time was about 4 h. Dexmedetomidine 2?5 and 5?0μg·kg-1 ·h-1 were intrave?nously infused for 1 h starting from 1 h prior to clipping the hepatic artery and portal vein in LD and HD groups, respectively. The rats were sacrificed after the end of operation, and the lungs were removed for determination of wet to dry weight ratio ( W∕D ratio) , cell apoptosis and expression of ERK mRNA, ERK, phosphorylated ERK ( p?ERK) , Bcl?2 and Bax in lung tissues and for examination of the pathological chan?ges ( with light microscope) and ultrastructure of lung tissues ( with transmission electron microscope) . The
injured alveolus rate ( IAR) , apoptosis index ( AI) and ratio of Bcl?2 to Bax expression ( Bcl?2∕Bax ratio) were calculated. Results Compared to group S, the W∕D ratio, IAR, AI, expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK, Bcl?2 and Bax and Bcl?2∕Bax ratio were significantly increased in LT, LD and HD groups ( P<0?05) . Compared to group LT, the W∕D ratio, IAR and AI were significantly decreased, the expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK and Bcl?2 and Bcl?2∕Bax ratio were significantly increased, and the expression of Bax was significantly down?regulated in LD and HD groups (P<0?05). Compared to group LD, the W∕D ratio, IAR and AI were significantly decreased, the expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK and Bcl?2 and Bcl?2∕Bax ratio were significantly increased, and the ex?pression of Bax was significantly down?regulated in group HD ( P<0?05) . The pathological changes of lung tissues were significantly attenuated in LD and HD groups as compared with group LT, and in group HD as compared with group LD. Conclusion The mechanism by which dexmedetomidine pretreatment mitigates cell apoptosis during acute lung injury is related to activation of ERK pathway in a rat model of liver trans?plantation.

Objective To evaluate the effect of penehyclidine hydrochloride on the damage to the non-ventilated lung in the pediatric patients undergoing one-lung ventilation (OLV).Methods One hundred and twenty pediatric patients of both sexes,aged 2-6 yr,with body mass index of 17-24 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or lⅡ and New York Heart Association class Ⅰ or Ⅱ,undergoing elective lobectomy performed via video-assisted thoracoscope,were randomly divided into 2 groups (n=60 each) using a random number table:control group (group C) and penehyclidine hydrochloride group (group P).At 10 rmin before anesthesia induction,penehyclidine hydrochloride 0.05 mg/kg was injected intravenously in group P,and the equal volume of normal saline was given in group C.At 5 min after drug intervention (T0),immediately after onset of OLV (T1),at 60 min of OLV (T2),immediately after the end of OLV (T3),at the end of surgery (T4),and at 24 h after surgery (T5),venous blood samples were collected for determination of serum tumor necrosis factor-alpha (TNF-o),interleukin-6 (IL-6) and IL-8 concentrations by enzyme-linked immunosorbent assay.The specimens of normal lung tissues around the lung lobe to be resected were obtained at T1 and T3 for determination of the injured alveolus count (with a light microscope) and cell apoptosis (using TUNEL) and for examination of the ultrastructure of epithelial cells (with a transmission electron microscope).The injured alveolus rate (IAR) and apoptosis index (AI) were calculated.Results Compared to the value at T0,the IAR and AI were significantly increased at T3,the serum TNF-α,IL-6 and IL-8 concentrations were significantly increased at T2-5 (P＜0.05),and the pathological changes were obvious in the two groups.Compared to group C,the IAR and AI were significantly decreased at T3,the serum TNF-α,IL-6 and IL-8 concentrations were significantly decreased at T2-5 (P＜0.05),and the pathological changes were significantly reduced in group P.Conclusion Penehyclidine hydrochloride can attenuate the damage to the non-ventilated lung in the pediatric patients undergoing OLV,and the mechanism is probably related to inhibition of systemic inflammatory responses and cell apoptosis in lung tissues.

Objective To investigate the effect of dexmedetomidine pretreatment on hippocampal endoplasmic reticulum stress-induced cell apoptosis after asphyxial cardiac arrest-resuscitation in rats. Methods A total of 60 pathogen-free male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-300 g, were divided into 3 groups (n= 20 each) by using a random number table: control group (C group), as-phyxial cardiac arrest-resuscitation group ( CA group) and dexmedetomidine pretreatment group ( Dex group). The anaesthetized rats were intubated with a 16G tracheal catheter which was connected to a rodent ventilator for mechanical ventilation. Cardiac arrest was induced by clamping the tracheal tube at the end of the exhalation until systolic blood pressure decreased to 25 mmHg lasting for 5 min, and then resuscitation was started. At 5 min before cardiac arrest, dexmedetomidine 4. 0 μg∕kg was intravenously injected in group Dex, and the equal volume of normal saline was given instead in C and CA groups. Rats were sacri-ficed at 6 h after successful resuscitation, brain tissues were removed for determination of wet to dry weight ratio ( W∕D ratio), and hippocampal tissues were obtained for examination of the pathological changes (with a light microscope) and ultrastructure (with an electron microscope) and for determination of cell ap-optosis (by TUNEL), expression of CCAAT∕enhancer-binding protein homologous protein (CHOP) and ac-tivated transcription factors (ATF4) and X-4 box binding protein 1 (XBP1) mRNA (by real-time polymer-ase chain reaction) and expression of CHOP, Bcl-2, Bax and caspase-3 (by Western blot). The apoptosis rate was calculated. Results Compared with group C, W∕D ratio of brain tissues was significantly in-creased, the apoptosis rate of hippocampal tissues was decreased, the expression of XBP-1, ATF4 and CHOP mRNA was up-regulated, the expression of CHOP, Bax and caspase-3 was up-regulated, and the expression of Bcl-2 was down-regulated in CA and Dex groups (P<0. 05). Compared with group CA, W∕D ratio of brain tissues was significantly decreased, the apoptosis rate of hippocampal tissues was decreased, the expression of XBP-1, ATF4 and CHOP mRNA was down-regulated, the expression of CHOP, Bax and caspase-3 was down-regulated, the expression of Bcl-2 was up-regulated (P<0. 05), and the pathological changes were significantly attenuated in group Dex. Conclusion The mechanism by which dexmedetomi-dine pretreatment mitigates brain injury after asphyxial cardiac arrest-resuscitation may be related to inhibi-ting cell apoptosis induced by endoplasmic reticulum stress in rats.