Objective To investigate the effect of microglia activation regulated by C-X3-C motif chemokine ligand 1(CX3CL1)-C-X3-C motif chemokine receptor 1(CX3CR1)pathway on memory function in hemorrhagic shock/resuscitation rats.Methods The experiment was divided into two parts.In the first part,the rats were randomly divided into sham group,model-0.5 hour group,model-1.5 hour group,model-3 hour group,10 rats in each group.There were differences in the time of hemorrhagic shock among each group.In the second part,rats were randomly divided into control group and CX3CL1 group,10 rats in each group.The rats in CX3CL1 group were treated with CX3CL1 protein factor(intraventricular injection),and the rats in control group were treated with saline.All rats were trained in Morris water maze experiments before model construction,and tests of Morris water maze experiments were carried out after 4 days of model construction.After completion,the whole brains were taken for HE staining and immunohistochemical staining.Cerebrospinal fluid was taken for detection of inflammatory cytokines,and hippocampus tissues were taken for Real-time PCR detection and Western blotting detection.Results Compared with the sham group,the escape latency of rats in model group increased,the number of platform crossings and the resident time in the third quadrant decreased.The neuronal state was impaired in HE staining in model group.In addition,compared with the sham group,the expression of ionized calcium binding adaptor molecule-1(Iba1)in the brain of the rats in model group increased,the contents of tumor necrosis factor-α(TNF-α)and interleukin(IL)-6 in the cerebrospinal fluid increased,and the M1-type microglia markers CD16,TNF-α,IL-1β and inducible nitric oxide synthase(iNOS)mRNA content increased.At the same time,compared with the sham group,the expressions of CX3CL1 and CX3CR1 in the brain of model group decreased,and the expressions of phosphorylated nuclear factor-κB(p-NF-κB)and nucleotide binding oligomerization domain(NOD)-like receptor protein 3(NLRP3)increased.However,compared with the control group,rats in CX3CL1 group had reduced escape latency,increased platform crossing times and quadrantⅢresident time,and recovered neuronal states.In addition,the expression of Iba1 in the brain of CX3CL1 group decreased,the contents of TNF-α and IL-6 in the cerebrospinal fluid decreased,the mRNA contents of M1-type microglia markers like CD16,TNF-α,IL-1β and iNOS decreased,and the mRNA contents of markers of M2-type microglia glial like CD206,transforming growth factor-β(TGF-β),arginase-1(Arg1),Chitinase 3-like protein 1(Ym 1)increased.Conclusion CX3CL1 can help inhibit the excessive activation of microglia,induce the polarization of microglia to M2 type,inhibit the polarization of M1 type,reduce the release of inflammatory cytokines,and alleviate the memory function damage induced by hemorrhagic shock/resuscitation.

【Objective】 To investigate the clinical application of self-developed magnetic anchoring device for assisting thoracoscopic pulmonary resection. 【Methods】 Eleven patients underwent thoracoscopic pulmonary assisted with resection magnetic anchoring technique at the Department of Thoracic Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, from March to May 2019. Their clinical data were retrospectively analyzed. The operation time, blood loss, blood transfusion volume, postoperative hospital stay, and postoperative complications were recorded. 【Results】 There were seven male and four female patients, with the average age of (51.6±13.9) years (range from 22 to 69 years). Three single-port and eight single-utility-port thoracoscopic surgeries were performed. Magnetic instruments provided good surgical field exposure in all operations. Among 11 surgeries, one was converted to thoracotomy and one to three-hole surgery due to enlargement and adhesion of hilar lymph nodes. The operation time was (107.8±63.1) minutes (range of 27-182 minutes). The blood loss was 50 (10-50)mL (range of 5-1 000 mL). No blood transfusion was needed during the operation. The postoperative hospital stay was (5.0±1.8) days (range of 3-9 days). No postoperative complications occurred in all the patients. 【Conclusion】 Magnetic anchor technique can effectively alleviate the "chopstick effect" in thoracoscopic surgery. Magnetic anchor technique is safe and feasible in assisting thoracoscopic pulmonary resection.

The Continuing Education Department of Chinese Medical Association has undertaken and participated in a number of tasks for the training of primary health care personnel in recent years. It has been recognized that the main measures to promote the development of primary continuing medical education including four aspects: national policies provide the direction of the development; medical progress is the output of the primary continuing medical education; the combination of multiple measures is a good way to carry out the primary continuing medical education; and technical means are the support of the development. Through understanding and grasping such factors as the national policies, medical development, education level, and technical conditions, and actively thinking about the relevant countermeasures, we can steadily and rapidly continue to promote the healthy development of continuing medical education at the grassroots level.

OBJECTIVE: To identify the main active components in Ⅲ and their targets and explore the mechanism by which Ⅲ alleviates proteinuria in chronic kidney disease (CKD) based on network pharmacology. METHODS: The active components of Ⅲ and their potential targets, along with the oral bioavailability and drug-like properties of each component were searched in the TCMSP database. The proteinuria-related targets were searched in the GeneCards database. The active component-target network was constructed using Cytoscape software, and the acquired information of the targets from ClueGO was used for enrichment analysis of the gene pathways. RESULTS: A total of 102 active components were identified from Ⅲ. These active components acted on 126 targets, among which 69 were related to proteinuria. Enrichment analysis revealed fluid shear stress- and atherosclerosisrelated pathways as the highly significant pathways in proteinuria associated with CKD. CONCLUSIONS We preliminarily validated the prescription of Ⅲ and obtained scientific evidence that supported its use for treatment of proteinuria in CKD. The findings in this study provide a theoretical basis for further study of the mechanism of Ⅲ in the treatment of proteinuria in CKD.
Biological Availability ; Drugs, Chinese Herbal ; chemistry ; pharmacokinetics ; therapeutic use ; Humans ; Proteinuria ; drug therapy ; etiology ; metabolism ; Renal Insufficiency, Chronic ; complications ; metabolism

AIM:To explore the effects of mammalian target of rapamycin (mTOR) double inhibitor AZD8055 on autophagy and apoptosis of human cholangiocarcinoma cell line HuCCT1. METHODS:The effect of AZD8055 on the viability of HuCCT1 cells was detected by MTT assay. Autophagosome was detected by acridine orange (AO) staining. Af-ter treated with AZD8055, the expression levels of apoptosis-related proteins Bcl-2, Bax and cleaved caspase-3 and auto-phagy marker proteins beclin 1, LC3 and p62 were determined by Western blot. Apoptotic rate was analyzed by flow cyto-metry with Annexin V-FITC/PI double staining. RESULTS:AZD8055 significantly inhibited the viability of HuCCT1 cells (P<0.05). AO staining showed that AZD8055 significantly increased orange granules in the cytoplasm. After treated with AZD8055, compared with the control group, the protein level of beclin 1 and the ratio of LC3-Ⅱ/LC3-Ⅰ were enhanced, while p62 was attenuated (P<0.05). The protein expression level of pro-apoptotic regulator Bax was down-regulated and anti-apoptotic regulator Bcl-2 was increased. The protein level of cleaved caspase-3 was reduced (P<0.05). The results of flow cytometry showed that AZD8055 inhibited cell apoptosis. CONCLUSION:AZD8055 inhibits the viability of cholangiocarcinoma cells, and the mechanism is closely related with autophagy induced by AZD8055.

Parasitic diseases are common infectious diseases closely related to poverty,which are mainly endemic in the trop-ical and subtropical regions.Africa is the major epidemic area of parasitic diseases,and the global burden of malaria and schisto-somiasis is over 85% in Africa.This paper reviews the disease burden,regional distribution and control strategies of the main parasitic diseases in Africa,in order to promote the prevention and control of parasitic diseases in this area.

ObjectiveTo study the correlation of high-risk human papillomavirus 16 and 18 (HPV16/18) infections with the risk of prostate cancer (PCa) and their association with the clinicopathologic indexes of PCa.

METHODSWe collected tissue samples from 75 cases of PCa and 73 cases of benign prostatic hyperplasia (BPH). We detected HPV16/18 infections in the samples by immunohistochemistry and PCR combined with reverse dot blot (RDB) assay.

RESULTSImmunohistochemistry revealed 16 cases of HPV16/18 positive in the PCa (21.3%) and 7 cases in the BPH samples (9.5%), with statistically significant difference between the two groups (P=0.049). PCR combined with RDB assay showed 17 cases of HPV16 infection (22.6%) and 13 cases of HPV18 infection (17.8%), including 4 cases of HPV16/18 positive, in the PCa group, remarkably higher than 6 cases of HPV16 infection (8.2%), 3 cases of HPV18 infection (4.1%) and no HPV16/18 positive in the BPH controls (P=0.001). No significant differences were observed between the result of immunohistochemistry and that of PCR combined with RDB assay (P=0.069). The risk of HPV16/18 infections was found to be correlated with the clinical T-stage and Gleason score of PCa (P<0.05 ) but not with the patient's age, PSA level or lymph node metastasis (P>0.05 ).

CONCLUSIONSHigh-risk HPV16/18 infections are correlated with the risk of prostate cancer.

Human papillomavirus 16 ; Human papillomavirus 18 ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Male ; Neoplasm Grading ; Papillomavirus Infections ; epidemiology ; Polymerase Chain Reaction ; Prostatic Hyperplasia ; epidemiology ; virology ; Prostatic Neoplasms ; epidemiology ; virology

OBJECTIVETo study the effects of peroxisome proliferator-activated receptor gamma agonists on angiotensin II-induced cellular response in cultured fibroblasts derived from patients with hypertrophic scars, so as to investigate its effects on preventing the formation of hypertrophic scars.

METHODSFibroblasts were freshly isolated from hypertrophic scars and cultured with angiotensin II, rosiglitazone and GW9662 at a certain concentration. Fibroblasts proliferation were assessed via Cell Counting Kit-8; the mRNA and protein expressions of Collagen I and Fibronectin (FN) were determined by quantitative real-time RT-PCR and Western blotting.

RESULTSThe absorbance of CCK-8 and relative expression of Collagen I, FN mRNA and protein were 1.082 5 +/- 0.007, 6.45 +/- 0.97, 4.92 +/- 0.86, 2.92 +/- 0.41, 2.78 +/- 1.04 in Ang II group; 0.722 4 +/- 0.012, 1.82 +/- 0.34, 1.78 +/- 0.27, 1.57 +/- 0.46, 1.68 +/- 0.39 in Ros + Ang II group; 0.554 7 +/- 0.012, 0.97 +/- 0.12, 1.07 +/- 1.08, 1.05 +/- 0.43, 1.14 +/- 0.36 in Ros group; 1.056 0 +/- 0.005, 5.83 +/- 0.24, 4.47 +/- 0.32, 2.69 +/- 0.35, 2.62 +/- 0.27 in GW9662 + ros + Ang II group. The results showed a significant difference between the Ang II group and the control group (P < 0.05). The effect of Ang II could be markedly inhibited by Ros (P < 0.05). In addition, Ros did not influence cell proliferation and production of extracellular matrix (P > 0.05). There was a significant difference between the GW9662 + Ros + Ang II group and the Ros + Ang II (P < 0.05).

CONCLUSIONSPPAR-gamma agonists inhibit Ang II-induced proliferation and extracellular matrix synthesis effectively in the hypertrophic scar fibroblasts. Thus PPAR-gamma agonists may have potential therapeutic effect for hypertrophic scar.

Angiotensin II ; pharmacology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cicatrix, Hypertrophic ; metabolism ; Collagen Type I ; biosynthesis ; Extracellular Matrix ; drug effects ; Fibroblasts ; drug effects ; metabolism ; pathology ; Fibronectins ; biosynthesis ; Humans ; PPAR gamma ; agonists

OBJECTIVETo investigate the bacterial distribution and drug resistance in patients with surgical infections, and provide the basis for the standardization treatment of the surgical infection.

METHODSRetrospectively analyzed from January 2008 to December 2011 surgical infection in our samples bacteria identification and drug sensitivity test results.

RESULTSA total of 3829 nonduplicate isolates from 3257 samples, Gram-negative bacteria accounted for 62.4% (the main microbes were P.aeruginosa, K. pneumonia and E.coli etc) and Gram-positive bacteria accounted for 37.6% (the main microbes were Enterococcus, Staphylococcus and coagulase negative Staphylococcus). Incidence of Staphylococcus aureus and Enterococcus faecalis were on an obvious increase. For the performance of the high level of sensitive to Imipenem, Amikacin, Piperacillin and Tazobactam by E. coli and K. pneumonia. The Pseudomonas aeruginosa and Acinetobacter baumannii to cephalosporins, Carbapenems and Fluoroqinolones were higher resistant with Multidrug resistance. No vancomycin and teicoplanin resistant Enterococcus faecium were found. The prevalence of ESBL E.coli was 45.6%-61.5% and ESBL K.pneumoniae isolates were fluctuated. The methicillin-resistant S.aureus (MRSA) isolates were relatively high (21.1%-55.8%), and methicillin-resistant Staphylococcus epidermidis was higher than the other Gram-positive cocci. Vancomycin for Staphylococcus performance was highly sensitive.

CONCLUSIONSThe main composition of surgical clinical infection pathogens are Gram-negative bacillus, and the emergency of resistance of bacteria to antibacterial drugs is a common phenomenon. The resistant rate shows ascendant trend; Drug resistance is significantly higher in Pseudomonas aeruginosa and Acinetobacter baumannii. Antimicrobial resistance is a serious and challenging issue.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anti-Bacterial Agents ; pharmacology ; Bacteria ; drug effects ; Child ; Child, Preschool ; Drug Resistance, Bacterial ; Female ; Humans ; Infant ; Male ; Microbial Sensitivity Tests ; Middle Aged ; Retrospective Studies ; Surgical Wound Infection ; microbiology ; Young Adult

OBJECTIVETo study the possible clonal origin of neuroendocrine cells in colorectal adenocarcinoma.

METHODSTwenty-six microsatellite loci were screened using laser capture microdissection, DNA extraction and whole genome amplification. Microsatellite instability (MSI) and loss of heterozygosity (LOH) in adenocarcinoma cells and neuroendocrine cells amongst 30 cases of colorectal carcinoma with neuroendocrine differentiation were detected using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP)-silver staining. The mutation status of p53 was evaluated by PCR-sequencing. The clonal origin of neuroendocrine cells in colorectal adenocarcinoma was determined.

RESULTSAmongst the 30 cases studied, the prevalence of MSI was 16.9% while that of LOH was 8.5%. The rate showed no statistically significant difference between adenocarcinoma cells and neuroendocrine cells. In 6 cases, the microsatellite alteration was entirely consistent. In 23 cases, the rate of microsatellite alteration consistency was greater than that of inconsistency. In 1 case, the consistency and inconsistency rates were identical. There was statistically significant difference between consistency and inconsistency of microsatellite alteration. The prevalence of p53 mutation was 16.7% which was the same for both adenocarcinoma cells and neuroendocrine cells.

CONCLUSIONSAdenocarcinoma cells and neuroendocrine cells in colorectal adenocarcinoma with neuroendocrine differentiation have similar biologic changes. It is likely that they are of identical origin.

Adenocarcinoma ; genetics ; pathology ; Colorectal Neoplasms ; genetics ; pathology ; DNA Mutational Analysis ; Humans ; Laser Capture Microdissection ; Loss of Heterozygosity ; Microsatellite Instability ; Neuroendocrine Cells ; pathology ; Tumor Suppressor Protein p53 ; genetics