Objective To study the safety and feasibility of tubeless percutaneous nephrostolithotomy by hemostasis gel closure of mini-percutaneous renal-channel.Methods Eighty patients after conventional percutaneous nephrostolithotomy are selected and divided into two groups according to the principle of randomization.Control group adopts conventional percutaneous nephrostolithotomy calculi lithotripsy with renal pelvis drainage tube placement whereas the experimental group adopts tubeless percutaneous nephrostolithotomy by hemostasis gel closure of mini-percutaneous renal channel.Both experimental group and control group will be scientifically and statistically analyzed via the incidence and the dose of using sedative for alleviating pain after operation,hospital stay,level of hemoglobin,and the occurrence of complications such as continuate hemorrhage,infection,urinary extravasation,etc.Results The operation of both groups are successful in phrase Ⅰ.The incidence and the dose of using sedative in control group are obviously higher than that in experimental group(45％ vs 20％).However,the incidence of postoperative complications like infection and hemorrhage and hospital stay between two groups are undifferentiated in statistics(P ＞ 0.05).Neither the experimental group nor the control group has perinephric hematoma,and seven cases of control group have urinary leakage after remove of fistula.Conclusion Tubeless percutaneous nephrostolithotomy by hemostasis gel closure of mini-percutaneous renal-channel is safe and feasible and it can reduce the incidence of postoperative pain and avoid urinary leakage.

Objective To study the growth suppressive effect of demethylation drug 5-aza-2'-deoxycytidine on bladder tumor cells. Methods The growth suppressive effect of DAC on 4 transitional cell carcinoma (TCC) cell lines was measured using the Cell Proliferation Reagent WST-1 assay.The effects of DAC on apoptosis induction and cell cycle arrest were analyzed by flow cytometric analysis. Caspase 3, 9 activities were analyzed by APOPCYTO Caspase Colorimetric Assay Kit and PCNA expression was also investigated by Western blot to clarify the mechanism of DAC against TCC. Results DAC inhibited the growth of all TCC cell lines tested in a dose-dependant manner, however,growth suppressive effect of DAC was independent of p53 status in TCC. DAC inhibited proliferation via inducing G2/M cell cycle arrest but not via inducing apoptosis. After treated with 0, 1 and 8 μmol/L DAC, cells of RTl 12 in G2/M phase was (36.3 ± 3.4) %, (46.2 ± 4.6) % and (56.5 ±6.2) %, TCCsup was (37.5 ± 3.8) %, (48.4 ±4.9) % and (60.1 ± 6.7) %, respectively. The expression of PCNA was decreased by DAC, but caspase3, 9 activities were not activated. Conclusion DAC could suppress the growth of TCC cells and might be a new strategy to treat bladder malignancy in the future.

Objective To investigate the safety of gemcitabine combined with cisplatin (GC) / carboplatin (GCa) regimen in adjuvant chemotherapy for upper urinary tract urothelial carcinoma.Methods The clinical and follow-up data of 80 patientswho underwent GC or GCa chemotherapy withinfourcycles of upper tract urothelial carcinoma (UTUC) admitted to Beijing Friendship Hospital,Capital Medical University from June 2012 to January 2018 were analyzed retrospectively,including 39 males and 41 females,aged 36 to 81 years,with a median age of 64.0 years.According to the chemotherapy regimen,all patients were divided into GC group (n =54) and GCa group (n =26).The software of SPSS 22.0 was used to calculate the incidence of adverse reactions of chemotherapy.The independent risk factors for serious adverse reactions were analyzed.The incidence of serious adverse reactions and the safety of renal function in patients with renal insufficiency during chemotherapy were explored.Results For adverse reactions to chemotherapy,GC group had 20 patients (37.0％) with severe myelosuppression,9 patients (16.4％) with non-hematological toxicity,3 patients (5.6％) with delayed chemotherapy due to serious chemotherapy adverse reactions,and 12 patients (22.2％) withdrawn chemotherapy early due to inability to tolerate chemotherapy toxicity.In GCa group,12 patients (46.2％) had severe myelosuppression,5 patients(19.2％) had severe non-hematologic toxicity,6 patients(23.1％) had delayed chemotherapy due to serious chemotherapy adverse reactions,and 6 patients (23.1％) had withdrawn chemotherapy early due to inability to tolerate chemotherapy toxicity.Pre-chemotherapye GFR ＜ 60 ml ·(min · 1.73 m2)-1 (OR =5.074,95％ CI:1.222-21.068) was an independent risk factor for severe myelosuppression in GC group (P ＜ 0.05).There was no significant difference in severe adverse reactions between the two groups (P ＜ 0.05).For the renal function decline between the two groups,Cr and eGFR decreased to a certain extent in the two groups during chemotherapy (P ＜ 0.05),but there was no significant difference in the extent and degree during chemotherapy (P ＜ 0.05).Conclusions Both GC and GCa adjuvant chemotherapy have certain toxicity and side effects.The process of chemotherapy needs to be closely monitored and timely symptomatic treatment if needed.Most patients can eventually endure chemotherapy.For patients with renal insufficiency,under the precondition of strict monitoring and adequate hydration,GC and GCa regimens adjuvant chemotherapy within four cycles may be the same safe level ofchemotherapy.

Objective To investigate the effect of cinobufacini on inhibiting colorectal cancer metastasis by regula-ting the polarization of M2 macrophages.Methods THP-1 was induced into M0 type macrophages.The condi-tioned medium of HCT116 cells was collected to stimulate M0 type macrophages.The polarization of M2 type mac-rophages was observed by flow cytometry,real-time quantitative PCR and ELISA experiments.The conditioned me-dium of M0 type macrophages and HCT116-Mφ cells was collected to stimulate HCT116 cells.The ability of migra-tion and invasion was observed by wound healing assay and Transwell assay.The effect of cinobufacini on the via-bility of HCT116 cells was detected by CCK-8 assay.The conditioned medium of HCT116 and HCT116+cinobufa-cini was collected to stimulate M0 type macrophages.The polarization of M2 type macrophages was observed by flow cytometry,real-time quantitative PCR and ELISA experiments.The conditioned media of HCT116-Mφ cells and(HCT116+cinobufacini)-Mφ cells were collected to stimulate HCT116 cells.The changes of migration and inva-sion ability were observed by wound healing assay and Transwell assay.Results After stimulation of M0 type mac-rophages in HCT116 cell conditioned medium,the morphology of M0 macrophages turned into fusiform cells,the proportion of CD11b+CD206+cells increased,and the expression of M2 macrophage markers IL-10 and TGF-β in-creased.The migration and invasion ability of HCT116 cells were significantly enhanced after stimulation in the conditioned medium of HCT1 16-Mφ cells.After the addition of cinobufacini,not only the polarization proportion of M2 macrophages decreased,but also the metastatic effect mediated by M2 macrophages was inhibited.Conclusion HCT116 cells can induce the polarization of M2 macrophages,while cinobufacini can inhibit the tumor metastasis mediated by M2 macrophages by inhibiting the polarization of M2 macrophages.

Objective To investigate the role of bufalin(BU)in inhibiting M2-type macrophage-mediated colorec-tal cancer metastasis.Methods Human acute leukemia mononuclear cells(THP-1)were differentiated into M0 macrophages using phorbol ester induction(PMA)for 48 hours.The M0 macrophages were then treated with IL-4 and IL-13 medium.Surface markers and morphological changes were observed through ELISA,morphology,and RT-qPCR experiments.RT-PCR and ELISA experiments were conducted to detect the surface markers TGF-β and IL-10 of M2 macrophages.The secretion level of IL-6 in the supernatant of M2 macrophages and colorectal cancer cells HCT116 was compared using ELISA.Additionally,the effect of conditioned medium on colorectal cancer cell HCT116 was assessed through Transwell,Wound healing,RT-qPCR,and Western blot experiments.Subsequent-ly,bufalin was added to the conditioned medium and the changes in AKT/PI3K protein,migration,and epithelial-mesenchymal transition ability in HCT116 were observed using Western blot,Transwell,Wound healing and RT-qPCR experiments.Results THP-1 were successfully differentiated into M2 macrophages.The activation of AKT/PI3K protein in HCT116 cells was induced by the secretion of IL-6 from M2 macrophages,which in turn promoted the migration and epithelial-mesenchymal transition ability of the HCT116 cells.The migration and epithelial-mes-enchymal transition mediated by M2 macrophages in HCT116 cells were effectively inhibited by Bufalin.Conclu-sion The release of IL-6 from M2 macrophages activates the AKT/PI3K signaling pathway in colorectal cancer cells,thereby promoting their migration and epithelial-mesenchymal transition capacity.Moreover,bufalin exhibits inhibitory effects on this effect.

Objective : To study the effect of bufalin on the proliferation and apoptosis of human colorectal cancer cell line HCT116，and to explore the role of endoplasmic reticulum stress ( ERS) in this process． Methods : The effect of bufalin on the proliferation of HCT116 cells was determined by CCK-8 assay．After HCT116 cells were treated with different concentrations of bufalin for 48 hours，cell apoptosis was detected by Annexin V / PI assay， and the expression of apoptosis-related proteins Bax and Bcl-2 was detected by Western blot．At the same time，the expression of ERS-related proteins glucose regulated protein 78 ( GRP78) ，phosphorylated protein kinase R like endoplasmic reticulum kinase ( p-PERK) ，eukaryotic translation initiation factor 2 α ( eIF2 α) ，phosphorylated eukaryotic translation initiation factor 2 α (p-eIF2 α) and C / EBP homologous protein ( CHOP) was detected by Western blot．HCT116 cells were divided into control group，bufalin group and combination group (bufalin + 4-phenylbutyric acid) ，and the expression of apoptosis-related proteins Bax and Bcl-2 was observed by Western blot. Results: CCK-8 assay showed that bufalin could inhibit the proliferation of HCT116 cells．Apoptosis assay showed that bufalin could induce apoptosis of HCT116 cells．The results of Western blot showed that bufalin could up-regulate the expression of pro-apoptotic protein Bax and down-regulate the expression of anti-apoptotic protein Bcl-2．It could also induce ERS and activate PERK / eIF2 α/ CHOP pathway．When bufalin combined with 4-phenylbutyric acid，the apoptosis-promoting effect of bufalin was inhibited． Conclusion Bufalin can effectively inhibit the prolif- erative activity and induce apoptosis of HCT116，which is achieved to some extent by activating ERS.

Few studies have described the key features and prognostic roles of lung microbiota in patients with severe community-acquired pneumonia (SCAP). We prospectively enrolled consecutive SCAP patients admitted to ICU. Bronchoscopy was performed at bedside within 48 h of ICU admission, and 16S rRNA gene sequencing was applied to the collected bronchoalveolar lavage fluid. The primary outcome was clinical improvements defined as a decrease of 2 categories and above on a 7-category ordinal scale within 14 days following bronchoscopy. Sixty-seven patients were included. Multivariable permutational multivariate analysis of variance found that positive bacteria lab test results had the strongest independent association with lung microbiota (R² = 0.033; P = 0.018), followed by acute kidney injury (AKI; R² = 0.032; P = 0.011) and plasma MIP-1β level (R² = 0.027; P = 0.044). Random forest identified that the families Prevotellaceae, Moraxellaceae, and Staphylococcaceae were the biomarkers related to the positive bacteria lab test results. Multivariable Cox regression showed that the increase in α-diversity and the abundance of the families Prevotellaceae and Actinomycetaceae were associated with clinical improvements. The positive bacteria lab test results, AKI, and plasma MIP-1β level were associated with patients' lung microbiota composition on ICU admission. The families Prevotellaceae and Actinomycetaceae on admission predicted clinical improvements.
Acute Kidney Injury/complications* ; Bacteria/classification* ; Chemokine CCL4/blood* ; Community-Acquired Infections/microbiology* ; Humans ; Lung ; Microbiota/genetics* ; Pneumonia, Bacterial/diagnosis* ; Prognosis ; RNA, Ribosomal, 16S/genetics*