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Objective:To analyze the operation efficiency of hospitals in 31 provinces in China from 2009 to 2019 based on the three-stage data envelopmeni analysis(DEA) model, for references to improve the operation efficiency of hospitals in China and promote the high-quality development of public hospitals.Methods:The data came from such sources as China health statistics yearbook and China general hospital ranking list of Fudan university.The number of hospitals, health technicians and beds in 31 provinces of China from 2009 to 2019 were used as input indicators, while that of hospital patients, discharged patients, hospitalized patients, reputational scoring of superior specialties and academic scoring of scientific research were used as output indicators.Government health expenditure, per capita GDP, population density and the proportion of tertiary hospitals were used as environmental variables.The three-stage DEA model was used to calculate the hospital operation efficiency and scale reward.Results:The environmental variables affected the operation efficiency of hospitals in China( P<0.05). After removing the impact, the average of comprehensive efficiency, pure technical efficiency and scale efficiency of hospitals in 31 provinces from 2009 to 2019 were 0.703, 0.961 and 0.726, respectively.Among them, the scale benefit of hospitals in 4 provinces remained unchanged, while those in 26 provinces increased progressively and 1 province decreased progressively. Conclusions:Pure technical efficiency could be the main factor to improve the operation efficiency of hospitals in China, while the low scale efficiency will affect the improvement of the operation efficiency of hospitals.The scale efficiency of hospitals in most provinces had great room for improvement.In order to improve the overall hospital operation efficiency in China, the authors suggested to expand hospital scale based on the precondition of quality, promote balanced distribution of high-quality medical resources, and play the positive role of the social, economic and environment variables.
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Objective@#To investigate the differences of gemstone spectral curve and CT value of gastric cancer with different pathological types and differentiation degrees.@*Methods@#91 cases of preoperative gemstone CT images with gastric cancer were collected, including 24 cases of mucinous carcinoma, 67 cases of non-mucinous carcinoma, 16 cases of signet ring cell carcinoma, 8 cases of mucinous adenocarcinoma, 32 cases of moderately differentiated adenocarcinoma and 35 cases of poorly differentiated adenocarcinoma. Gemstone CT spectral imaging was performed preoperatively, and the spectral curve of the lesion in venous phase was obtained by using GSI Viewer software, the slope of the curve was calculated, and 11 monoenergetic CT values of 40~140 keV (10 keV interval) were measured. The gemstone spectral curves and CT values of gastric cancer with different pathological types and differentiation degrees are compared.@*Results@#The curve slopes of non-mucinous carcinoma, signet ring cell carcinoma and poorly differentiated adenocarcinoma were -1.92±0.53, -1.73±0.37 and -2.14±0.54, respectively. The absolute values were higher than those of mucinous carcinoma (-1.45±0.54), mucinous adenocarcinoma (-0.90±0.34) and moderately differentiated adenocarcinoma (-1.67±0.41), and the differences were all statistically significant (P<0.05). There were significant differences in monoenergetic CT values between mucinous and non-mucinous carcinomas at 40-140 keV (all P<0.05). The former was lower than the latter in different degrees, and the lower the energy, the greater the difference was. There were significant differences in monoenergetic CT values between signet ring cell carcinoma and mucinous adenocarcinoma at 40-100 keV (all P<0.05); monoenergetic CT values between poorly differentiated adenocarcinoma and moderately differentiated adenocarcinoma at 40-90 keV showed statistically significant differences (P<0.05).@*Conclusions@#Gastric cancer with different pathological types and differentiation degrees have their characteristic spectral curves in venous phase, and the monoenergetic CT values are significantly different at low energy. The spectral curve of gemstone CT may be helpful to evaluate the pathological type and differentiation degree of gastric cancer before operation.
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Aim Toinvestigatetheeffectsoftotalsap-onin of Dioscorea (TSD)on rats with monosodium u-rate crystal-induced acute gouty arthritis (AGA)and mechanisms.Methods Totally72Wistarratswere randomly devided into six groups,Each group was giv-en corresponding drug before,then rat acute gouty ar-thritis model was made by injection of monosodium u-rate in the ankle joint cavity.The gait,articular swell-ing degree and physiological changes of rats were ob-served.The concentration of TNF-α,IL-1β,IL-18 in serum were detected by ELISA.The levels of pro-IL-1β, NALP3, ASC, pro-caspase-1, and cleaved caspase-1 were detected by Western blot.Results AllTSDgroupsandcolchicinesignificantlychangedthe gait of rats and TSD high and middle groups signifi-cantly reduced joint swelling and diminished the patho-logical changes.The levels of TNF-α,IL-1β,IL-18 in serum were significantly decreased,and the levels of pro-IL-1β,NALP3,ASC,pro-caspase-1 and cleaved caspase-1 were apparently reduced in TSD high and middlegroups.Conclusion TSDpossessesanti-goutfunction and the mechanism may be related to sup-pressing the NALP3 inflammasome activation and in-hibiting the cytokine production.
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Generally,the pathological changes of multiple sclerosis(MS) is mostly on lesion of the central white matter (WM). However,the clinical symptoms such as cognitive impairment cannot be fully explained just by the WM damage. Therefore, central gray matter(GM)damage has attracted more attention. The development of magnetic resonance imaging(MRI)makes in vivo detection of GM while showing the clinical symptoms possible. Yet,the correlation between the patient clinical symptoms and GM dam?age particularly in cortex still need to be elucidated. Hence,we summarize the historical background and give an overview of the corre?lation between GM damage and MS clinical symptoms in terms of cognitive impairment and epilepsy.
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Transforming growth factor-β1(TGF-β1)has become an important biological marker and therapeutic target of clinical progression of chronic kidney diseases. Sma- and Mad-related protein (Smad)is a downstream signal transduction protein of the TGF-β family. TGF-β1 activates Smad2 and Smad3 before increasing the transcription of connective tissue growth factors in the nucleus. Smad3 promotes mesangial cell proliferation,extracellular matrix accumulation,epithelial-mesenchymal transition, leading to renal fibrosis. However,Smad2 and Smad7 play a negative regulatory role by inhibiting renal fibrosis. TGF-β1 specific inhibitor (SB431542,etc.) has antifibrosis effect,most of which is in the preclinical stage. The drugs on the market that are effective for DN,such as benzodiazepines,atorvastatin, losartan,and pirfenidone,can inhibit the expression of TGF-β1,while tripterygium wilfordii,cordyceps sinensis,and berberine can delay the process of diabetic nephropathy by reducing TGF-β1 levels.
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OBJECTIVE:To study the in vitro dissolution of Enalapril maleate and folic acid tablet. METHODS:HPLC was performed on the column of Agilent HC-C18 with mobile phase A of acetonitrle-phosphate buffer solution(70:30,V/V) and mobile phase B of acetonitrle-phosphate buffer solution(5:95,V/V)(gradient elution) at a flow rate of 1.0 ml/min,detection wavelength was 215 nm,column temperature was 50 ℃,and volume injection was 80 μl. Media were water,hydrochloric acid solution(pH 1.2),phosphate buffer solution(pH 5.0)and phosphate buffer solution(pH 6.8),medium volume was 900 ml and rotation speed was 50 r/min. The dissolution behavior of enalapril maleate in Enalapril maleate and folic acid tablet in 4 media were studied and compared with the dissolution behavior in vitro in original preparation of Enalapril maleate tablet,meanwhile,the dissolution behar-ior of folic acid in Enalapril maleate and folic acid tablet in phosphate buffer solution(pH 5.0)were studied and compared with dis-solution data of folic acid preparation in Japanese Orange Book to evaluate the intrinsic quality. RESULTS:The linear range was 0.561-14.03μg/ml for enalapril maleate(r=0.999 9)and 0.043-1.085μg/ml for folic acid(r=0.999 9),respectively;RSDs of pre-cision and stability tests were lower than 2.0%;recoveries of enalapril maleate in 4 media were 100.63%-102.33%(RSD=0.72%, n=9),99.27%-100.44%(RSD=0.41%,n=9),99.71%-100.29%(RSD=0.15%,n=9)and 96.74%-99.19%(RSD=0.79%,n=9),respectively. Recoveries of folic acid were 100.18%-101.63%(RSD=0.48%,n=9),97.73%-101.81%(RSD=1.32%,n=9),99.60%-102.24%(RSD=0.74%,n=9)and 100.00%-102.76%(RSD=0.90%,n=9),respectively. In 15 min,the dissolution of enalapril maleate of 2 preparations in 4 dissolution media were more than 85%;dissolution speed of folic acid in Enalapril male-ate and folic acid tablet was faster than that in folic acid preparation in phosphate buffer solution(pH 5.0). CONCLUSIONS:The method is suitable to determine the dissolution of Enalapril maleate and folic acid tablet;the in vitro dissolution curve of enalapril maleate in Enalapril maleate and folic acid tablet is similar to Renitec,and the in vitro dissolution of folic acid is better than folic acid preparation.
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Homocysteine ( Hcy) is an independent risk factor for a variety of diseases and closely related to cardiac-cerebralvascu-lar diseases, neurological diseases, diabetes and diabetic com-plications. High homocysteine levels can significantly increase the recurrence risks of cardiac-cerebralvascular events and stroke in patients with stroke, leading to high all-cause mortality. The risk of Alzheimer’s disease is increased by 1. 8 fold when the concentration of Hcy is over 14 μmol·L-1 . For each 5 μmol· L-1 increase in plasma Hcy in diabetes patients, the mortality rate increases by 5 fold in the next five years. High Hcy triggers the pathogenesis of diseases via multiple mechanisms including oxidative stress, lesions of vascular endothelial cells, prolifera-tion of vascular smooth muscle cells, dysfunction of coagulation and lipid metabolism and genomic hypomethylation etc.
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Microglia are the inherent macrophages and immune surveillance cells in the central nervous system (CNS) and compose the first guard of immune defense in CNS .The activation of microglia is one of the pathological features of many CNS diseases and acts as an important role during the multiple sclerosis (MS) process.MS is a CNS disease characterized by neuroinflammatory infiltration , demyelination and axonal damage.Accumulation of activated microglia at the injury site has been observed in brains of MS patients and experimental animals with complicated mechanisms.Microglia have both detrimental and beneficial roles .For instance, microglia have been shown to recruit and reactivate T cells in the CNS and release many detrimental molecules such as proteases , inflammatory cytokines, and free radicals.Conversely, they have also been observed to aid in axonal regeneration and remyelination as well as assist in the clearance of inhibitory myelin debris .In addition, microglia have been shown to release a variety of neurotrophic factors . Cuprizone [oxalic acid bis (cyclohexylidene hydrazide )] is a well-known copper-chelating agent.Cuprizone ingestion in mice induces a highly reproducible demyelination of distinct brain regions .Discussion on the detrimental and beneficial aspects of microglia in cuprizone animal models will serve to better understand the development of MS and find out new therapeutic targets.This review will further our understanding of the dichotomous roles of microglia in cuprizone -induced demyelination in animal models of multiple sclerosis .
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ObjectiveInvasive fungal infection(IFI) can be a lethal complication in patients with diffuse connective tissue diseases(DCTD).The aim of this study was to determine the characteristics of hospitalized DCTD patients with IFI,and identify the risk factors.MethodsData from 33 DCTD in patients with IFI at Shanghai Renji Hospital between Jan 2007 and Jan 2011 were collected retrospectively.DCTD patients with either active M.tuberculosis (n=33) or other bacterial infections (n=34) at the same period were taken as controls.Systemic lupus erythematosus (SLE) inpatients with IFI (n=11 ) from Jan 2002 to Dec 2006 were also considered as a historical control group.The method of univariate analysis of data depended on the data distribution type.Variables that suggested association in the univariate analysis P＜0.1 were entered into a stepwise logistic regression model.ResultsThe leading underlying diseases of DCTD with IFI were SLE(n=18,55％),systemic vasculitis(n=4,12％),and inflammatory myopathy(n=4,12％).The most frequent pathogen was Candida spp(n=13,39％ ),followed by Cryptococcus neoformans(n=10,30％ ),and Aspergillus (n=3,9％).The infection locations included lung (n=19,58％),central nervous system (n=9,27％ ),and disseminated IFI(n=4,12％ ).Six patients(18％) died from IFI.Compared with non-IFI infections,patients with IFI infection had a shorter duration of underlying disease and were exposed to high doses of prednisolone prior to infection.More patients with IFI infection had elevated alanine aminotransferase,higher fasting glucose and lower C-reactive protein levels when compared to patients with non-IFI infections.Compared with the two historical SLE-IFI groups, the short-term survival improved in lupus patients complicated with IFI infection over time(64％ vs 83％).ConclusionUnderstanding disease spectrums and risk factors of IFI in DCTD,along with advances in antifungal treatment,will help clinicians to manage those patients with invasive fungal infection effectively to achieve favourable prognosis.
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Aim To investigate the rationality and the dose of TSD combined with TSA on reducing serum uric acid and anti-inflammatory.Methods Mice hyperuricemic models were made by uric acid intraperitoneal injection or yeast extract paste intragastric administration.Mice ear swelling model was induced by locally painting dimethylbenzene.Optimized combination dosage of TSD and TSA was obtained using the Codrug software.Results In the mice hyperuricemic models,the serum uric acid in TSD group,TSD plus TSA group and positive control groups was significantly reduced compared with the model group(P
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Uric acid is an end product of purine degradation in humans and normally depends upon renal excretion for the majority. Hyperuricemia is likely to cause gout, renal disease, or stones, and associated with cardiovascular impairment over the long term. The prevalence of gout and hyperuricemia appears to be on the increase in recent years. The present paper reviews the relationships between hyperuricemia and insulin resistance,purine metabolism and uric acid elimination , the genetics study and the mechanisms of hyperuricemia.
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AIM This paper was to review the methods of establishing experimental animal models of intrauterine growth retardation (IUGR) and their observed index. METHODS Passive smoking, passive smoking plus drinking wine, NG nitro-L-arginine methyl ester, dactinomycin, thiamine deficiency plus pyrithiamine, or ligating the uterine artery during pregnancy were used.RESULT The fatal and maternal body weight was lower body length; was shorter; infant physique and nerve system development was slow.CONCLUSION The above methods could establish animal models of IUGR.
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AIM To establish hyperuricemia animal model. METHODS The mice were given uric acid by ip and then the level of uric acid in serum was detected. RESULTS Uric acid 125,250,500, 1 000 mg?kg -1 ip significantly increased the level of uric acid in mouse serum. The level of uric acid in mouse serum was attained peak at 10 min and the hyperuricemia could lasted over 4 hours after uric acid 250 mg?kg -1 given. CONCLUSION Uric acid given by ip can form mouse hyperuricemia model, the dosage of 250 mg?kg -1 is better.
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Hyperuricemia is induced by the mechanism of the elevated production of uric acid or the decreased renal excretion of uric acid. At present, there are three major methods to establish models for hyperuricemia: first, it will elicit pronounced hyperuricemia when feeding or injecting the animal with hypoxanthine 600～1000 mg?kg -1 , xanthine 600 mg?kg -1 , adenine 150～300 mg?kg -1 , yeast 15～30 g?kg -1 , uric acid 250 mg?kg -1 or 350～700 mg?kg -1 because of the elevated serum uric acid. Such effect will be also observed as administrating the animal with the inhibitors of uric acid excretion such as ethambutol 250 mg?kg -1 , nicotinic acid 100 mg?kg -1 at the same time of the above steps. Second, being an uricase inhibitor, when fed the rats 0 4 g?d -1 and uric acid 0 6 g?d -1 for 3～4 weeks, oxonic acid is able to cause the continuously elevated serum uric acid. Similarly, when potassium oxonate 300 mg?kg -1 ip only once, the serum uric acid in mice will be also elevated. Third, to destruct the urate oxidase gene (EC 1.7.3.3) in the mouse by homologous recombination in embryonic stem cells, and then the oxidase deficient mutant mouse as the hyperuricemia model, is generated by gene recombination.The rats and the mice have urate oxidase, which can decompose the uric acid to allantoin, while the avian (such as chicken, coturnix and so on) have not.
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AIM To establish mice hyperuricemia model METHOD Yeast extract paste 7 5～30 g?kg -1 was given to mice by ig once daily for 7,14,21,28 consecutive days, and detected the level of uric acid in serum RESULT The serum uric acid level in mice were (271 8?53 2),(215 4?31 5),(195 9?56 0),(142 1?30 7) ?mol?L -1 in 30 g?kg -1 group after administration 1,2,3,4 weeks;and (226 8?40 7),(148 67?30 4),(176 9?27 0),(119 3?27 4) ?mol?L -1 in 15 g?kg -1 group after administration 1,2,3,4 weeks;In 7 5 g?kg -1 group the serum uric acid level was (117 0?29 0) ?mol?L -1 after 1 week, respectively CONCLUSION Yeast extract paste (15～30) g?kg -1 given by ig could form mice hyperuricemia model, and the hyperuricemia could last 1～2 weeks
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AIM To study the effect of polysaccharides 2b from Mudan cortex (PSM 2b) on type 2 diabetes mellitus (T2DM) rats and explore its mechanism. METHODS T2DM rat model was established by low dosage streptozotocin and high sucrose fat diet. The drugs were administrated by ig for 5 weeks. The serum glucose was assayed with GOD POD method. Insulin was determined by radioimmunoassay. Insulin receptors of the plasma membrane from rat liver were determined with radioligand binding assay of receptors (RBAR). RESULTS PSM 2b could significantly lower fasting blood glucose (FBG), improve impaired glucose telarance (IGT) and dyslipidemia. It could also remarkably raise receptor total (RT2) of the low affinity insulin receptor (InsR) and insulin sensitivity index (ISI) in T2DM rats. CONCLUSION PSM 2b has an obvious therapeatic effect on T2DM in rats. Its mechamsm is relatively improve insulin resistance (IR) in T2DM rats by raising the number of InsR.
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We first report the pharmacokinetics of paeoniflorin ( PF), that is a main component of paeony roots, in dogs by HPLC analysis. The experimental results were shown that after i .v . of 11.25 mg/kg PF in 4 dogs, the curve of plasma concentrations versus times for PF was fitted well to a open 2 compartment model, the T1/2 (?) was 6.29?1.80min T1/2 ( ? ) was 133.41?84.89 min, VB was 0.54 ? 0.10 L/kg, andCL was 3.41 ? 1.01ml/min?kg-1 .The results also were shown that PF was rapidly removed from the blood by kidney and the accumulated recovery amounts of excretion was 36.85% and 79.33% of total i .v . doses during 20 min and 7h administrations respectively. The elimination of PF by liver was lower than by kidney, and the accumulated amount of PF in bile was only 3.77% within 7h after iv.