Objective To investigate the effects of the interaction between human hepatoma cells and hepatic stellate cells on their growth state,and study its role of interaction on the progression of hepatocellular carcinoma.Methods Human hepatoma cell line HepG2 and hepatic stellate cell line hepatic stallate cells (HSC)-T6 were used and the methods including methyl thiazolyl tetrazolium (MTT) assay,flow cytometry (FCM) analysis,immunohistochemistry,and electron microscopy were employed in this experiment.The effects of conditioned medium (CM) of HepG2 on the activation and proliferation of HSC were explored.The effects of activated HSC CM on HepG2 proliferation were investigated.The uhrastructural changes of the two co-cultured cells were observed.Results MTT assay result showed that HepG2/HSC CM could promote HSC/HepG2 proliferation.FCM result demonstrated that HepG2/HSC CM could influence the cell cycle distribution in HSC/HepG2.Immunohistochemistry exhibited that after the treatment of HepG2/HSC CM,the expression ofα-smooth muscle actin (α-SMA) in HSC and proliferating cell nuclear antigen (PCNA) in HepG2 were increased.When HepG2 and HSC were co-cultured,the ultrastructure of HSC displayed an activated feature.Conclusions HepG2 cells can induce the activation and proliferation of HSC,and the activated HSC can also stimulate the proliferation of HepG2.Interaction between hepatoma cells and hepatic stellate cells may play an important role in the progression of hepatocellular carcinoma.

The effects of A-L tonic capsule on DNA content in rat experimental hepatocarcinogenesis induced by diethylnitrosamine (DENA) were observed. The experimental rats were divided into 4 groups. With exception of group D in which the rats were only administered with DENA, the rats in the groups A, B, C were previously, simultaneously and subsequently fed with A-L tonic capsule respectively while they were administered with DENA. The DNA content of all rat livers was measured using automatic image analysis technique 20 weeks after administration of DENA. The results showed that the highest and lowest DNA contents were respectively seen in the groups D and A. There was significant difference in DNA contents between the groups A or B or C and D, and also between the groups A and B or C (both P < 0.01). 4 components (4C) and > or = 5C cells were predominant in the group D, while 2C cells were the minority. The number of 2C cells in the groups A, B, C was significantly higher than that in the group D, and the number of > or = 5C cells in the groups A, B, C was markedly lower than that in the group D (P < 0.01). Also, there was very significant difference in the number of 2C and > or = 5C cells between group A and B or C (P < 0.01). It was concluded that A-L tonic capsule could effectively inhibit the increase of DNA content of hepatocytes and improve the distribution of DNA content in rat hepatocarcinogenesis, especially in group A.
Animals ; Astragalus membranaceus ; chemistry ; Capsules ; Carcinogenicity Tests ; DNA, Neoplasm ; analysis ; Diethylnitrosamine ; Drugs, Chinese Herbal ; pharmacology ; Hepatocytes ; chemistry ; Ligustrum ; chemistry ; Liver Neoplasms, Experimental ; chemically induced ; chemistry ; genetics ; Male ; Rats ; Rats, Sprague-Dawley

Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.

Objective To investigate the function and molecular mechanism of tacrolimus in podocyte injury and restoration.Methods Cultured podocytes were stimulated by Angiotensin Ⅱ (Ang Ⅱ) or Ang Ⅱ plus tacrolimus.Cells were collected at different time points (0 h,12 h and 24 h).The distribution of F-actin was observed after immunofluorescence staining,and the protein expression of nephrin and podocin were detected by Western Blot (WB).Results In normal control podocytes,F-actin was arranged in cytoplasm powerfully.Ang Ⅱ induced the disruption and discontinuity of F-actin.Tacrolimus inhibited the effect of Ang Ⅱ,stabilized the regular arrangement the F-actin.Compared to normal cells,the protein expression of nephrin in Ang Ⅱ group significantly decreased at 24 h after stimulation (0.76 ± 0.32 in AngⅡ group vs.1.18 ± 0.40 in normal group,P ＜ 0.05).And tacrolimus stabilized the expression of nephrin protein (1.00 ± 0.19 in treatment group vs.0.76 ± 0.32 in Ang Ⅱ group,P ＜ 0.05).Ang Ⅱ and tacrolimus did not affect the expression of podocin protein.Conclusion Tacrolimus inhibits podocyte injury induced by Ang Ⅱ,stabilizes the regular arrangement of cytoskeleton and protein expression of nephrin.

Objective To explore the prognostic value of hs-cTnⅠ in patients with suspected acute coronary syndrome(ACS)in emergency department.Methods A large-scale,prospective observa-tional study was conducted on totally 966 patients with suspected ACS admitted in Fuwai Hospi-tal from January 2017 to October 2020.Their baseline serum/plasma hs-cTnⅠ level was detected at admission,conventional treatment was performed,and relevant data were collected.Logistic regression analysis was used to predict the risk of primary and secondary endpoint events within 30 d by hs-TnⅠ concentration,and subgroup analysis was performed.Results Among the 966 patients,the time from chest pain to visit was 5.0(2.5,13.0)h,and 284 patients had primary end-point events within 30 d,including 283 cases of myocardial infarction(99.6％)at the first visit,1 case of recurrent myocardial infarction(0.4％),5 cases of cardiovascular death(1.8％),and 1 case of unplanned revascularization(0.4％).When hs-cTnⅠ was at the minimum detection limit of 2 ng/L,the incidence of adverse events was 5.8％,when the limit of 70 ng/L,the incidence was 49.2％,and when of 316 ng/L,the incidence reached 100％.The model could correctly classify 92.3％of the patients.Conclusion The hs-cTn sequence has a good predictive effect for the risk of short-term cardiovascular adverse events in Chinese population.

The community-friendly program " Online mobile payment of medical insurance" , launched by Guangzhou Municipal Medical Insurance Bureau, poses new challenges to hospital medical insurance management and information intelligence. To this end, the Second Affiliated Hospital of Guangzhou Medical University staged from January 2017 to March 2019 kept upgrading its IT system and built an intelligent monitoring system for medical insurance. These efforts prepared adequately for the medical insurance mobile payment, and explored a mode of medical insurance management, evolving from extensive management to standard and fine management.

Objective To explore the strategies of drug treatment and pharmaceutical care for children with bacterial meningitis. Methods The anti-infective therapy, therapeutic drug monitoring and dose adjustment of vancomycin in children with bacterial meningitis were analyzed and discussed according to relevant guidelines and literatures. Results Clinical pharmacists analyzed therapeutic regimen. According to the results of etiology and drug sensitivity, meropenem was discontinued and rifampicin was added. Based on drug monitoring of vancomycin, it is suggested to extend the infusion time of vancomycin to reach the target concentration. The child was discharged from hospital. Conclusion Recommendations of the relevant drug treatment guidelines and the latest medical research evidence should be provided by clinical pharmacists in order to promote reasonable and effective clinical uses of medicine.

Anti-seizure medications (ASMs) are the main therapy for epilepsy.There are many kinds of ASMs with complex mechanism of action, so it is difficult for pharmacists to examine prescriptions.This paper put forward some suggestions on the indications, dosage forms/routes of administration, appropriateness of usage and dosage, combined medication and drug interaction, long-term prescription review, individual differences in pathophysiology of children, and drug selection when complicated with common epilepsy, for the reference of doctors and pharmacists.

BACKGROUND: Cell competition is an important feature in pancreatic cancer (PC) progression, but the underlying mechanism remains elusive. This study aims to explore the role of exosomes derived from normal pancreatic ductal epithelial cells involved in PC progression. METHODS: PC cells and pancreatic stellate cells (PSCs) were treated with exosomes isolated from pancreatic ductal epithelial cells. Cell proliferation was assessed by CCK8 assays. Cell migration and invasion were assessed by Transwell assays. PC and matched adjacent non-tumor tissue specimens were obtained from 46 patients pathologically diagnosed with PC at Peking University First Hospital from 2013 to 2017. Tissue miR-485-3p and p21-activated kinase-1 (PAK1) expression was examined by real-time polymerase chain reaction (RT-PCR), and the relationship of the two was analyzed using Pearman's product-moment correlation. The clinical significance of miR-485-3p was analyzed using the Chi-square test, Wilcoxon rank-sum test, and Fisher exact probability, respectively. The binding of miR-485-3p to PAK1 5'-untranslated region (5'-UTR) was examined by luciferase assay. PC cells were xenografted into nude mice as a PC metastasis model. RESULTS: Exosomes from pancreatic ductal epithelial cells suppressed PC cell migration and invasion as well as the secretion and migration of PSCs. MiR-485-3p was enriched in the exosomes of pancreatic ductal epithelial cells but deficient in those of PC cells and PSCs, in accordance with the lower level in PSCs and PC cells than that in pancreatic ductal cells. And the mature miR-485-3p could be delivered into these cells by the exosomes secreted by normal pancreatic duct cells, to inhibit PC cell migration and invasion. Clinical data analysis showed that miR-485-3p was significantly decreased in PC tissues (P < 0.05) and was negatively associated with lymphovascular invasion (P = 0.044). As a direct target of miR-485-3p, PAK1 was found to exert an inhibitory effect on PC cells, and there was a significantly negative correlation between the expression levels of miR-485-3p and PAK1 (r = -0.6525, P < 0.0001) in PC tissues. Moreover, miR-485-3p could suppress PC metastasis in vivo by targeting p21-activated kinase-1. CONCLUSIONS Exosomal miR-485-3p delivered by normal pancreatic ductal epithelial cells into PC cells inhibits PC metastasis by directly targeting PAK1. The restoration of miR-485-3p by exosomes or some other vehicle might be a novel approach for PC treatment.
Animals ; Mice ; MicroRNAs/metabolism* ; Mice, Nude ; p21-Activated Kinases/metabolism* ; Cell Line, Tumor ; Pancreatic Neoplasms/genetics* ; Epithelial Cells/metabolism* ; Pancreatic Ducts/pathology* ; Cell Proliferation ; Cell Movement ; Gene Expression Regulation, Neoplastic