The scientific indexes and methods for checking utilization and intact rates of analytical instruments are established by cybernetic principles, fozzy mathemetical mdthods, theories of systematic engineering, and actual conditions of working units. it is proved that the realization of scientific management and control to manipulators, instruments and working enviroment can raise the utilization and intact rates of analytical instruments, guarantee the assay quality of drugs, increase the efficiency of supervision and promote the research work in drug analysis. Definite social and economic results are thus obtained.

BACKGROUND:Reperfusion injury salvage kinase (RISK) pathway plays an important role in protective mechanism against ischemia reperfusion injury (IRI) induced by both ischemic pre-and post-conditioning. Many researches have been carried out on RISK pathway mechanism underlying ischemic post-conditioning conferring cardioprotection against IRI;however, there is less research about its effect on IRI in the skeletal muscle.
OBJECTIVE:To investigate the protective effect of an optimized protocol of ischemic post-conditioning on IRI in rat skeletal muscle and its underlying mechanism.
METHODS:Eighteen male Sprague-Dawley rats were equivalently randomized into IRI, ischemic post-conditioning and control groups. Rats were given occlusion or disocclusion of the right femoral artery of the right lower limb. Subsequently, the IRI group rats were subjected to 24 hours of reperfusion;the ischemic post-conditioning group immediately given 4 cycles of 30 seconds reperfusion/30 seconds ischemia, followed by 24 hours of reperfusion;the control group given no intervention.
RESULTS AND CONCLUSION:Hematoxylin-eosin staining showed that in the ischemic post-conditioning group, the morphology of muscle fibers changed little, with fewer inflammatory lesions and milder edema compared with the IRI group. The infarct size with TTC staining in the ischemic post-conditioning group was smaller than that in the IRI group. Western blot analysis revealed that the expressions of phospho-Akt and phosphorylated endothelial nitric oxide synthase-S1177 were significantly increased, but the expression of phosphorylated type endothelial nitric oxide synthase-Thr495 was much decreased in the ischemic post-conditioning group compared with the IRI group. The measurement of mitochondrial permeability transition pore opening with Ca2+induction showed that the absorbance values in the ischemic post-conditioning group were significantly lower than those in the IRI group (P<0.05). These results indicate that ischemia-reperfusion injury can be improved by applying an optimal protocol of ischemic post-conditioning in rat skeletal muscle. The underlying mechanism may be associated with the activation of RISK signaling pathway to inhibit opening of mitochondrial permeability transition pore, thereby contributing to the enhanced tolerance to IRI in rat skeletal muscle.

BACKGROUND: Ischemic postconditioning protects the myocardium from ischemia/recursion injury via maintaining 3-minute acidosis initially. But its effect on the skeletal muscle remains unclear. OBJECTIVE: To dynamically measure the pH values in rat skeletal muscle after ischemia, and then to simulate acidic perfusate infusion to investigate the effect of ischemic postconditioning on ischemia/reperfusion injury. METHODS: Based on the ischemia/reperfusion injury model and ischemic postconditioning protocol in previous study, dynamic measurement of pH values in rat skeletal muscle was conducted using pH instrument at the global ischemia, ischemic postconditioning (30/30 seconds) and reperfusion period, and then the acidic perfusate equivalent to pH in ischemic postconditioning period was prepared with lactic acid and normal saline. Twenty-five healthy adult male Sprague-Dawley rats were randomly divided into sham, ischemia/reperfusion, ischemic postconditioning, lactic acid, and normal saline groups (n=5 per group). Blood samples were collected to detect lactate dehydrogenase level. The samples from gastrocnemius were harvested to calculate the wet/dry ratio, level of myeloperoxidase, and infarct size through triphenyltetrazolium chloride staining. The samples from the right tibialis anterior muscle were taken to detect the expression level of Erk1/2 in the MAPK signaling pathway by western blot assay. RESULTS AND CONCLUSION: A prolonged acidic platform was detected in the early reperfusion during ischemic postconditioning, on which the pH value was 6.81±0.133, and the duration was 2 minutes and 40 seconds. The levels of lactate dehydrogenase and myeloperoxidase as well as the wet/dry ratio in the ischemic postconditioning and lactic acid groups were significantly lower than those in the ischemia/reperfusion group (P < 0.05). Western blot assay results showed that the expression level of p-Erk in the ischemic postconditioning, lactic acid and normal saline groups was significantly higher than that in the ischemia/reperfusion group (P < 0.05). Triphenyltetrazolium chloride staining results showed that compared with the ischemia/reperfusion group, the infarct area was significantly reduced in the postconditioning and lactic acid groups (P < 0.05). These findings suggest the existence of a short acidosis during ischemic postconditioning in the early reperfusion, and acidic perfusate can simulate the ischemic postconditioning and effectively attenuate ischemia/reperfusion injury in the rat skeletal muscle via activating Erk1/2 in RISK signaling pathway.

Objective To compare the scalp nerve block versus local infiltration of incision for in-tracranial aneurysm clipping under general anesthesia. Methods Fifty-seven American Society of Anesthe-siologists physical statusⅠorⅡpatients of both sexes, aged 18-64 yr, scheduled for elective intracranial aneurysm clipping under general anesthesia, were divided into 3 groups ( n=19 each) using a random num-ber table method:control group ( group C) , scalp nerve block group ( group S) and local infiltration of in-cision group ( group I) . Anesthesia was induced by intravenously injecting propofol, sufentanil and cisatra-curium. Bilateral supraorbital nerve (2 ml), supratrochlear nerve (2 ml), zygomaticotemporal nerve (2 ml), auriculotemporal nerve (2 ml), greater occipital nerve (3 ml), lesser occipital nerve (3 ml) and the third occipital nerve ( 1 ml) blocks were performed with 0. 75％ ropivacaine after tracheal intubation in group B. Local infiltration of incision was carried out with 0. 75％ ropivacaine 15 ml in group I. Anesthesia was maintained by intravenously infusing propofol and remifentanil to maintain bispectral index value at 40-60. The fluctuation range of mean arterial pressure and heart rate was not more than 20％ of the baseline, and vasoactive agents were administered when necessary. Oxycodone 0. 1 mg∕kg was intravenously injected at 30 min before the end of surgery to perform preemptive analgesia. When visual analogue scale score>3 with-in 48 h after surgery, oxycodone 2 mg was intravenously injected as rescue analgesic, and administration was repeated when necessary ( at an interval>15 min) . The intraoperative consumption of propofol, remifen-tanil and vasoactive agents was recorded. Arterial blood samples were collected before anesthesia induction and at 3, 12, 24, 48 and 72 h after surgery for determination of serum interleukin-6 ( IL-6) , IL-10 and C-reactive protein ( CRP ) concentrations by enzyme-linked immunosorbent assay. The time of the first postoperative requirement for oxycodone and consumption of oxycodone within 48 h after surgery were recor-ded. The development of adverse reactions such as postoperative fever, nausea and vomiting, dizziness, respiratory depression, pruritus, local anesthetic intoxication, subcutaneous hematoma, and scalp infec-tion was also recorded. Results Compared with group C, the intraoperative consumption of remifentanil and requirement for nicardipine were significantly decreased, the concentration of serum IL-6 was decreased at 3 h after surgery, the concentration of serum CRP was decreased at 12 h after surgery, the concentration of serum IL-10 was increased at 12 and 24 h after surgery, the time of the first postoperative requirement for rescue analgesia was prolonged, the consumption of oxycodone was reduced, and the incidence of nausea and vomiting was decreased in group B, and the intraoperative consumption of remifentanil was significantly reduced in group I (P<0. 05). Compared with group I, the intraoperative consumption of remifentanil was significantly reduced, the requirement for nicardipine was decreased, the concentration of serum IL-6 was decreased at 3 h after surger-y, the concentration of serum CRP was decreased at 12 h after surgery, the concentration of serum IL-10 was in-creased at 12 and 24 h after surgery, the time of the first postoperative requirement for rescue analgesia was pro-longed, the consumption of oxycodone was reduced, and the incidence of nausea and vomiting was decreased in group B (P<0. 05). Conclusion Compared with local infiltration of incision, scalp nerve block is helpful in carrying out anesthetic model of low-consumption opioids and in maintaining intraoperative hemodynamics stable and is more helpful in inhibiting perioperative inflammatory and pain responses when used for the patients under-going intracranial aneurysm clipping under general anesthesia.

Osteoarthritis (OA), in which M1 macrophage polarization in the synovium exacerbates disease progression, is a major cause of cartilage degeneration and functional disabilities. Therapeutic strategies of OA designed to interfere with the polarization of macrophages have rarely been reported. Here, we report that SHP099, as an allosteric inhibitor of src-homology 2-containing protein tyrosine phosphatase 2 (SHP2), attenuated osteoarthritis progression by inhibiting M1 macrophage polarization. We demonstrated that M1 macrophage polarization was accompanied by the overexpression of SHP2 in the synovial tissues of OA patients and OA model mice. Compared to wild-type (WT) mice, myeloid lineage conditional Shp2 knockout (cKO) mice showed decreased M1 macrophage polarization and attenuated severity of synovitis, an elevated expression of cartilage phenotype protein collagen II (COL2), and a decreased expression of cartilage degradation markers collagen X (COL10) and matrix metalloproteinase 3 (MMP3) in OA cartilage. Further mechanistic analysis showed thatSHP099 inhibited lipopolysaccharide (LPS)-induced Toll-like receptor (TLR) signaling mediated by nuclear factor kappa B (NF-κB) and PI3K-AKT signaling. Moreover, intra-articular injection of SHP099 also significantly attenuated OA progression, including joint synovitis and cartilage damage. These results indicated that allosteric inhibition of SHP2 might be a promising therapeutic strategy for the treatment of OA.