Neoadjuvant camrelizumab (an anti-PD-1 antibody) plus chemotherapy or apatinib (a VEGFR-2 inhibitor) for initially unresectable stage II-III non-small-cell lung cancer: a multicentre, two-arm, phase 2 exploratory study.

This multicentre, two-arm, phase 2 study aimed to explore the efficacy and safety of neoadjuvant camrelizumab plus chemotherapy or apatinib in patients with initially unresectable stage II-III non-small-cell lung cancer (NSCLC). Eligible patients regardless of PD-L1 expression received neoadjuvant camrelizumab 200 mg and platinum-doublet chemotherapy every 3 weeks (arm A) or those with PD-L1-positive tumors received neoadjuvant camrelizumab and apatinib 250 mg once daily (arm B), for 2-4 cycles, followed by surgery. The primary endpoint was major pathological response (MPR) rate. Thirty patients in arm A and 21 in arm B were enrolled. Surgery rates were 50.0% (15/30) in arm A and 42.9% (9/21) in arm B, with all patients achieving R0 resections. Of these patients, the MPR and pathological complete response rates were both 20.0% (95% CI 4.3-48.1) in arm A and were 55.6% (95% CI 21.2-86.3) and 11.1% (95% CI 0.3-48.2) in arm B, respectively. The corresponding objective response rates were 33.3% (95% CI 11.8-61.6) and 55.6% (95% CI 21.2-86.3). With a median follow-up of 22.4 months (95% CI 19.0-26.0), the median event-free survival was not reached (NR; 95% CI 13.6-NR) in arm A and 16.8 months (95% CI 8.6-NR) in arm B. Grade 3 or above treatment-related adverse events occurred in eight (26.7%) patients in arm A and three (14.3%) in arm B. Biomarker analysis showed baseline TYROBP expression was predictive of treatment response in arm B. Neoadjuvant camrelizumab plus chemotherapy or apatinib exhibits preliminary efficacy and manageable toxicity in patients with initially unresectable stage II-III NSCLC.

CRYAB reduces cigarette smoke-induced inflammation, apoptosis, and oxidative stress by retarding PI3K/Akt and NF-κB signaling pathways in human bronchial epithelial cells.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a familiar airway disease characterized by chronic immune response in the lungs. More and more evidences have assured that cigarette smoking is the primary reason for the progression of COPD, but its related regulatory mechanism requires further clarification. The α-B-crystallin (CRYAB) has been identified to exhibit vital functions in different diseases, and is down-regulated in the alveoli of mice mediated by cigarette smoke extract (CSE). METHODS: The messenger RNA expression of CRYAB was assessed by reverse transcription--quantitative polymerase chain reaction. The proteins' expressions were tested using Western blot method. The cytotoxicity was measured by lactate dehydrogenase assay. The levels of malondialdehyde, superoxide dismutase, catalase, myeloperoxidase, tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 were assessed through enzyme-linked-immunosorbent serologic assay (ELISA). RESULTS: In this study, it was discovered that the expression of CRYAB was markedly decreased with the increased time of cigarette smoking. Moreover, CRYAB overexpression increased cell viability and decreased cell apoptosis induced by cigarette smoke. In addition, the strengthened oxidative stress and inflammation mediated by CSE treatment was relieved after overexpression of CRYAB. Eventually, results OF Western blot method confirmed that CRYAB retarded the activation of phosphatidylinositol 3-kinase-Ak strain transforming (PI3K-Akt) and nuclear factor kappa B (NF-κB) signaling pathways. CONCLUSION: Our results manifested that CRYAB reduced cigarette smoke-induced inflammation, apoptosis, and oxidative stress in normal and diseased bronchial epithelial (NHBE) and human bronchial epithelial (BEAS-2B) cells by suppressing PI3K/Akt and NF-κB signaling pathways, which highlighted the functioning of CRYAB in preventing or treating COPD.

Effects of Preserving the Pulmonary Vagus Nerve Branches on Cough After Pneumonectomy During Video-Assisted Thoracic Surgery.

Background: Cough is one of the most common complications of early-stage non-small cell lung cancer (NSCLC) after video-assisted thoracoscopic surgery (VATS). The vagus nerve plays an important role in pulmonary inflammation and the cough reflex. In this study, we attempted to reduce the incidence of postoperative chronic cough and other complications by preserving the pulmonary vagus nerve branches. Patients and Methods: This study was a randomized controlled double-blinded trial of subjects and observers. A total of 158 NSCLC patients were enrolled. We randomly assigned 79 patients to Group A (pulmonary branch of vagus nerve preservation group) and 79 cases to Group B (conventional surgical treatment group). In the final analysis, 72 patients from Group A and 69 patients from Group B were included. The main outcome measure of the study was the occurrence of CAP or other postoperative complications within five weeks. This trial was registered with ClinicalTrials.gov (number NCT03921828). Results: There was no significant difference in preoperative general clinical data between the two groups. No death during the perioperative period occurred in either of the two groups. There was no significant difference between the two groups in operation time, intraoperative bleeding, number of lymph nodes sent for examination, number of cases transferred to ICU after operation, postoperative catheterization time, or postoperative hospital stay (P>0.05). There was no significant difference in other pulmonary and cardiovascular complications between the two groups, including pulmonary infection (2.78% vs. 8.70%, P = 0.129), atelectasis (1.39% vs. 0%, P = 0.326), pleural effusion (2.78% vs. 1.45%, P = 0.585), persistent pulmonary leakage (2.78% vs. 2.90%, P = 0.965), arrhythmia (2.78% vs. 1.45%, P = 0.585), and heart failure (0% vs. 1.45%, P = 0.305). The incidence of CAP in Group A was significantly lower than that in Group B (13.89% vs. 30.43%, P = 0.018). The LCQ-MC scores in Group A were significantly higher than those in Group B at two and five weeks after operation (P<0.05). Univariate and multivariate analysis showed that the risk factors for postoperative CAP were surgical side (right lung), surgical lung lobe (upper lobe), preservation of pulmonary branch of the vagus nerve during operation, and duration of anesthesia. Conclusions: Preserving the pulmonary vagus nerve branches during VATS in patients with stage IA1-2 NSCLC can reduce the incidence of postoperative CAP.

PTBP3 mediates TGF-ß-induced EMT and metastasis of lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is associated with a poor prognosis due to early metastasis to distant organs. TGF-ß potently induces epithelial-to-mesenchymal transition (EMT) and promotes invasion and metastasis of cancers. However, the mechanisms underlying this alteration are largely unknown. PTBP3 plays a critical role in RNA splicing and transcriptional regulation. Although accumulating evidence has revealed that PTBP3 exhibits a pro-oncogenic role in several cancers, whether and how PTBP3 mediates TGF-ß-induced EMT and metastasis in LUAD remains unknown. The expression levels and prognostic value of PTBP3 were analyzed in human LUAD tissues and matched normal tissues. siRNAs and lentivirus-mediated vectors were used to transfect LUAD cell lines. Various in vitro experiments including western blot, qRT-PCR, a luciferase reporter assay, chromatin immunoprecipitation (ChIP), transwell migration and invasion assay and in vivo metastasis experiment were performed to determine the roles of PTBP3 in TGF-ß-induced EMT and metastasis. PTBP3 expression was significantly upregulated in patients with LUAD, and high expression of PTBP3 indicated a poor prognosis. Intriguingly, we found that PTBP3 expression level in LUAD cell lines was significantly increased by exogenous TGF-ß1 in a Smad-dependent manner. Mechanistically, p-Smad3 was recruited to the PTBP3 promoter and activated its transcription. In turn, PTBP3 knockdown abolished TGF-ß1-mediated EMT through the inhibition of Smad2/3 expression. Furthermore, PTBP3 overexpression increased lung and liver metastasis of LUAD cells in vivo. PTBP3 is indispensable to TGF-ß-induced EMT and metastasis of LUAD cells and is a novel potential therapeutic target for the treatment of LUAD.

Spontaneous Rupture of Esophageal Diverticulum-A Case Report and Literature Review.

The spontaneous rupture of the esophageal diverticulum is a rare condition that occurs without any warning signs. Its incidence is low, but the mortality rate is high. This paper reports a case of spontaneous esophageal diverticulum rupture and analyzes it along with 13 other cases to explore its prevention and treatment measures. When patients suffer from chronic swallowing difficulties and chest pain or vomiting that cannot be explained after meals, they should be suspected to have a possible spontaneous rupture of the esophageal diverticulum, which is critical to the patient's prognosis.

A methyltransferase-like 14/miR-99a-5p/tribble 2 positive feedback circuit promotes cancer stem cell persistence and radioresistance via histone deacetylase 2-mediated epigenetic modulation in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a highly aggressive and treatment-resistant tumor. The biological implications and molecular mechanism of cancer stem-like cells (CSCs) in ESCC, which contribute to therapeutic resistance such as radioresistance, remain elusive. METHODS: Quantitative real-time polymerase chain reaction, western blotting, immunohistochemistry, and in situ hybridization assays were used to detect methyltransferase-like 14 miR-99a-5p tribble 2 (METTL14/miR-99a-5p/TRIB2) expression in ESCC. The biological functions of METTL14/miR-99a-5p/TRIB2 were demonstrated in vitro and in vivo. Mass spectrum analysis was used to identify the downstream proteins regulated by TRIB2. Chromatin immunoprecipitation (IP), IP, N6 -methyladenosine (m6 A)-RNA IP, luciferase reporter, and ubiquitination assays were employed to explore the molecular mechanisms underlying this feedback circuit and its downstream pathways. RESULTS: We found that miR-99a-5p was significantly decreased in ESCC. miR-99a-5p inhibited CSCs persistence and the radioresistance of ESCC cells, and miR-99a-5p downregulation predicted an unfavorable prognosis of ESCC patients. Mechanically, we unveiled a METTL14-miR-99a-5p-TRIB2 positive feedback loop that enhances CSC properties and radioresistance of ESCC cells. METTL14, an m6 A RNA methyltransferase downregulated in ESCC, suppresses TRIB2 expression via miR-99a-5p-mediated degradation of TRIB2 mRNA by targeting its 3' untranslated region, whereas TRIB2 induces ubiquitin-mediated proteasomal degradation of METTL14 in a COP1-dependent manner. METTL14 upregulates miR-99a-5p by modulating m6 A-mediated, DiGeorge critical region 8-dependent pri-mir-99a processing. Hyperactivation of TRIB2 resulting from this positive circuit was closely correlated with radioresistance and CSC characteristics. Furthermore, TRIB2 activates HDAC2 and subsequently induces p21 epigenetic repression through Akt/mTOR/S6K1 signaling pathway activation. Pharmacologic inhibition of HDAC2 effectively attenuates the TRIB2-mediated effect both in vitro and in patient-derived xenograft models. CONCLUSION: Our data highlight the presence of the METTL14/miR-99a-5p/TRIB2 axis and show that it is positively associated with CSC characteristics and radioresistance of ESCC, suggesting potential therapeutic targets for ESCC treatment.

Upregulation of glucosamine-phosphate N-acetyltransferase 1 is a promising diagnostic and predictive indicator for poor survival in patients with lung adenocarcinoma.

Lung adenocarcinoma, a type of non-small cell lung cancer, is the leading cause of cancer death worldwide. Great efforts have been made to identify the underlying mechanism of adenocarcinoma, especially in relation to oncogenes. The present study by integrating computational analysis with western blotting, aimed to understand the role of the upregulation of glucosamine-phosphate N-acetyltransferase 1 (GNPNAT1) in carcinogenesis. In the present study, publicly available gene expression profiles and clinical data were downloaded from The Cancer Genome Atlas to determine the role of GNPNAT1 in lung adenocarcinoma (LUAD). In addition, the association between LUAD susceptibility and GNPNAT1 upregulation were analyzed using Wilcoxon signed-rank test and logistic regression analysis. In LUAD, GNPNAT1 upregulation was significantly associated with disease stage [odds ratio (OR)=2.92, stage III vs. stage I], vital status (dead vs. alive, OR=1.89), cancer status (tumor status vs. tumor-free status, OR=1.85) and N classification (yes vs. no, OR=1.75). Cox regression analysis and the Kaplan-Meier method were utilized to evaluate the association between GNPNAT1 expression and overall survival (OS) time in patients with LUAD. The results demonstrated that patients with increased GNPNAT1 expression levels exhibited a reduced survival rate compared with those with decreased expression levels (P=8.9×10-5). In addition, Cox regression analysis revealed that GNPNAT1 upregulation was significantly associated with poor OS time [hazard ratio (HR): 1.07; 95% confidence interval (CI): 1.04-1.10; P<0.001]. The gene set enrichment analysis revealed that 'cell cycle', 'oocyte meiosis', 'pyrimidine mediated metabolism', 'ubiquitin mediated proteolysis', 'one carbon pool by folate', 'mismatch repair progesterone-mediated oocyte maturation' and 'basal transcription factors purine metabolism' were differentially enriched in the GNPNAT1 high-expression samples compared with GNPNAT1 low-expression samples. The aforementioned pathways are involved in the pathogenesis of LUAD. The findings of the present study suggested that GNPNAT1 upregulation may be considered as a promising diagnostic and prognostic biomarker in patients with LUAD. In addition, the aforementioned pathways may be pivotal pathways perturbed by the abnormal expression of GNPNAT1 in LUAD. The findings of the present study demonstrated the therapeutic value of the regulation of GNPNAT1 in lung adenocarcinoma.

Direct Electrochemical Defluorinative Carboxylation of gem-Difluoroalkenes with Carbon Dioxide.

We report a facile and economical synthesis of α-fluoroacrylic acids via direct electrochemical defluorinative carboxylation of gem-difluoroalkenes with CO2. By using a platinum plate as the working cathode and a cheap nickel plate as the anode in a user-friendly undivided cell under constant current conditions, the reactions proceed smoothly under room temperature, without the use of expensive transition metal catalysts, ligands, external base or reductant, affording the desired adducts in up to 83% yield and 20:1 Z/E ratio, with good functional group tolerance. A cyclic voltammetry study was conducted and suggested a novel ECEC process.

Direct electrochemical defluorinative carboxylation of α-CF3 alkenes with carbon dioxide.

An unprecedented γ-carboxylation of α-CF3 alkenes with CO2 is reported. This approach constitutes a rare example of using electrochemical methods to achieve regioselectivity complementary to conventional metal catalysis. Accordingly, using platinum plate as both a working cathode and a nonsacrificial anode in a user-friendly undivided cell under constant current conditions, the γ-carboxylation provides efficient access to vinylacetic acids bearing a gem-difluoroalkene moiety from a broad range of substrates. The synthetic utility is further demonstrated by gram-scale synthesis and elaboration to several value-added products. Cyclic voltammetry and density functional theory calculations were performed to provide mechanistic insights into the reaction.

Multifunctional 1,3-diphenylguanidine for the carboxylative cyclization of homopropargyl amines with CO2 under ambient temperature and pressure.

Herein, we report that 1,3-diphenylguanidine (DPG) could be utilized for the carboxylative cyclization of homopropargyl amines with CO2 under ambient temperature and pressure, in combination with AgSbF6, which enabled the synthesis of both chiral and achiral 2-oxazinones efficiently. A mechanistic study revealed that the multi-functionality of DPG is critical to the success of the reaction.

Association of multiple genetic variants with chronic obstructive pulmonary disease susceptibility in Hainan region.

BACKGROUND AND AIMS: Recent genome-wide association studies have shown associations between variants in loci (4q28.1, 6p21.32, 6p21.1, 6q16.1, 10q22.1 and 10q22.3) and chronic obstructive pulmonary disease (COPD) or smoking behaviors. The objective of this study was to look for associations between 16 single nucleotide polymorphisms (SNP) at these six loci and COPD susceptibility in Hainan region. METHODS: A case-control cohort was composed of 200 COPD cases and 401 controls that were genotyped and analyzed statistically. Odds ratios (OR) and 95% confidence intervals (CIs) were computed by chi-square (χ2 ) test and genetic models by unconditional logistic regression. RESULTS: After Hardy-Weinberg equilibrium (HWE) P value screening, we excluded the SNP rs12220777 with P < 0.001. By χ2 test only rs9296092 which located on 6p21.32 was provided the strongest evidence of an increasing risk of COPD with an OR of 3.28 (95% CI = 1.03 - 2.32; P = 0.003) between cases and controls. By genetic models analysis, we not only found rs9296092 increased COPD risk, but also found in the over-dominant model the genotype 'C/T' (OR = 0.55; 95% CI = 0.33 - 0.93; P = 0.023) of rs950063 was proved to be associated with decreased COPD risk. CONCLUSIONS: This study is the first to provide evidence of importance of rs9296092 and rs950063 for risk of COPD in Hainan Province. Further studies are needed to characterize the functional sequences that cause COPD.

A general and efficient Lewis acid catalysed Mukaiyama-aldol reaction of difluoroenoxysilanes and ketones.

We report a general and highly efficient Mukaiyama-aldol reaction of ketones and difluoroenoxysilanes. While the reaction of aryl ketones worked efficiently in the presence of Bi(OTf)3, that of aliphatic ketones required the use of Sc(OTf)3. In addition, Sc(OTf)3 was capable of achieving excellent 1,2-selectivity in the corresponding reaction of α,ß-unsaturated ketones. This method provides a facile access to differently substituted ß-hydroxy α,α-difluoro ketones, versatile synthons for difluomethylated tertiary alcohols.

Early growth response gene-1 decoy oligonucleotides inhibit vascular smooth muscle cell proliferation and neointimal hyperplasia of autogenous vein graft in rabbits.

OBJECTIVES: The excess proliferation of vascular smooth muscle cells (VSMCs) and the development of intimal hyperplasia is a hallmark of vein graft failure. This study aimed to verify that a single intraoperative transfection of early growth response gene-1 (Egr-1) decoy oligonucleotide (ODN) can suppress vein graft proliferation of VSMCs and intimal hyperplasia. METHODS: In a rabbit model, jugular veins were treated with Egr-1 decoy ODN, scrambled decoy ODN, Fugene6, or were left untreated, then grafted to the carotid artery. The vein graft samples were obtained 48 h, 1, 2 or 3 weeks after surgery. The thickness of the intima and intima/media ratio in the grafts was analysed by haematoxylin-eosin (HE) staining. The expression of the Egr-1 decoy ODN transfected in the vein was analysed using fluorescent microscopy. Egr-1 mRNA was measured using reverse transcription-polymerase chain reaction. The expression of Egr-1 protein was analysed by Western blot and immunohistochemistry. RESULTS: Transfection efficiency of the ODN was confirmed by 4', 6-diamidino-2-phenylindole staining. In the grafts treated with Egr-1 decoy ODN, our study achieved statistically significant inhibition of intimal hyperplasia by ∼58% at 3 weeks. Transfection of Egr-1 decoy ODNs decreased the protein expression of Egr-1 and Egr-1 mRNA. CONCLUSIONS: We confirmed that gene therapy using in vivo transfection of an Egr-1 decoy ODN significantly inhibits proliferation of VSMC and intimal hyperplasia of vein grafts in a rabbit model.

Myeloperoxidase-mediated oxidation targets serum apolipoprotein A-I in diabetic patients and represents a potential mechanism leading to impaired anti-apoptotic activity of high density lipoprotein.

BACKGROUND: It is demonstrated that levels of protein-bound chlorotyrosine, nitrotyrosine and myeloperoxidase (MPO), a protein that catalyzes generation of chlorinating and nitrating oxidants, serve as independent predictors of cardiovascular disease. METHODS: Immunoprecipitation and Western blot were used to analyze protein concentration, nitration and chlorination. LC-MS/MS was used to identify nitrated and chlorinated sites of Tyr from immunoprecipitated serum proteins. RESULTS: Apolipoprotein A-I (apoA-I), the primary protein constituent of high density lipoprotein (HDL), was identified as a selective target for MPO-catalyzed nitration and chlorination in patients with type 2 diabetes. The serum proteins from diabetic subjects showed that the levels of apoA-I nitration and chlorination were clearly increased, whereas apoA-I concentration and cholesterol efflux activity were significantly decreased. MPO as a likely mechanism for oxidative modification of apoA-I in vivo was apparently facilitated by MPO binding to apoA-I. Subsequently, it was found that Tyr 192 was the major nitration and chlorination site in apoA-I from diabetic serum. Further studies in vitro revealed that besides the classic inhibition in cholesterol efflux activities, MPO-catalyzed oxidation could result in a loss of anti-apoptotic activity of lipoprotein. CONCLUSIONS: ApoA-I undergoes MPO-mediated oxidation in serum from diabetic patients compared to non-diabetic subjects and MPO-catalyzed modification may impair the anti-apoptotic properties of HDL in vitro.

Early results after surgical treatment of left ventricular aneurysm.

BACKGROUND: Left ventricular aneurysm (LVA) is a serious complication of myocardial infarction and reduces the chances of survival. Controversy still exists regarding the optimal surgical technique for LVA repair. We analyze the efficacy of two techniques, linear vs. endoventricular circular patch plasty, for repair of LVA and the efficacy of surgical ventricular restoration (SVR) on beating heart. METHODS: This study included 62 patients who underwent SVR from 1086 consecutive patients were subjected to coronary artery bypass grafting (CABG) between 2000 and 2009. All selected patients were divided either into group liner or patch according to the choice of the repair technique depended on factors such as localization, size and dimension of the scar. The patients also were divided either into group beating heart or cardioplegia. The pre-, intra- and postoperative relevant data of all selected patients were analyzed. RESULTS: The mortality was not significantly different between linear and patch repair groups, also the actuarial survival rates within 24 months (p= 0.529). Postoperative echocardiographic findings showed significant improvements in left ventricular function in both groups. The beating heart technique reduced postoperative peak release by 27% for Cardiac troponin I (cTnI) compared with the cardioplegia group (0.46 ± 0.06 ng/mL versus 0.63 ± 0.09 ng/mL, p= 0.004), and increased the perioperative survival by 9% (97.2% versus 88.5%), but the actuarial survival rates were not significantly different between the groups from 2 to 24 months (p= 0.151). CONCLUSIONS: Both techniques (linear and patch) achieved good results with respect to mortality, functional status and survival. The choice of surgical technique should be adapted in each patient. The beating heart technique may to some extent relieve myocardial injury in patients undergoing SVR.

Timing of continuous veno-venous hemodialysis in the treatment of acute renal failure following cardiac surgery.

The purpose was to study optimum timing of continuous veno-venous hemodialysis (CVVHD) for acute renal failure (ARF) after cardiac surgery. CVVHD was performed in two groups [elapsed time between urine output (UO) <0.5 ml/kg/h and dialysis of no more than 12 h in group A and >12 h in group B] with a total of 58 adult patients. Survivors in groups A and B were entered into groups A1 and B1, respectively. Compared to group A, the acute physiology and chronic health evaluation III score, peak values of urea and creatinine before CVVHD, major complications, period of ICU and hospitalization were significantly higher in group B. In-hospital mortality in group B was significantly higher than that in group A (37.5 vs. 8.8%, p = 0.02). Kaplan-Meier curves confirmed significantly better postoperative survival in group A (χ² = 6.966, p = 0.008). Time elapse from UO < 0.5 ml/kg/h until dialysis among the survivors was significantly lower than that among the dead (12.0 ± 6.2 vs. 20.8 ± 9.1 h, p = 0.0002). Additionally, duration of dialysis, length of ICU stay, duration of ventilator support and time elapse from dialysis until UO > 1 ml/kg/h were significantly higher in group B1 as compared to those in group A1. All of them correlated positively with the time elapse from UO < 0.5 ml/kg/h until dialysis. Early beginning of CVVHD is extremely important.

Combination of irbesartan and amiodarone to maintain sinus rhythm in patients with persistent atrial fibrillation after rheumatic valve replacement.

BACKGROUND: Atrial fibrillation (AF) after rheumatic valve replacement is the most common arrhythmic complication. Previous studies reported angiotensin-II receptor blocker can prevent AF. This study aimed to assess the effect of a combination of irbesartan and amiodarone on the maintenance of sinus rhythm after cardioversion of AF in patients with post-rheumatic valve replacement in a randomized, controlled trial. METHODS AND RESULTS: Eighty-five consecutive patients undergoing rheumatic valve surgery were enrolled and randomly assigned to an irbesartan plus amiodarone (irbesartan 150 mg/d, n=43) or an amiodarone group (n=42) starting 10 days before scheduled electrical cardioversion. The primary end-point was recurrence of AF. Pharmacological conversion was documented in 7 patients, and electrical conversion in 68 patients (87.2%). A higher rate of maintenance of sinus rhythm (69.8% vs 40.5%, P=0.01) and a better AF-free survival (chi(2)=7.466, P=0.006) were observed in the irbesartan plus amiodarone group compared to the amiodarone group during the 1-year follow-up period. Cox regression showed that use of irbesartan was an independent factor associated with the maintenance of sinus rhythm after cardioversion (OR=0.43, P=0.018), whereas increased left atrium diameter was associated with increased risk (OR=1.54, P=0.005). CONCLUSIONS: In patients with post-rheumatic valve replacement, the combination of amiodarone and irbesartan demonstrated a lower rate of AF recurrence after cardioversion than amiodarone alone, which might be due to preventing the atrial remodeling.

[Clinical and pathological analysis of 114 cases with non-ductal pancreatic adenocarcinoma occupying lesions].

OBJECTIVE: To improve the diagnosis and treatment of non-ductal pancreatic adenocarcinoma-occupying lesions. METHODS: A retrospective analysis was made for 114 cases of pancreatic non-ductal adenocarcinoma-occupying pathologically confirmed lesions. RESULTS: (1) There were 36 males (31.6%) and 78 females (68.42%); (2) presenting symptoms and signs were abdominal pain (n = 56, 49.1%), back pain (n = 24, 21.1%), weight loss (n = 18, 15.8%) and obstructive jaundice (n = 8, 0.07%); (3) the positive rates of CA19-9, CA242 and CEA were 21.1%, 19.7% and 5.6% respectively; (4) pancreaticoduodenectomy was performed in 26 patients, distal pancreatectomy in 53, tumor enucleation in 15, segmental pancreatectomy in 9, partial resection in 3, duodenum-preserving pancreatic head resection in 1 and palliative surgery (either cholecystojejunostomy anastomosis or gastrojejunostomy) in 7; (5) pathologic analysis revealed 35 solid pseudopapillary neoplasm of pancreas, 28 pancreatic endocrine tumors, 18 focal chronic pancreatitis, 11 serous cystic neoplasms, 9 mucinous cystic neoplasms, 4 pancreatic cysts, 3 acinar cell carcinomas, 2 pancreatic cavernous hemangiomas, 1 sarcoma of pancreas, 1 sarcomatoid carcinoma of pancreas, 1 pancreatic schwannoma and 1 pancreatic neuroblastoma. CONCLUSION: The non-ductal pancreatic adenocarcinoma-occupying lesions have no specific clinical presentation or serum tumor marker. An understanding of the natural history of these lesions is important for optimal management.

Effect of preoperative atorvastatin therapy on atrial fibrillation following off-pump coronary artery bypass grafting.

BACKGROUND: Atrial fibrillation (AF) after coronary artery bypass grafting (CABG) is still the most common postoperative arrhythmic complication. Previous studies report that patients undergoing preoperative statin therapy had a lower incidence of postoperative AF. This study aimed to assess the effect of preoperative atorvastatin therapy on preventing AF following off-pump CABG in a randomized, controlled trial. METHODS AND RESULTS: The 140 consecutive patients undergoing elective off-pump CABG, without a history of AF or previous statin treatment, were enrolled and randomly assigned to a statin (atorvastatin 20 mg/day, n=71) or a control group (placebo, n=69) starting 7 days preoperatively. The primary endpoint was the occurrence of postoperative AF; secondary endpoints were major adverse in-hospital cardiac and cerebrovascular events and identification of variables predicting postoperative AF. Atorvastatin significantly reduced the incidence of postoperative AF and the postoperative peak C-reactive protein (CRP) level vs placebo (14% vs 34%, P=0.009; 126.5 +/-22.3 vs 145.2 +/-31.6 mg/L, P<0.0001). Logistic regression analysis showed preoperative atorvastatin treatment was an independent factor associated with a significant reduction in postoperative AF (odds ratio (OR) 0.219, P=0.005), whereas a high postoperative CRP level was associated with increased risk (OR 2.011, P=0.013). CONCLUSIONS: Administration of atorvastatin 20 mg/day, initiated 1 week before elective off-pump CABG and continued in the postoperative period, significantly decreases postoperative AF.