Objective To evaluate the therapeutic effect of steam inhalation of ?2-adrenergic agents combined with anticholinergic agents for patients with chronic obstructive lung disease(COPD) acute attack.Methods 64 patients with COPD acute attack were divided into two groups at random.The control group were under regular treatment,the therapy group were treated with steam inhalation of ?2-adrenergic agents combined with anticholinergic agents besides regular treatment.Results Symptoms and pulmonary function showed distinctly better in therapy group than in control group.Conclusion Steam inhalation of ?2-adrenergic agents combined with anticholinergic agents is an efficacious way to treat the patients with COPD acute attack.

Objective The biological half-life in vivo of local anesthesia is short, high concentration in local tissue is in-clined to cause central nerve and cardiovascular toxicity due to the drug absorption into blood by blood vessels.The research was to pre-pare the poly ( lactide-co-glycolide) nanoparticle loaded with ropivacaine ( RVC-PLGA-NPS) , optimize its process, and determine its characteristics in vitro. Methods An oil-in-water emulsion solvent evaporation technique was adopted to prepare the RVC-PLGA-NPS.The formulation was optimized by central composite design/response surface method(CCD-RSM), with the encapsulation effi-ciency( EE) , drug loading( DL) and particle size as the indexes.Research was also made on itsin vitro release by fitting different model equations. Results The acquired nanoparticals were smooth, with the mean particle size (331.21±2.11) nm, DL (13.81±1.35)%and EE (74.82±2.53)%.The accumulative release rate of the nanoparticals was about 73%in 96 h, which showed that Higuchi func-tion fitted the release curve. Conclusion The RVC-PLGA-NPS made by emulsion solvent evaporation technique have obvious drug-release behaviour in vitro.

Objective To establish the model of serum-caused damage to pulmonary microvascular endothelial cells (PMVECs) of mice with renal ischemia-reperfusion (I/R) injury.Methods Mice PMVECs were cultured to measure the standard trans-endothelial electrical resistance (TER) in the monolayer of PMVECs.When PMVECs were cultured and arranged in compact monolayer and TER was achieved,they were divided into 4 groups (n =3 each) using a random number table:serum of normal mice group (NS group) and different concentrations (5％,10％ and 20％) of serum of mice with renal I/R injury groups (IRS5 group,IRS10group and IRS20 group).The PMVECs were cultured for 1 h in the serum-free endothelial culture medium.The 0.8 and 0.2 ml culture medium containing 20％ serum of normal mice were then added to the upper and lower chambers,respectively,in group NS.The 0.8 and 0.2 ml culture medium containing 5％,10％ and 20％ serum of mice with renal I/R injury were then added to the upper and lower chambers in IRS5,IRS10 and IRS20 groups,respectively.100 μg/ml FITC-BSA 100 μl was added to the upper chamber in the four groups.At 3,6,9,12,15,18,21 and 24 h of incubation,the PMVEC monolayer permeability (apparent permeability coefficient,Pa) was detected.Results Compared with NS group,the Pa was significantly increased at 12 and 15 h of incubation in IRS5 group,and the Pa was increased at 6-24 h of incubation in IRS10 and IRS20 groups.Compared with IRS5 group,the Pa at 21 and 24 h in IRS10 group and at 9-24 h in IRS20 group were significantly increased.Conclusion Both 10％ and 20％ serum of mice with renal I/R injury can successfully establish the model of damage to PMVECs,and 20％ serum causes a more severe damage.

Objective To find the differentially expressed long non-coding RNA (lncRNA) between db/db mice that with nephropathy (DN) or not (DM).Methods In this study,3 DM db/db mice and 2 DN db/db mice proven by renal biopsy were randomly selected,and 3 healthy db/m mice as normal control group.Then,differentially expressed lncRNAs,mRNAs and their fragments per kilobase million (FPKM) in kidney samples were detected by high-throughput next generation sequencing technology.Sequencing data were analyzed to filter out the differentially expressed lncRNA,and theirfunction was preliminarily investigated by bioinformatics analysis and functional enrichment analysis to predict their target genes.Total RNAs of kidneys from these 8 mice were extracted to run real time PCR (RT-qPCR) for verifying the outcomes of the high-throughput sequencing.Results The urinary microalbumin/creatinine ratio (UACR),serum creatinine,and glomerular basement membrane thickness of DN db/db mice were higher than those of DM db/db mice (all P ＜ 0.05),while there was not significant difference in glucose between DM and DN mice.Totally 160 lncRNAs were up-regulated and 99 lncRNAs were down-regulated in kidneys of DN mice compared with those of DM mice,in which the differentially expressed lncRNAs with FPKM value≥2 and differential expression≥ 1 fold between groups were screened and verified by RT-qPCR.Finally three lncRNAs whose variation trend were consistent with the outcomes of the high-throughput sequencing were obtained.Conclusion There was a significantly different expression pattern of lncRNA between the kidneys of DN and DM mice,which may be involved in the progress of DN.

Objective To evaluate the effects of melatonin on the excitability of pyramidal neurons in the prefrontal cortex and the role of melatonin receptor 1 (MT1 R)-cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway.Methods Brains were obtained from male SpragueDawley rats between 14 and 21 days after birth.The brain slices of 350-μm thick were prepared and placed in artificial cerebrospinal fluid.The brain slices were divided into 5 groups (n =6 each) using a random number table method:control group (C group),melatonin group (M group),MT1/2R antagonist luzindole plus melatonin group (L+M group),MT2R antagonist 4P-PDOT plus melatonin group (P+M group) and PKA inhibitor Rp-cAMPS plus melatonin group (R+M group).Cells were perfused for 2 min with artificial cerebrospinal fluid in group C.Cells were perfused for 2 min with 1 μmol/L melatonin in group M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT1/2R antagonist luzindole and 1 μmol/L melatonin in group L+M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT2R antagonist 4P-PDOT and 1 μmol/L melatonin in group P+M.In group R+M,1 mmol/L PKA inhibitor Rp-cAMPS was continuously added to the pipette solution,and cells were perfused for 2 min with 1 μmol/L melatonin.The whole-cell patch-clamp technique was used to record the membrane potential and clamp current of pyramidal neurons in the prefrontal cortex.Results Compared with group C,the clamp current was significantly increased,and the membrane potential was decreased in group M (P＜0.05).Compared with group M,the clamp current was significantly decreased,and the membrane potential was increased in L + M and R + M groups (P＜0.05),and no significant change was found in the clamp current or membrane potential in group P+M (P＞0.05).Conclusion Melatonin inhibits the excitability of pyramidal neutrons in the prefrontal cortex,and the mechanism is related to activating MT1 R-cAMP-PKA signaling pathway.

Objective To evaluate the relationship between prefrontal cortex and propofol-induced cognitive dysfunction in rats. Methods SPF healthy male Sprague-Dawley rats, weighing 300-350 g, aged 16 weeks, were used in this study. Thirty rats in which catheters were successfully implanted into the prefrontal lobe were divided into 2 groups ( n=15 each ) using a random number table method: control group (group C) and propofol group (group P). In group P, 50μmol/L propofol 0. 5μl was microinjected into the prefrontal cortex at day 7 after operation, and the equal volume of normal saline was given instead in group C. T-maze test and open field test were performed at 15 min after administration. Results Com-pared with group C, the correct rate of selection in T-maze was significantly decreased ( P＜0. 05) , and no significant change was found in the total locomotor or number of rearing in open field test in group P ( P＞0. 05) . Conclusion Prefrontal cortex may be involved in propofol-induced cognitive dysfunction in rats.

Objective To analyze the factors related to early allograft dysfunction(EAD)after liver transplantation and to construct a predictive model.Methods A total of 375 patients who underwent liver transplantation in our hospital from December 2008 to December 2021 were collected,including 90 patients with EAD and 266 patients without EAD.Thirty items of baseline data for the 2 groups were compared and analyzed.Aftergrouping in a ratio of 7∶3,univariate and multivariate logistic regression analyses were used in the training set to evaluate the factors related to EAD and construct a nomogram.Receiver operating characteristic(ROC)curve,decision curve analysis(DCA),sensitivity,specificity,positive predictive value,negative predictive value,Kappa value and other indicators were used to evaluate the model performance.Results The incidence of EAD after liver transplantation was 24%.Multivariate logistic regression analysis showed that preoperative tumor recurrence history(OR=3.15,95%CI:1.28～7.77,P=0.013)and operation time(OR=1.22,95%CI:1.04～1.42,P=0.015)were related to the occurrence of EAD after surgery.After predicting the outcome according to the cut-off point of 0.519 identified by the Youden index,the model performance in the both training set and validation set was acceptable.DCA suggested the model has good clinical applicability.Conclusion The risk factors for EAD after liver transplantation are preoperative tumor recurrence history and operation time,and the established model has predictive effect on prognosis.