Cost accounting is an important measure in hospital economic management.This article approaches the problems and their causes in cost accounting in army hospitals in terms of the correlation between income and cost,the normality of asset management,the accuracy of internal service cost,the advancedness of cost accounting techniques and so on.It also proposes a some corresponding countermeasures based on our work experience.

Human CD3AK cells were prepared from peripheral blood mononuclear cells by culturing with recombinant IL-2 and antiCD3AK McAb. The mechanism and regulation of CD3AK cytotoxic activity with cytokines (rhIFN-?, rhIFN-?, TNF) and chernotherapeutic agents (CDDP or ADM) were observed by LDH-release assay, ABC-CELISA and the flow cytometric assay. The results showed: (1) Adhesion molecules ICAM-l/LFA-1 participated in CD3AK-mediated killing of tumor cells, hrlFN-? and TNF enhanced cytotoxicity of CD3AK through this pathway. (2) CD3AK could indirectly kill tumor cells by releasing soluable cytotoxic factors. (3) The membrane-associated TNF may be involved in CD3AK-mediated cytotoxicity. (4) CD3AK cells could induce the apoptosis of tumor cells. (5) Pretreatment of tumor cells with CDDP or ADM resulted in the increased vulnerability of tumor cells to CD3AK-mediated killing, the enhancement of CD3AK-mediated cytotoxicity by CDDP was relative to the increased expression of ICAM-1, HLA-ABC on tumor cell membrane.

Objective:To explore the possible mechanism of astragaloside involved in the mouse podocytes injury induced by TGF-β1 in vitro.Methods:Mouse podocytes were cultured in vitro and then all cell were divided into 5 groups:normal control group , TGF-β1 treatment group ,TGF-β1 treatment +astragaloside low dose group ,TGF-β1 treatment +astragaloside middle dose group and TGF-β1 treatment +astragaloside high dose group.The proliferation rate of each group was investigated by MTT assay ,the expression of TRPC6 protein and mRNA were measured by Western blot and RT-PCR respectively after 48 hours.Results:TGF-β1 can significantly inhibit the proliferation of podocytes ( P<0.05) ,fusions of foot processes or even effaced of podocytes were observed .TGF-β1 could also increase the expression of TRPC6.Astragaloside could reduce the inhibition of TGF-β1 to the proliferain of podocytes significantly ,make the cell shape tend to be normal,and reduce the expression of TRPC6 mRNA and protein with dose-effect relation.Conclusion:TRPC6 play an impor-tant role in the TGF-β1 induecd podocytes injury .Astragaloside can alleviate podocytes injury by reduce the expression of TRPC 6.

Objective To explore the mechanism by which the anti-human P185erbB2 scFv-Fc-IL-2(HFI)modulates tumor surface molecules and activates immune effector cells in vitro. MethodsMTT assay was used to test the proliferation and the LAK-like cytotoxicity. Flow cytometry assay was used to test the expression of ICAM-1, Fas and erbB2 receptors in tumor cells and the expression levels of CD molecules FasL and LFA-1 in human PBMC. Antibody-dependent cell-mediated cytotoxicity(ADCC)mediated by HFI against SKOV3, MCF-7 and SGC-7901 tumor cells was explored hv LDH release assay. Results The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI were upregulated, from 24.85％ and 0.53％ to 85.36％ and 59.19％ respectively, while the expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI were downregulated, from 98.48％, 42.60％ and 36.66％ to 94.01％,30.95％ and 12.36％ respectively. HFI could significantly enhance the proliferation activity of human PBMC, and CD3+ CD8+ T cells and CD3- CD16+ CD56+ NK cells were elevated, from 24.37％ and 6.90％ to 38.80％ and 13.45％ respectively. The expression levels of CD25, LFA-1 and FasL were significantly enhanced from 3.99％, 86.52％ and 5.02％ to 12.96％, 99.06％ and 16.19％. The LAK-like cytotoxicity of human PBMC treated with HFI against SKOV3, MCF-7,SGC-7901 tumor cells was significantly improved:HFI was effective in mediating ADCC against SKOV3,MCF-7 and SGC-7901 tumor cells which expressed high,medium and low levels of erbB2,respectively,and HFI-induced ADCC was correlated with the degrees of erbB2 expression on the tumor cells. Conclusion The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI are significantly upregulated. The expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI are downregulated. HFI can significantly enhance the proliferation activity of human PBMC. The LAK-like eytotoxicity of human PBMC treated with HFI against tumor cells is significantly enhanced. HFI iS effective in mediating ADCC and the activity of HFI-induced ADCC is correlated with the degrees of erbB2 expression on the tumor cells.

Objective To evaluate the role of Toll-like receptor 4 (TLR4)-p38 mitogen-assoliated protein kinase (p38MAPK)-nuclear factor kappa B (NF-κB) signaling pathway in sevoflurane-induced decrease in cognitive function of aged rats.Methods Sixty SPF healthy male Sprague-Dawley rats,aged 20 months,weighing 550-750 g,were divided into 5 groups (n =12 each) using a random number table method:control group (C group),sevoflurane group (S group),TAK242 plus sevoflurane group (TS group),SB202190 plus sevoflurane group (SS group),and PDTC plus sevoflurane group (PS group).All the rats were intubated after anesthesia and connected to an animal ventilator.TAK242,SB202190 and PDTC 10 μl were injected into the lateral cerebral ventricle in TS,SS and PS groups,respectively,and normal saline containing the equal volume of DMSO was given in C and S groups.Starting from 10 min after lateral cerebral ventricle injection,4％ sevoflurane was inhaled for 6 h via the tracheal tube,with the inhaled oxygen concentration 30％ and oxygen flow rate 2 L/min.The mixture of air and oxygen was inhaled in C group.The learning and memory ability was assessed by Morris water maze test at 7 days after the end of sevoflurane anesthesia,and the escape latency and swimming distance were recorded.Animals were sacrificed after the end of Morris water maze test,and brains were removed and hippocampi were isolated for determination of neural apoptosis (by TUNEL),contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in hippocampal tissues (by enzyme-linked immunosorbent assay),and expression of caspase-3,phosphorylated p38MAPK (p-p38MAPK),total p38MAPK (t-p38MAPK) and NF-κB in nucleus (by Western blot).The apoptosis rate and p-p38MAPK/t-p38MAPK ratio were calculated.Results Compared with C group,the escape latency and swimming distance were significantly prolonged at each time point,the apoptosis rate and contents of TNF-oα and IL-1β were increased,the expression of caspase-3,p-p38MAPK and NF-κB was up-regulated,and p-p38MAPK/t-p38MAPK ratio was increased in the other four groups (P＜0.05).Compared with S group,the escape latency and swimming distance were significantly shortened at each time point,the apoptosis rate and contents of TNF-α and IL-1β were decreased,and the expression of caspase-3 was down-regulated in TS,SS and PS groups,the expression of NF-κB was significantly down-regulated in TS and SS groups,and the expression of p-p38MAPK was significantly down-regulated,and p-p38MAPK/t-p38MAPK ratio was decreased in TS group (P＜0.05).Compared with TS group,the escape latency and swimming distance were significantly prolonged at each time point,the apoptosis rate and contents of TNF-α and IL-1β were increased,the expression of caspase-3 and p-p38MAPK was up-regulated,and p-p38MAPK/t-p38MAPK ratio was increased in SS and PS groups,and the expression of NF-κB was significantly up-regulated in PS group (P＜0.05).The expression of NF-κB was significantly up-regulated in PS group when compared with SS group (P＜0.05).Conclusion TLR4-p38MAPKNF-κB signaling pathway is involved in sevoflurane-induced decrease in cognitive function of aged rats.

Objective To evaluate the role of Toll-like receptor 4 (TLR4) signaling pathway in sevoflurane anesthesia-induced cognitive dysfunction in aged rats.Methods Twenty-seven SPF healthy male Sprague-Dawley rats,aged 20 months,weighing 550-750 g,were divided into 3 groups (n =9 each) using a random number table:control group (C group),sevoflurane anesthesia group (S group) and TLR4 antagonist plus sevoflurane anesthesia group (TS group).TLR4 monoclonal antibody 30 μl was injected into the lateral cerebral ventricle in group TS,and the equal volume of serum containing no antibody was injected into the lateral cerebral ventricle in C and S groups.At 10 min after completion of injection,S and TS groups inhaled the mixture of 4％ sevoflurane and 30％ oxygen for 6 h,and group C only inhaled the mixture of air and oxygen.Morris water maze test was performed at 24 h after the end of sevoflurane anesthesia.The animals were sacrificed after completion of Morris water maze test,brains were removed and hippocampi were isolated for determination of nerve cell apoptosis (using TUNEL) and expression of activated caspase-3 (using immunofluorescent staining).Nerve cell apoptosis rate was calculated.The expression of high-mobility group box 1 protein (HMGB1) mRNA in hippocampi was measured by Northern blot assay at 6 h after the end of sevoflurane anesthesia.The expression of amyloid precursor protein (APP) and amyloid beta protein (Aβ) in hippocampi was assessed by Western blot at 24 h after the end of sevoflurane anesthesia.Results Compared with C group,the escape latency was significantly prolonged,nerve cell apoptosis rate was increased,the expression of activated caspase-3,HMGB1 mRNA,APP and Aβ was up-regulated in group S,and nerve cell apoptosis rate was increased,the expression of activated caspase-3,HMGB1 mRNA,APP and Aβ was up-regulated (P＜0.05),and no significant change was found in the escape latency in group TS (P＞0.05).Compared with S group,the escape latency was significantly shortened,nerve cell apoptosis rate was decreased,and the expression of activated caspase-3,HMGB1 mRNA,APP and Aβ was down-regulated in group TS (P＜0.05).Conclusion Activation of TLR4 signaling pathway is involved in the mechanism of sevoflurane anesthesia-induced cognitive dysfunction in aged rats.

Objective To explore the effect of erythropoietin (EPO) attenuating apoptosis in old rat hippocampal neuronal cells exposed to sevoflurane and the role of toll like receptor 4.Methods Twenty months old SD rats,male,550-750 g,in accordance with the random number table,were divided into 3 groups (n =9):control group (group C),sevoflurane treatment (group S),and sevoflurane plus EPO treatment (group ES).The rats in group S and ES were subjected to inhale 4％ sevoflurane for 6 h,but the rats in group C were inhaled air-oxygen only.The rats in group ES were injected with EPO into caudal vein at 24 h,48 h,and 72 h after sevoflurane exposure.The cognitive ability was assessed by Morris water maze test;the effects of hippocampal apoptosis were assessed by TUNEL assays;the expressions of TLR4 mRNA was measured by RT-PCR assay;mitochondrial membrane potential (MMP) was assessed by JC-1 fluorescence;the expressions of APP and Aβ were assessed by western blot.Results Compared with group C,there were significant increases of escape latency period,neuronal apoptosis,TLR4 mRNA,and APP and Aβ expression,but a decrease of MMP in group S (P＜0.05).Compared with group S,there were significant decreases of escape latency period,neuronal apoptosis,TLR4 mRNA,and APP and Aβ expression,but a increase of MMP in group ES (P＜0.05).Conclusion The attenuation of rat hippocampal neuronal apoptosis induced by EPO could be associated with inhibition of TLR4,improvement of MMP,as well as inhibition of APP and Aβ activity.

Objective To explore the changes of cognitive ability in elderly rats induced by sevoflurane exposure,and their relation with Toll like receptor 4 (TLR4)-MyD88 signal pathway.Methods Forty-eight male SD rats,weighting 550-750 g,in accordance with the random number table,were divided into 4 groups (n=12):control group (C group),sevoflurane treatment group (S group),sevoflurane plus TAK242 treatment group (TS group),and sevoflurane plus ST2825 treatment group (SS group).The rats in S,TS and SS groups were subjected to inhale 4％ sevoflurane for 6 h,but the rats in C group were inhaled by air-oxygen only.The rats in TS and SS group were injected with 20 μL TAK242 (1 g/L) or 20 μL ST2825 (1 g/L) via lateral ventricle 10 min before sevoflurane exposure,respectively.The cognitive ability was assessed by Morris water maze test and open field test;the levels of hippocampal tumor necrosis factor (TNF)-α and interleukin (IL)-1β were assessed by ELISA;the Aβ expressions was assessed by Western blotting.Results As compared with those in the C group,significant increase of escape latency,time of the animals spent in the central square,and TNF-α,IL-1β and Aβ expressions,but decrease of number of crossing the grid,and smaller number of standing on the back legs were noted in the S group (P＜0.05).As compared with S group,TS and SS group had significantly decreased escape latency,time of the animals spent in the central square,and TNF-oα,IL-1β and Aβ expressions,but statistically larger number of crossing the grid and number of standing on the back legs (P＜0.05).Conclusion The cognitive dysfunction of elderly rats induced by sevoflurane exposure could be associated with TLR4-MyD88 signal pathway.

Objective To evaluate the role of mitochondrial ATP sensitive potassium ( mito-KATP ) channel in dexmedetomidine-induced inhibition of subarachnoid hemorrhage ( SAH )-caused programmed cell death ( PCD) in cardiomyocytes of rats. Methods On hundred and twenty clean-grade healthy male Sprague-Dawley rats, aged 9-10 weeks, weighing 350-400 g, were divided into 5 groups ( n=24 each) using a random number table method: sham operation group ( group Sham ) , SAH group, SAH plus dexmedetomidine group ( group SD) , 5-HD plus SAH and dexmedetomidine group ( group HSD) and 5-HD plus SAH group ( group HS) . The rats were subjected to SAH by intracranial vascular puncture after being anesthetized with pentobarbital sodium. Dexmedetomidine 5 μg∕kg was infused for 10 min via the jugular vein starting from the time point after intracranial vascular puncture, followed by a continuous infusion of 5μg·kg-1 ·h-1 for 1 h in SD and HSD groups. 5-HD 30 mg∕kg was intraperitoneally injected at 1 h before intracranial vascular puncture in HSD and HS groups. Blood samples were collected from the abdominal aor-ta at 24 h after intracranial vascular puncture for determination of serum cardiac troponin I ( cTnI) concen-trations. The animals were then sacrificed, and myocardial specimens were collected for determination of PCD rate ( by TUNEL) , reactive oxygen species ( ROS) activity ( by DCFH-DA assay) , and expression of cleaved caspase-3, cleaved caspase-1 and interleukin-1beta ( IL-1β) ( by Western blot) . Results Com-pared with group Sham, the serum concentrations of cTnI, PCD rate and ROS activity were significantly in-creased, and the expression of cleaved caspase-3, cleaved caspase-1 and IL-1βwas up-regulated in SAH, SD, HSD and HS groups ( P<0. 05) . Compared with group SAH, the serum concentrations of cTnI, PCD rate and ROS activity were significantly decreased, and the expression of cleaved caspase-3, cleaved caspase-1 and IL-1βwas down-regulated in group SD, and the serum concentrations of cTnI, PCD rate and ROS activity were significantly increased, and the expression of cleaved caspase-3, cleaved caspase-1 and IL-1βwas up-regulated in group HS ( P<0. 05) . Compared with group SD, the serum concentrations of cT-nI, PCD rate and ROS activity were significantly increased, and the expression of cleaved caspase-3, cleaved caspase-1 and IL-1β was up-regulated in group HSD ( P<0. 05) . Compared with group HSD, the serum concentrations of cTnI, PCD rate and ROS activity were significantly increased, and the expression of cleaved caspase-3, cleaved caspase-1 and IL-1βwas up-regulated in group HS ( P<0. 05) . Conclusion mito-KATP channel is involved in dexmedetomidine-induced inhibition of PCD in cardiomyocytes of rats with SAH.

Objective:To explore the application effect of WeChat-based IIFAR combined with progressive exercise prescription in patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI) .Methods:Using the convenient sampling method, a total of 90 ACS patients from the First Affiliated Hospital of Air Force Military Medical University were selected as the research objects from June 2017 to June 2019. The patients were divided into the observation group and the control group, with 45 cases in each group by random number method. Patients in the control group adopted conventional nursing methods, while patients in the intervention group used WeChat-based IIFAR combined with progressive exercise prescription intervention. Coronary Self-Management Behavior Scale (CSMS) , 6 min walking test and exercise load test were used to compare the effects of the intervention.Results:A total of 3 cases in the control group and 1 case in the observation group dropped out. None of the patients had any adverse cardiac events during the study period. The scores of daily life management, social emotional management and medical disease management behaviors of the observation group were higher than those of the control group at 3 months after operation, and the differences were statistically significant ( P<0.05) . Three months after the operation, the 6-min walking distance and maximum exercise load of the observation group were higher than those of the control group, and the differences were statistically significant ( P<0.05) . Conclusions:WeChat-based IIFAR combined with progressive exercise prescription can improve the exercise load and self-management behavior of ACS patients after PCI.