Objective To evaluate the safety and efficacy of percutaneous nephrolithotomy (PCNL) with B ultrasound-guided renal access in the lateral decubitus flank position for complex renal calculi. Methods From June 2004 to August 2009, 650 patients with renal stones≥20 mm underwent PCNL with B ultrasound-guided renal access in the lateral decubitus flank position. 512 men and 138 women,with a mean age of 38 years(range 11 - 78 years)and a mean stone size of 31 mm(range 20 - 58 mm). Results Successful access was achieved in 650 patients (100%). Minimally PCNL and PCNL were performed in 493 and 157 patients. Complete stone clearance rate was 86. 6% (563/ 650). The mean operative time was 72 min(range 35 - 145 min), and the mean hospital stay was 18d (range 9 - 32 d). There were no visceral injuries. Conclusions PCNL with B ultrasound-guided renal access in the lateral decubitus flank position is safe and convenient, and prevents harmful effects of radiation for the surgeon, the surgical team, and the patient.

Objective To investigate various types and quantities of fetal cells getting into peripheral blood of pregnant women and immune status related to pregnancy induced hypertension syndrome (PIH) and analyze the etiology of PIH.Methods (1) Three markers of fetal nucleated red blood cells (fNRBCs) in normal pregnant women(n=43)and PIH patients (n=39)were measured by flow cytometry: CD71,HbF/iAg and HbF/CA.(2)We detected the levels of sub-groups of lymphocytes and some plasma cytokines.such as TNF-α and IL-6.The blood samples were from normal pregnant subjects and patients of PIH.Results In the peripheral blood of patients of PIH and normal pregnant subjects,(1) The quantities of fetal cells using three different methods in PIH [6.56(11.37)%、0.09(0.16)%、0.06(0.11)%]were significantly different from normal pregnant subjects[1.58(3.35)%、0.04(0.08)%、0.02(0.06)%],Z= -5.31,-2.97,-4.13 respectively,P＜0.01.(2)Except CD8,the levels of CD3 (76.4±8.5)%,CD4(42.6±6.4)%,CD4/CD8(1.5±0.4)%,CD19(10.5±3.9)%,CD16/CD56 (12.2±7.7)%,TNF-α (1.4 ±0.6)μg/L and IL-6(89.6±12.9)μg/L in PIH were significantly different from normal pregnant subjects[CD3(70.4±8.3)%,CD4(35.3±6.9)%,CD4/CD8(1.2±0.4)%,CD19(8.2±2.8)%,CD16/CD56(20.5±8.9)%,TNF-α(0.5±0.2)μg/L and IL-6(22.0±5.7)μg/L,respectively,P＜0.001].There were no significant differences observed in the level of CD8(P＞0.05).Conclusion The increment of fNRBCs getting into peripheral blood of pregnant women and associated immune status were implicated in the development of PIH.

(Hp) is widely disseminated in human, and Hp infection causes various gastrointestinal diseases, including gastric cancer. Different genotypes of Hp may cause different diseases, so the genotyping is important for clinical and basic research of Hp. This article introduces the methods for Hp genotyping, including multilocus sequence typing, pulsed-field gel electrophoresis, random amplified polymorphic DNA, amplified fragment length polymorphism, and whole-genome sequencing. By reviewing the application of these techniques in Hp genotyping and comparing their advantages and disadvantages, the article provides a theoretical basis for research into the pathogenesis, antibiotic resistance, and epidemiology of Hp infection.
Amplified Fragment Length Polymorphism Analysis ; Genotype ; Helicobacter Infections ; microbiology ; pathology ; Helicobacter pylori ; genetics ; Humans ; Polymerase Chain Reaction ; Research

Objective To assess the causality between 14 malignant tumors and hypertension.Methods Publicly available datasets from genome-wide association study were used,from which independent genetic variants strongly associated with hypertension and 14 malignant tumors were extracted as instrumental variables for bidirectional Mendelian randomization(MR)analysis,including random effect inverse variance weighted(IVW),simple mode,weighted median,weighted mode and MR-Egger to evaluate the causal effect.Sensitivity analysis was used to test the validity and robustness of the analytical results,and multivariate MR method was used to further control for the effects of confounding factors.Results In the MR analysis of malignant melanoma and hypertension,the study included a total of 11 single nucleotide polymorphisms(SNPs)strongly associated with malignant melanoma.After Bonferroni correction,the IVW-based results showed a causal relationship between malignant melanoma and hypertension(OR=1.67,95％CI:1.27-2.21,P＜0.001).Cochran's Q test,Mendelian randomization pleiotropy residual sum and outlier test and MR-Egger intercept test showed that there were no outliers and no horizontal pleiotropy among the instrumental variables,and the sensitivity analysis of the leave-one-out method showed that there was no single SNP that had a significant impact on the overall results.In the analysis of hypertension and leukemia,the preliminary analysis results showed that there may be a relationship between the two,but after adjusting for confounders,the effect of hypertension on the risk of leukemia was no longer significant.Conclusion Malignant melanoma may be a risk factor in the development of hypertension.

Disturbance of macrophage-associated lipid metabolism plays a key role in atherosclerosis. Crosstalk between autophagy deficiency and inflammation response in foam cells (FCs) through epigenetic regulation is still poorly understood. Here, we demonstrate that in macrophages, oxidized low-density lipoprotein (ox-LDL) leads to abnormal crosstalk between autophagy and inflammation, thereby causing aberrant lipid metabolism mediated through a dysfunctional transcription factor EB (TFEB)-P300-bromodomain-containing protein 4 (BRD4) axis. ox-LDL led to macrophage autophagy deficiency along with TFEB cytoplasmic accumulation and increased reactive oxygen species generation. This activated P300 promoted BRD4 binding on the promoter regions of inflammatory genes, consequently contributing to inflammation with atherogenesis. Particularly, ox-LDL activated BRD4-dependent super-enhancer associated with liquid-liquid phase separation (LLPS) on the regulatory regions of inflammatory genes. Curcumin (Cur) prominently restored FCs autophagy by promoting TFEB nuclear translocation, optimizing lipid catabolism, and reducing inflammation. The consequences of P300 and BRD4 on super-enhancer formation and inflammatory response in FCs could be prevented by Cur. Furthermore, the anti-atherogenesis effect of Cur was inhibited by macrophage-specific Brd4 overexpression or Tfeb knock-out in Apoe knock-out mice via bone marrow transplantation. The findings identify a novel TFEB-P300-BRD4 axis and establish a new epigenetic paradigm by which Cur regulates autophagy, inhibits inflammation, and decreases lipid content.

Inflammation-driven endothelial dysfunction is the major initiating factor in atherosclerosis, while the underlying mechanism remains elusive. Here, we report that the non-canonical stimulator of interferon genes (STING)-PKR-like ER kinase (PERK) pathway was significantly activated in both human and mice atherosclerotic arteries. Typically, STING activation leads to the activation of interferon regulatory factor 3 (IRF3) and nuclear factor-kappa B (NF-κB)/p65, thereby facilitating IFN signals and inflammation. In contrast, our study reveals the activated non-canonical STING-PERK pathway increases scaffold protein bromodomain protein 4 (BRD4) expression, which encourages the formation of super-enhancers on the proximal promoter regions of the proinflammatory cytokines, thereby enabling the transactivation of these cytokines by integrating activated IRF3 and NF-κB via a condensation process. Endothelium-specific STING and BRD4 deficiency significantly decreased the plaque area and inflammation. Mechanistically, this pathway is triggered by leaked mitochondrial DNA (mtDNA) via mitochondrial permeability transition pore (mPTP), formed by voltage-dependent anion channel 1 (VDAC1) oligomer interaction with oxidized mtDNA upon cholesterol oxidation stimulation. Especially, compared to macrophages, endothelial STING activation plays a more pronounced role in atherosclerosis. We propose a non-canonical STING-PERK pathway-dependent epigenetic paradigm in atherosclerosis that integrates IRF3, NF-κB and BRD4 in inflammatory responses, which provides emerging therapeutic modalities for vascular endothelial dysfunction.