Objective To evaluate the efficacy of hydromorphone for patient-controlled intravenous analgesia (PCIA) after hip replacement in elderly patients.Methods Seventy patients, aged 65-75 yr, weighing 40-70 kg, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ , undergoing elective unilateral hip replacement, were randomly divided into either analgesia with hydromorphone group (group H, n =35) or analgesia with fentanyl group (group F, n=35).After a loading dose of 20 μg/kg of hydromorphone was injected at the beginning of skin closure, a PCA pump was connected, and the PCIA solution contained hydromorphone 0.25 mg/kg and tropisetron 10 mg in 120 ml of normal saline in group H.After a loading dose of 1 μg/kg of hydromorphone was injected at the beginning of skin closure, a PCA pump was connected, and the PCIA solution contained fentanyl 25 μg/kg and tropisetron 10 mg in 120 ml of normal saline in group F.The PCA pump was set up with a 0.5 ml bolus dose, a 15 min lockout interval and the background infusion at a rate of 2 ml/h in both groups.Tramadol 0.5 mg/kg was injects intravenously as rescue analgesic, and visual analogue scale score was maintained ≤ 3.The Ramsay sedation score,the number of attempts and the number of tramadol administration were recorded at 24 and 48 h after operation.The adverse effects within 48 h after operation and patient's satisfaction with analgesia were recorded.Results There was no significant difference in the Ramsay sedation score, the number of attempts and the number of Tramadol administration between H and F groups.Compared with group F, the incidence of adverse effects such as postoperative nausea, vomiting, respiratory depression, drowsiness, urinary retention, was significantly decreased, and the level of satisfaction with analgesia was increased in group H.Conclusion Hydromorphone provides accurate efficacy for PCIA after hip replacement in elderly patients, with fewer adverse effects and higher level of patient' s satisfaction.

OBJECTIVE:To investigate the mechanism of cross allergy reaction during the application of β-lactam antibiotics, and to provide reference for rational drug use in clinic. METHODS:Based on study experience of author in UIC and its affiliated hospital during advanced study,according to the experience of drug use safety management in patients allergic to β-lactam antibiot-ics from Rush University Medical Center,the mechanism of cross allergy reaction during the application of β-lactam antibiotics was summarized,and the disposal procedure for patients allergic to β-lactam antibiotics in the Affiliated Hospital of UIC was intro-duced. RESULTS:The principal reason for cross allergy reaction induced by β-lactam antibiotics were same or similar side chains between drugs. Cross allergy reaction occurred when IgE recognized these side chains. The disposal procedure for patients allergic to β-lactam antibiotics in the Affiliated Hospital of UIC included that the indication of β-lactam use was evaluated;standard penicil-lin skin testing according to evaluation results,anti-infection treatment by Grade challenge β-lactam antibiotics and course and rap-id drug tolerance induction. CONCLUSIONS:The disposal method for patients allergic to β-lactam antibiotics in the Affiliated Hos-pital of UIC can provide new thought for domestic clinical pharmacists in rational drug use among the patiens with reported aller-gies to special group as pregnant women,children.

ObjectiveTo investigate the effects of propofol on calcium/calmodulin-dependent protein kinase Ⅱ α ( CaMK Ⅱ α) activity in hippocampus in mentally depressed rats after electroconvulsive therapy (ECT).MethodsHealthy adult male SD rats aged 2-3 months weighing 180-220 g were used in this study.Mentally depressed model was induced by chronic unpredictable mild stress.Forty mentally depressed rats were randomly divided into 4 groups (n =10 each): mental depression group (group D),propofol group (group P),ECT group (group E),propofol + ECT group (group DPE).Groups D and P received intraperitoneal normal saline 8 ml/kg or propofol 80 mg/kg once a day for 7 consecutive days respectively.Group E received ECT once a day for 7 consecutive days.Group DPE received propofol 80 mg/kg + ECT once a day for 7 consecutive days.Sucrose preference test was performed at 1 d before and 1 d after treatment,and Morris water maze test was performed at 1 d before and 3 d after treatment.The rats were sacrificed after Morris water maze test,and hippocampi were removed for determination of CaMK Ⅱ α and phosphorylated CaMK Ⅱ α(pCaMK Ⅱ α )expression,and pCaMK Ⅱ α/CaMK Ⅱ α ratio was caculated.ResultsCompared with group D,the sucrose preference percentage was significantly increased in groups E and DPE,the escape latency prolonged and space exploration time shortened,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α down-regulated,pCaMK Ⅱ α/CaMK Ⅱ α ratio decreased in group E,the escape latency was significantly shortened and space exploration time prolonged,and the expression of pCaMK Ⅱ α up-regulated in group DPE ( P ＜ 0.05).Compared with group E,the escape latency was significantly shortened,space exploration time prolonged,and the expression of CaMK Ⅱ α and pCaMK Ⅱ α up-regulated,and pCaMK Ⅱ α/CaMK Ⅱ α ratio increased in group DPE ( P ＜ 0.05).ConclusionPropofol can reduce the cognition impairment induced by ECT in mentally depressed rats through enhancing CaMK Ⅱ α activity in hippocampus.

Objective To evaluate antimicrobial effect and mechanism of meropenem in the model of PA infection by C.elegans.Methods To evaluate drug effects of PA infection with caenorhabditis elegans by different concentrations of culture medium, determinate the lethal rate of C.elegans.Western blot detected mitogen activated protein kinase ( Mitogen-activated protein kinase MAPK ) activity change, and PCR detected antimicrobial peptide genes expression in C.elegans after PA infection,the effect of meropenem on MAPK activity change and antimicrobial peptide genes expression.Results Compared with the control group (OP-50), the death rate of C.elegans in PA infection group changed significantly (P<0.01). Meropenem showed protective effect after C.elegans infection ( P <0.01 ) .Detection of MAPK kinase activity showed that PA infection caused PMK-1 kinase activation, further study showed that antibiotics meropenem did not affect the activation of PMK-1 kinase (no significant difference).C.elegans antimicrobial peptide gene Lys-1, clec-85, F55G11.7, K08D8.5 activity increased in PA infection (P<0.01).Meropenem promoted the expression of the antimicrobial peptide gene increased (P<0.01),with synergistic effects.Conclusion Our results show that a C.elegans pathogenicity model can be applied screening drug susceptible to pathogens infection quickly and easily.

Objective To elucidate the function of phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling pathway underlying the regulation of Na+-I-symporter (NIS) and the influence of different levels of iodine on PI3K-AKT signaling pathway in lactating breast cells.Methods The primary cultured mammary gland cells were divided into three groups:①control group [0 μmol/L LY294002 + 0 μg/L insulin-like growth factor Ⅰ (IGF-Ⅰ)];②stimulation group (50 μg/L IGF-Ⅰ);③inhibition group (40 μmo]/L LY294002 + 50 μg/L IGF-Ⅰ).In addition,the cells were treated with different iodine contents (0,5,50,1 000,3 000 μg/L) for low iodine groups 1 and 2,iodine group,high iodine groups 1 and 2,and IGF-Ⅰ (50 μg/L) was used to stimulate PI3K-AKT signaling pathway.The expressions of AKT and NIS mRNA and protein were determined by real-time quantitative PCR and Western blotting,respectively.Results The expression of AKT mRNA (1.497 ± 0.550) in stimulation group was higher than that in inhibition group (0.777 ± 0.108,P ＜ 0.05),while the expression of NIS mRNA and protein in stimulation group (0.783 ± 0.187,0.618 ± 0.103) was lower than those in inhibition group (2.430 ± 1.423,1.417 ± 0.250,all P ＜ 0.05).With the iodine concentration increasing,except high iodine group 1 (1.090 ± 0.356),the expression of AKT mRNA in low iodine groups 1 and 2,iodine group,high iodine group 2 (1.758 ± 0.893,1.320 ± 0.538,1.003 ± 0.006,0.745 ± 0.307) tended to decline;total AKT protein (0.640 ± 0.106,0.601 ± 0.081,0.583 ± 0.089,0.555 ± 0.097,0.532 ± 0.023) and NIS mRNA (2.259 ± 0.682,1.823 ± 0.332,1.409 ± 0.366,1.321 ± 0.405,1.150 ± 0.454) tended to decline in low iodine groups 1 and 2,iodine group,high iodine groups 1 and 2;except low iodine group 2 (0.484 ± 0.179),NIS protein expression tended to decline (0.556 ± 0.199,0.502 ± 0.179,0.455 ± 0.126,0.435 ± 0.138);however,except low iodine group 2 (0.076 ± 0.045),the p-AKT protein expressions (0.078 ± 0.049,0.079 ± 0.040,0.085 ± 0.055,0.095 ± 0.051) were on the rise.Conclusion PI3K-AKT signaling pathway may play an inhibition role in the expression of NIS in lactating breast cells.

Objective:To investigate whether chitosan-polyelectrolyte complex (CS-PEC) can be used as scaffold for chondrocyte culture and for cartilage regeneration in vivo.Methods:Condylar chondrocytes of fetal mouse were seeded onto the three-dimension gel scaffolds of CS-PEC and cultured.The cultured chondrocytes/CS-PEC complex samples were transplanted subcutaneously into nude mice and the CS-PEC scaffold without chondrocyte was used as the control.The animals were sacrificed 4 and 8 weeks after operation respectively.Cartilage formulation was observed by histological and immunohistochemical methods.Results:In the in vitro culture the majority of cells attached to the CS-PEC surface and expanded rapidly. 4 weeks after transplantation,in the chondrocytes/CS-PEC complex the scaffold maintained mostly the original structure. Hypertrophic chondrocytes appeared in scaffold materials. CollagenⅡwas positive in the new cartilage. 8 weeks after transplantation the scaffold degraded almost completely and new cartilage could be observed. CollagenⅡ and cartilage matrix was positive in the new cartilage and the collagen I was positive in the surrounding fibroblast-like cells. In control transplants,8 week after transplantation some fibre-like tissue formed in the circumference, but there was no new cartilage formation and the collagen II and the cartilage matrix was negative.Conclusions:CS-PEC may be used as scaffold for fibre-cartilage regeneration.

Objective: To evaluate the effect of exogenous insulin on endoplasmic reticulum stress in myocardial tissues during insulin resistance in the rabbits undergoing cardiopulmonary bypass (CPB). Methods: Forty healthy adult New Zealand white rabbits of both sexes, weighing 2.5-3.0 kg, were divided into 4 groups (n=10 each) using a random number table method: control group (group C), CPB group, CPB plus insulin group (group I) and CPB plus normal saline group (group NS). Group C received no treatment.An insulin resistance model was established in group CPB.Insulin was continuously infused (the infusion rate was adjusted according to the blood glucose) starting from establishing CPB to 1 day after operation in group I. The equal volume of normal saline was given starting from establishing CPB to 1 day after operation in group NS.Blood samples were collected from the left femoral artery, and myocardial tissues obtained before CPB (T₁) and at 15, 30 and 60 min after aortic opening (T_2-4). The level of blood glucose was determined using oxidase method, the level of glucagon was detected by the radioimmunoassay method, and the insulin resistance index was calculated.The expression of inositol-requiring protein-1α(IRE1α), XBP1 and caspase-12 was measured by Western blot.The expression of IRE1α, XBP1 and caspase-12 mRNA was measured by fluorescent quantitative real-time polymerase chain reaction.Cell apoptosis was detected by TUNEL. Results: Compared with group C, blood glucose and glucagon levels at T_2-4 and insulin resistance index at T₄ were significantly increased, and the expression of inositol-requiring protein-1α(IRE1α), XBP1 and caspase-12 protein and mRNA was up-regulated at T₄ in CPB, I and NS groups (P<0.05). Compared with group CPB, blood glucose and glucagon levels at T_2-4 and insulin resistance index at T₄ were significantly decreased, and the expression of IRE1α, XBP1 and caspase-12 protein and mRNA was down-regulated at T₄ in group I (P<0.05). Conclusion Exogenous insulin significantly improves insulin resistance in myocardial tissues, and the mechanism is related to inhibiting endoplasmic reticulum stress and reducing cell apoptosis in the rabbits undergoing CPB.

This experimental study was designed to explore the possible mechanisms of Cariporide, a kind of Na+/H+ exchanger inhibitor, for protecting the lung from warm ischemia/reperfusion injury (WI/RI) of isolated rat lung model. Thirty isolated rat lungs were established on the Langendorff apparatus and randomly divided to three groups (n = 10, each): control group (C group), ischemia/reperfusion group (IR group) and Cariporide group (CP group). Mean pulmonary artery pressure (MPAP) and peak airway pressure (pAwP) were monitored continuously. At the end of reperfusion, right bronchoalveolar lavage was performed, bronchoalveolar lavage fluid (BALF) recovery rate (BALFRR) was recorded, and protein content in BALF was measured. Lung water content (LWC), malondialdehyde (MDA) and superoxide dismutase (SOD)of left lung tissue were measured; histomorphology evaluation was performed under light microscope and transmission electron microscope. In comparison with the data from IR group, BALF protein concentration, LWC, MDA content and MPAP content of reperfusion were significantly decreased, but SOD activity was increased in CP group. Histomorphologic feature also showed that pathological change significantly reduced in CP group. In this rat WI/RI model, the mechanism by which the selective Na+/H+ exchanger inhibitor (Cariporide) attenuates lipid peroxidation induced by WI/IR may be: preventing Ca2+ overload via inhibiting the transport of Na+/H2 exchanger-1 (NHE1) in the context of the coupled exchanger, thereby reducing the activation of xanthine oxidase pathway and oxygen free radical liberation which is dependent on certain intracellular Ca2+ concentration, and lastly promoting the endogenous antioxidative mechanism.
Animals ; Antioxidants ; pharmacology ; Guanidines ; pharmacology ; In Vitro Techniques ; Ischemic Preconditioning ; Lung ; blood supply ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; etiology ; prevention & control ; Sodium-Hydrogen Exchangers ; antagonists & inhibitors ; Sulfones ; pharmacology ; Superoxide Dismutase ; metabolism ; Warm Ischemia

OBJECTIVE:To explore the importance and necessity of clinical pharmacists in drug therapy for chronic disease patients,the feasibility of developing medication reconciliation (MR),and to provide reference for establishing the internal medicine working model of clinical pharmacy.METHODS:During May to Jul.2016,inpatients were selected from respiratory department of our hospital as subjects.After detailed pharmaceutical consultation,clinical pharmacist conducted MR for newly inpatients at the first day in the hospital.RESULTS:Through clinical pharmacists classified and organized the problems of drug use in the inpatients during medication,MR records of 98 inpatients were collected,involving 296 medical orders and 96 items of medication errors.Among MR patients,there were only 44 cases of good compliance (44.9％);some problems about drug use existed in other cases,including optional medication,improper usage and dosage,fearing of drug side effects and refusing to use drugs,drug withdrawal due to ADR,follow-up failure of special disease leading to excessive or inadequate dose,poor communication with doctors leading to medication errors,forgetting to take medication or missing,excessive medical treatment and so on.Most common medication error-inducing drugs type was cardiovascular drug,followed by respiratory drug and endocrine system drug.CONCLUSIONS:The development of MR by clinical pharmacists is helpful to identify and correct medication error,avoid potential medication error,and control disease.It can be used as a project of pharmaceutical care in department of internal medicine.

Objective To evaluate the effect of exogenous insulin on inositol-requiring protein 1α (IRE1α)-X-box-binding protein 1 (XBP1) signaling pathways in pancreatic tissues during cardiopulmonary bypass (CPB)-caused insulin resistance in rabbits.Methods Forty healthy adult New Zealand white rabbits of both sexes,weighing 2.5-3.0 kg,were divided into 4 groups (n =10 each) using a random number table method:control group (group C),group CPB,insulin group (group I),and normal saline control group (group NS).CPB was established in group CPB.Insulin was intravenously infused in a dose of 1.2 ml/h from establishing CPB to 1 day after operation,and the infusion rate of insulin was regulated according to the blood glucose (maintaining at 7.2-8.3 mmol/L) in group I.CPB was established,and normal saline was intravenously infused from the beginning of operation to 1 day after operation in group NS.Before CPB (T1) and at 15,30 and 60 min after aortic opening (T2-4),blood samples were collected from the left femoral artery,the plasma was separated,the blood glucose level was detected by oxidase method,the level of glucagon was detected by the radioimmunoassay method,and the insulin resistance index was calculated.Animals were sacrificed at T4,and pancreatic tissues were obtained for determination of the expression of IRE1α,XBP1,c-Jun N-terminal kinase (JNK) and caspase-12 protein and mRNA (by Western blot or fluorescent quantitative real-time polymerase chain reaction) and for examination of the pathological changes (by haematoxylin and eosin staining).Results Compared with group C,blood glucose and glucagon concentrations and insulin resistance index were significantly increased at T2-4,and the expression of IRE1α,XBP1,JNK and caspase-12 was up-regulated at T4 in CPB,I and NS groups (P＜0.05).Compared with group CPB or group NS,blood glucose and glucagon concentrations and insulin resistance index were significantly decreased at T2-4,the expression of IRE1α,XBP1,JNK and caspase-12 was down-regulated at T4 (P＜0.05),and the pathological changes of pancreatic tissues were significantly attenuated in group I.There was no significant difference in the parameters mentioned above between group CPB and group NS (P＞0.05).Conclusion The mechanism by which exogenous insulin reduces CPB-caused insulin resistance may be related to inhibiting IRE1α-XBP1 signaling pathways in pancreatic tissues of rabbits.