Objective To evaluate the efficacy of preoperative femoral nerve block on preemptive analgesia in the elderly patients undergoing total knee arthroplasty under general anesthesia.Methods Sixty ASA physical status Ⅰ-Ⅲ patients of both sexes,aged 65-75 yr,scheduled for elective total knee arthroplasty,were randomly divided into 3 groups (n =20 each) using a random number table:control group (group Ⅰ),preoperative femoral nerve block group (group Ⅱ) and postoperative femoral nerve block group (group Ⅲ).Single-injection femoral nerve block was performed with 0.375％ ropivacaine 20 ml injected around the nerve under thc guidance of ultrasound immediately before induction of anesthesia and at the end of surgery in Ⅱ and Ⅲ groups,respectively.Patient-controlled intravenous analgesia (PCIA) with sufentanil (background infusion 2 ml/h,bolus dose 2 ml,lockout interval 15 min) was used until 2 days after surgery,and VAS score was maintained ≤ 3.When VAS score＞3,flurbiprofen axetil 50 mg was injected intravenously as rescue medication.The consumption of sufentanil per hour,requirement for rescue medication,and development of adverse reactions were recorded within 24 h after surgery.Sufentanil-sparing degree was calculated.Results Compared with group Ⅰ,the consumption of sufentanil per hour,requirement for rescue medication and the incidence of nausea and vomiting were significantly decreased within 24 h after surgery in Ⅱ and Ⅲ groups.The consumption of sufentanil per hour,requirement for rescue medication and the incidence of nausea and vomiting were significantly lower within 24 h after surgery in group Ⅱ than in group Ⅲ.The consumption of sufentanil per hour was decreased by 35％ in group Ⅱ as compared with group Ⅰ,and decreased by 18％ in group Ⅱ as compared with group Ⅲ.Conclusion Preoperative femoral nerve block can provide good preemptive analgesia in the elderly patients undergoing total knee arthroplasty under general anesthesia.

Objective To investigate the role of nucleotide-binding oligomerization domain 2(NOD2)modified by palmitoyltransferase(ZDHHC5)in brain injury after cardiopulmonary resuscitation(CPR)in mice.Methods Twenty-four male C57BL/6J mice were divided into the blank group,the control group,the ZDHHC5-si group and the NOD2-si group,with 6 mice in each group.Except for the blank group without any treatment,CPR modeling was performed in the other three groups.At 24 h before CPR,mice in the ZDHHC5-si group and the NOD2-si group were injected with ZDHHC5 siRNA and NOD2 siRNA via tail vein,respectively.The modified neurological deficit scale(mNSS)was used to evaluate the neurological function at 24 h,48 h and 72 h in each group.Blood samples and brain tissue were collected 72 h after modeling.Real-time fluorescent quantitative PCR(qPCR)was used to detect ZDHHC5 and NOD2 in brain tissue.The protein expression levels of IL-1β,TNF-α and IL-6 in plasma were detected by enzyme-linked immunosorbent assay(ELISA).Colorimetric method and thiobarbituric acid(TBA)method were used to detect protein expression levels of MDA and MPO in brain tissue,respectively.Western blot assay was used to detect expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 in brain tissue.HE pathological sections of brain tissue were observed under light microscope.The pathological sections of brain tissue were observed by TUNEL under fluorescence microscope.Results Compared with the blank group,the mNSS score,the expression levels of IL-1β,TNF-α,IL-6,MDA and MPO,and the protein expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 were significantly increased(P＜0.05),and brain tissue damage and cell apoptosis were aggravated in the other three groups.Compared with the control group,the above indicators were significantly decreased in the ZDHHC5-si group and the NOD2-si group(P＜0.05),and brain tissue damage and cell apoptosis were significantly attenuated.Compared with the NOD2-si group,the above parameters were significantly decreased(P＜0.05),and brain tissue damage and cell apoptosis were further attenuated in the ZDHHC5-si group.Conclusion In the mouse CPR model,NOD2 can produce palmitoylated NOD2 after regulated by ZDHHC5,which further promotes the release of inflammatory factors and causes neuronal apoptosis,ultimately damaging brain tissue and affecting neurological function.