Using the enterprise resource planning(ERP)management mode,the paper analyzed the present medical insurance payment audit accounts at public hospitals,and probed into the establishment of an information management platform for medical insurance payment audit accounts in the ERP environment.The purpose is to perfect the management of medical insurance payment audit accounts,increase the efficiency of hospital's working capital,strengthen the quality and efficiency of hospital management.

【Objective】 To study the technology of separating and purifying C1 esterase inhibitor (C1-INH) by using the waste washing liquid as raw materia during the preparation of human prothrombin complex (PCC) l. 【Methods】 C1-INH was isolated and purified by a two-step method of polyethylene glycol (PEG) 4000 precipitation and cation chromatography. The pH of raw materials and the concentration of PEG4000 were adjusted to investigate the optimal conditions of PEG4000 precipitation method. After PEG was precipitated and centrifuged, the supernatant is treated as the loading solution for cation exchange chromatography, using Fractogel EMD SE HiCap(M) gel and CM Sepharose FF gel for ion exchange chromatography. The most suitable gel and separation conditions were selected by comparing the C1-INH antigen yield, activity yield and specific activity. 【Results】 Under the condition of pH 6.1, when the mass fraction of PEG4000 was 14%, the recovery rate of C1 esterase inhibitor was close to 70%, and the removal rate of ceruloplasmin was more than 95% after stirring for 10 minutes. As fractogel EMD SE HiCap(M) gel was used for cation exchange chromatography, when the eluent salt concentration was 0.25 M sodium chloride, the activity yield of C1 esterase inhibitor was greater than 80%, and the specific activity was greater than 5 IU/mg. 【Conclusions】 Using the waste washing liquid as the raw material during the preparation of PCC, the C1 esterase inhibitor with high specific activity can be prepared through PEG precipitation and purification by Fractogel EMD SE HiCap(M) ion exchange chromatography.

Objective To investigate the expressions of ABCG2 and V-ATPase in NSCLC and their expression rates in pathological classification, TNM stages and pathological grades and the expression correlation between ABCG2 and V-ATPase. Methods Expressions of ABCG2 and V-ATPase were accessed with EnVinsion immunohistochemistry in tumor samples from 92 NSCLC patients. The corresponding data was analyzed statistically. Results Expressions of ABCG2 and V -ATPase were found both in the lung adenocarcinoma and lung squamous cell cancer, and the difference between these two kinds of tumors was significant (P =0.003,0.000). ABCG2 expression was significantly different among TNM stages of lung adenocarcinoma (P=0.004) as well as among pathological grades of lung adenocarcinoma (P =0.028) and squamous cell carcinoma (P =0.000), while no significant difference was found among TNM stages of squamous cell lung carcinoma. The level of V-ATPase expression was associated with TNM stages of lung adenocarcinoma (P =0.026) and pathological grades of lung squamous cell carcinoma (P =0.002), however, among TNM stages of lung squamous cell carcinoma and pathological grades of lung adenocarcinoma, the difference was not significant. Additionally, the significant correlation was found between expression of ABCG2 and V-ATPase in all samples, adenocarcinoma and squamous cell carcinoma (P<0.001). Conclusion The significant correlation is found between expression of ABCG2 and V-ATPase, which indicate that they may co-work to participate in the mechanism of anticancer drug resistance.

Objective To explore the effect of advanced glycation end products (AGEs) on proliferation of bone marrow mesenchymal stem cells (MSCs) and related mechanism.Methods The bone marrow MSCs were isolated from male Sprague Dawley rats and cultured in vitro.The flow cytometer was used to identify the bone marrow MSCs by detecting positive labels (CD29 and CD90) and negative labels (CD34 and CD45).The advanced glycation end products-bovine serum albumin (AGE-BSA),one of the AGEs,was used in this study.The methyl thiazolyl tetrazolium (MTT) method was used to detect the effect of AGE-BSA on proliferation of the bone marrow MSCs.In MTT test,there were 3 groups:AGE-BSA group,BSA group,and control group.In AGE-BSA group,different doses of AGE-BSA (0,25,50,100 and 200 μg/ml) was used to stimulate the bone marrow MSCs for 6 h,12 h or 24 h.In BSA group,the 200 μg/ml BSA was used to stimulate the bone marrow MSCs for 6 h,12 h or 24 h.Gene chips detection was used to detect change of genes expression in bone marrow MSCs.Results The proliferation of the bone marrow MSCs could be inhibited by AGE-BSA,in a dose- and time-related manner.Compared with the BSA group,after being treated with 100 μg/ml AGE-BSA for 24 h or 200 μg/ml AGE-BSA for 12 h and 24 h,the proliferation of the bone marrow MSCs decreased obviously.The gene chips detection found that there were changes in expression of 17 genes in the bone marrow MSCs after being treated with AGE-BSA (200 μ.g/ml) for 12 h or 24 h,and the genes were same at the two time points.Among 17 genes,the expression of 12 genes increased,including four inflammatory factors (CCL3,CCL2,CCL4 and IL-1β),and 5 genes decreased.Conclusion AGE-BSA can inhibit the proliferation of bone marrow MSCs,which may be related to the onset of the diabetic osteoporosis.

Osteoarthritis (OA) is a common chronic joint disease,whose main pathological changes are the degeneration of articular cartilage and secondary bone hyperplasia.The limitation of current treatment methods including pain relief and joint replacement surgery is that they cannot fundamentally improve the damage of articular cartilage.The emergence of disease-modifying osteoarthritis drugs (DMOAD) may break the above limitations.They fundamentally inhibit the structural degeneration of articular cartilage by participating in the regulation of cartilage metabolic balance, regulation of subchondral bone remodeling,and control of local inflammation.Thereby,OA patients will get symptom improvement including pain relief and joint function restoration,delay the artificial joint replacement surgery, and improve the quality of life. There are still no DMOAD drugs widely available on the market worldwide.This paper reviews the background of R&D,the classification of mechanisms of action and research progress of representative drugs under different inechanisms so as to provide reference for future research.

Objective:To observe the changes of varicella zoster virus (VZV)-DNA load in aqueous humour samples in VZV-induced acute retinal necrosis (ARN) in the early stages of antiviral treatment.Methods:A retrospective observational clinical study. From April 2016 to April 2018, 24 patients with 24 eyes of VZV-induced ARN who were diagnosed by Department of Ophthalmology, Eye and ENT Hospital of Fudan University and received complete aqueous humor sampling were included in the study. Among them, there were 13 males with 13 eyes, 11 females with 11 eyes; 12 left eyes and 12 right eyes; the age was 52.0±9.5 years old (39-71 years old). The time from the onset of ocular symptoms to the diagnosis of ARN was 16.6±6.1 days (7-30 days). Best-corrected visual acuity (BCVA) and ultra-wide-field fundus imaging were performed in all affected eyes. The BCVA examination was carried out using the Snellen visual acuity chart, which was converted into the logarithm of the minimum angle of resolution (logMAR) visual acuity. All patients were given intravitreal injection of 40 mg/ml ganciclovir 0.1 ml (including 4 mg of ganciclovir), 2 times a week, until the active necrotizing retinal lesions subsided, at most after the diagnosis 4 weeks, with a maximum of 9 injections. The follow-up period was 12.8±5.6 months. The aqueous humor samples were collected at presentation and 4, 7, 14, 21, 28 days after the initiation of antiviral therapy, and the VZV-DNA load was detected by real-time quantitative polymerase chain reaction. A plateau phase and a logarithmic reduction phase of the DNA load changes were observed after antiviral treatment began. Wilcoxon rank sum test was used to compare and analyze the differences in BCVA between the eyes at baseline and last follow-up.Results:The mean viral load at presentation was 8.6×10 7±1.3×10 8 copies/ml. The initial plateau phase last for an average of 7.4±2.4 days. In the following logarithmic reduction phase, the mean slope of the decline in viral load was -0.13±0.04 log/day, and the expected time for half reduction of the initial viral load was 2.5±0.7 days. After 28 days antiviral treatment, the viral load decreased to 1.7×10 5±1.8×10 5 copies/ml. In the course of the disease, rhegmatogenous retinal detachment occurred in 16 eyes. Before treatment and at the last follow-up, the logMAR BCVA of the affected eye was 1.1±0.6 and 0.8±0.7, respectively. The results of correlation analysis showed that the logMAR BCVA at the last follow-up was correlated with the initial VZV-DNA load ( r=0.467, P=0.033). Conclusion:The VZV-DNA load in the aqueous humor of eyes with VZV-induced ARN is significantly decreased after antiviral treatment, which is closely related to the clinical process of ARN.

The situation of population aging is grim.And scientific and technological innovation is an important strategic support means to solve the problem of population aging.President Xi Jinping has put forward the guiding ideology of "Four Facing" of scientific and technological innovation, pointing out the direction of using science and technology to support the high-quality development of the aging cause and to realize healthy aging.The scientific and technological innovation of population aging has always been highly integrated with exploring international science frontiers, serving main economic sectors, meeting major national needs and safeguarding people's life and health.This paper elaborates on the deep integration between the aging population and the "four facing" of scientific and technological innovation, in order to better construct a new development pattern, and for science to help actively cope with the smooth implementation of the national strategy of population aging.

【Objective】 To explore the effects of nerve growth factor （NGF） on bladder function and axon injury repair in rats with traumatic spinal cord injury （t-SCI） so as to explore its molecular mechanism. 【Methods】 Traumatic spinal cord injury model was constructed in 30 male SD rats by modified Allen’s beating method. The rats were randomly divided into sham-operation group， injury group and NGF group， with 10 rats in each group. We used the BBB score to observe the motor function of the rats’ hind limbs before and after the operation. The BL-420 biometer experimental system detected the urodynamics. Six anterior roots of the left lumbar taken from the distal end of the anastomosis were stained with toluidine blue， and the number of myelinated axons was counted. We used HE to stain rat bladder tissue， TUNEL to stain the rats’ severely injured spinal cord， and observed the spinal cord apoptosis rate. Western blotting was used to detect the protein expressions of Raf-1， p-MEK-2， MEK-2， ERK1/2， and p-ERK1/2 in spinal cord tissue. 【Results】 The BBB score results showed that there was no difference in the scores of the sham-operation group， the injury group and the NGF group before the operation. After the operation， the scores of the injury group and the NGF group were significantly lower than those in the sham-operation group （P<0.05）. The maximum detrusive pressure and the number of axons were significantly lower in the injury group than in the sham-operation group and the NGF group （P<0.05）， but the residual urine volume and bladder cell apoptosis rate in the injury group were notablely higher than those in the other two groups （P<0.05）. HE staining results showed that bladder edema in the injury group was severe and the detrusor muscle structure was loose， while the NGF group had reduced bladder injury. Western blot results showed that the protein ratio of p-ERK1/2/ERK1/2 and p-MEK-2/MEK-2 and the expression of Raf-1 in the injury group were significantly higher than those in the sham operation group and NGF group （P<0.05）. However， there was no significant difference between the sham operation group and the NGF group in maximum detrusive pressure， the number of myelin axons， residual urine volume， bladder cell apoptosis rate， or protein （P>0.05）. 【Conclusion】 NGF may hinder the conduction of MAPK/ERK pathway， thereby affecting the repair of axon damage and improving the bladder function of t-SCI rats.

Severe muscle injury is hard to heal and always results in a poor prognosis. Recent studies found that extracellular vesicle-based therapy has promising prospects for regeneration medicine, however, whether extracellular vesicles have therapeutic effects on severe muscle injury is still unknown. Herein, we extracted apoptotic extracellular vesicles derived from mesenchymal stem cells (MSCs-ApoEVs) to treat cardiotoxin induced tibialis anterior (TA) injury and found that MSCs-ApoEVs promoted muscles regeneration and increased the proportion of multinucleated cells. Besides that, we also found that apoptosis was synchronized during myoblasts fusion and MSCs-ApoEVs promoted the apoptosis ratio as well as the fusion index of myoblasts. Furthermore, we revealed that MSCs-ApoEVs increased the relative level of creatine during myoblasts fusion, which was released via activated Pannexin 1 channel. Moreover, we also found that activated Pannexin 1 channel was highly expressed on the membrane of myoblasts-derived ApoEVs (Myo-ApoEVs) instead of apoptotic myoblasts, and creatine was the pivotal metabolite involved in myoblasts fusion. Collectively, our findings firstly revealed that MSCs-ApoEVs can promote muscle regeneration and elucidated that the new function of ApoEVs as passing inter-cell messages through releasing metabolites from activated Pannexin 1 channel, which will provide new evidence for extracellular vesicles-based therapy as well as improving the understanding of new functions of extracellular vesicles.
Creatine/metabolism* ; Extracellular Vesicles ; Muscle, Skeletal/metabolism* ; Myoblasts/metabolism* ; Regeneration ; Connexins/metabolism*