Risk factors for diaphragmatic injury in subxiphoid video-assisted thoracoscopic surgery.

BACKGROUND: Subxiphoid video-assisted thoracoscopic surgery (VATS) is considered a safe and feasible operation for anterior mediastinal mass resection. However, diaphragmatic injury, presented as tearing or puncturing, may occur during subxiphoid VATS despite of low incidence. This study aims to explore risk factors for diaphragmatic injury in subxiphoid VATS, as well as strategies to reduce occurrence of the injury. METHODS: We retrospectively reviewed clinical records of 44 consecutive adult patients who underwent subxiphoid VATS. These patients were divided into two groups: diaphragmatic injury group and non-injury group. Perioperative outcomes and anatomic features derived from 3D CT reconstructions were compared between the two groups. RESULTS: Significant differences were observed in operation time (223.25 ± 92.57 vs. 136.28 ± 53.05, P = 0.006), xiphoid length (6.47 ± 0.85 vs. 4.79 ± 1.04, P = 0.001) and length of the xiphoid below the attachment point on the diaphragm (24.86 ± 12.02 vs. 14.61 ± 9.25, P = 0.029). Odds ratio for the length of the xiphoid below the attachment point on the diaphragm was 1.09 (1.001-1.186), P = 0.048 by binary logistic regression analysis. CONCLUSIONS: We identified the length of the xiphoid below the attachment point on the diaphragm as an independent risk factor for diaphragm injury during subxiphoid VATS. Prior to subxiphoid VATS, a 3D chest CT reconstruction is recommended to assess the patients' anatomic variations within the xiphoid process. For patients with longer xiphoid process, a higher incision at the middle and upper part of the xiphoid process, and partial xiphoid process resection or xiphoidectomy is preferred.

Silencing of m6A methyltransferase KIAA1429 suppresses the progression of non-small cell lung cancer by promoting the p53 signaling pathway and ferroptosis.

KIAA1429, an important component of the N6-methyladenine methyltransferase complex, is involved in the pathology of many types of cancer. In this study, the mechanisms through which KIAA1429 promotes non-small cell lung cancer (NSCLC) progression were explored using in vitro and in vivo experiments. Additionally, bioinformatics analysis of publicly available data was used to determine the relationship between KIAA1429 expression and NSCLC patient survival. The results showed that KIAA1429 was upregulated in NSCLC tissues and cells, and its high expression level was associated with low overall survival. Transcriptome analysis of KIAA1429-silenced NSCLC cells identified 346 differentially expressed genes, which were enriched in ferroptosis and the p53 signaling pathway. KIAA1429 silencing using small interfering (si) RNA promoted erastin-induced ferroptosis in NSCLC cells and activated the p53 signaling pathway. Moreover, si-KIAA1429 inhibited the proliferative, migratory, and invasive abilities of NSCLC cells in vitro and tumor growth in vivo. These in vitro effects were weakened by pifithrin-µ, a p53 inhibitor. Therefore, given its effects on ferroptosis and the p53 signaling pathway, targeting KIAA1429 could be an effective strategy for treating NSCLC.

A Novel m6A-Related LncRNA Signature for Predicting Prognosis, Chemotherapy and Immunotherapy Response in Patients with Lung Adenocarcinoma.

N6-methyladenosine (m6A) and long non-coding RNA (lncRNA) have been associated with cancer prognosis and the effect of immunotherapy. However, the roles of m6A-related lncRNAs in the prognosis and immunotherapy in lung adenocarcinoma (LUAD) patients remain unclear. We evaluated the m6A modification patterns of 695 samples based on m6A regulators, and prognostic m6A-related lncRNAs were identified via a weighted gene co-expression network analysis. Twelve abnormal m6A regulators and nine prognostic lncRNAs were identified. The tumor microenvironment cell-infiltrating characteristics of three m6A-related lncRNA clusters were highly consistent with the three immune phenotypes of tumors, including immune-excluded, immune-inflamed and immune-desert phenotypes. The lncRNA score system was established, and high lncRNA score patients were associated with better overall survival. The lncRNA score was correlated with the expression of the immune checkpoints. Two immunotherapy cohorts supported that the high lncRNA score enhanced the response to anti-PD-1/L1 immunotherapy and was remarkably correlated with the inflamed immune phenotype, showing significant therapeutic advantages and clinical benefits. Furthermore, the patients with high lncRNA scores were more sensitive to erlotinib and axitinib. The lncRNA score was associated with the expression of miRNA and the regulation of post-transcription. We constructed an applied lncRNA score-system to identify eligible LUAD patients for immunotherapy and predict the sensitivity to chemotherapeutic drugs.

B3GNT3 as a prognostic biomarker and correlation with immune cell infiltration in lung adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is the most common malignant cancer in humans and because of low long-term survival rates, exploration of the molecular mechanisms underlying its progression, as well as novel prognostic predictors, is urgently needed. B3GNT3, a type II transmembrane protein located in the Golgi apparatus, is essential for forming extended core 1 oligosaccharides and is reportedly involved in malignant transformation. Methods: The Cancer Genome Atlas (TCGA) and GSE68465 were used to analyze the expression of B3GNT3 in LUAD and normal tissues and overall survival. Real time quantitative polymerase chain reaction (qPCR) and western blot were conducted to measure the mRNA and protein levels of B3GNT3, respectively. Functional enrichment of differentially expressed genes was explored using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. We performed univariate and multivariate Cox regression analyses and a meta-analysis to reveal an independent factor for LUAD. We evaluated the correlation between immune infiltration levels and cumulative survival in the TIMER database. The correlation between B3GNT3 and immune cell infiltration was assessed via Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT). The association of DNA methylation of B3GNT3 and prognosis was determined. A nomogram that incorporated expression and clinical features was additionally built for prognostic prediction. Cell proliferation, cloning, and invasion were conducted to validate the roles of B3GNT3 in LUAD. Results: B3GNT3 was more highly expressed in LUAD tissues than in normal lung tissues, consistent with the mRNA and protein levels in LUAD cells. B3GNT3 was an independent factor for LUAD. Moreover, the levels of B3GNT3 were related to immune cell infiltration in LUAD microenvironments. DNA methylation of B3GNT3 correlated with the mRNA of B3GNT and overall survival of LUAD patients. The expression of B3GNT3 was highly valuable for the prediction of diagnosis. Knockdown of B3GNT3 inhibited LUAD cell viability and cloning ability, and hindered invasion. Conclusions: B3GNT3 was highly associated with immune cell infiltration, acting as an important biomarker for the prognosis and diagnosis of LUAD.

Elucidating the anatomy of the quadrivial pattern of the right upper lobe bronchus using 3D-CT images.

Background: A preoperative understanding of the thoracic anatomy of the patients with the quadrivial pattern of branching of the right upper lobe is key to successful surgery. We analyzed the quadrivial pattern of division of the right upper lobe bronchus of patients using three-dimensional (3D) computed tomography (CT) angiography and bronchography. Methods: A total of 212 consecutive adult patients who had undergone thoracic CT scans before surgery at the Zhujiang Hospital of the Southern Medical University from August 2020 to August 2021 was used for retrospective study. The 3D-CT images were taken using Mimics software. Radiology technicians processed all the 3D images, and thoracic surgeons confirmed the validity of all the reconstructions. Results: Six (2.83%) were identified as having a quadrivial pattern of division of the right upper lobe bronchus with 1 female, and 5 males. Based on the number of pulmonary artery branches, 5 (83.3%) and 1 (16.7%) were classified as "trunk superior (Tr.sup) + ascending artery (A.asc) and Tr.sup + trunk inferior (Tr.inf) + ascending artery (A.asc) (1/6, 16.7%). Based on the number of ascending artery branches, the patients were also divided into type A (3/6, 50%) and type B (3/6, 50%). The patients were also divided into 1 of the following three types based on the origins of the A2: (I) A2 originates from A6 (1/6, 16.7%); (II) A2 originates from the pulmonary trunk (4/6, 66.7%); and (III) A2a originates from A3, and A2b originates from the pulmonary artery stem (1/6, 16.7%). According to the number of A1b branches, patients were divided into two types: (I) 1 branch (4/6, 66.7 %); and (II) 2 branches (2/6, 33.3 %). In the present study, anterior + central type was observed which classified into two types: (I) type Iab, the anterior vein ran from V1a to V1b (4/6, 66.7%); and (II) type Ib, the anterior vein ran from V1b only (2/6, 33.3%). Conclusions: 3D-CT was successfully used for analyzing the quadrivial bronchovascular patterns of the right upper lobe bronchus. Our study provides certain references to perform anatomical pulmonary segmentectomy, which should improve the success rate of operations.

Nursing Observation of Improved Administration Route of Protamine Sulfate Neutralizing Heparin.

In this study, we have evaluated and examined various nursing effects of improved administration of protamine sulfate neutralizing heparin after cardiopulmonary bypass. For this purpose, retrospective analysis was made about the nursing records and clinical data of 216 patients who underwent cardiac operation under cardiopulmonary bypass in our hospital from January 2018 to December 2020. Among the enrolled patients, 118 patients were given subinterval administration of protamine sulfate neutralizing heparin via aortic root with the assistance of the scrub nurse at the end of cardiac surgery (improved group). A total of 98 patients were administered by the circulating nurse via the central vein (regular group). The changes of body temperature, blood pressure, oxygen saturation before and after heparin neutralization, and the total volume of thoracic drainage within 24 hours after operation were observed in the two groups, so as to evaluate the application effect of the improved administration of protamine sulfate neutralizing heparin from the perspective of nursing. There was no significant difference in age, gender, and other basic characteristics between the two groups (P > 0.05). The volume of drainage in the improved group and the regular group within 24 hours after surgery was 234 ± 26.3 ml and 307 ± 31.8 ml, respectively, P < 0.01, and the difference was statistically significant. The incidence of adverse reactions in the improved group was much lower than that in the regular group, P < 0.01. The administration route of the improved group was beneficial to maintain the stability of hemodynamics when using the protamine sulfate to neutralize heparin, which is worthy of clinical nursing promotion.

Circ_0072088 knockdown contributes to cisplatin sensitivity and inhibits tumor progression by miR-944/LASP1 axis in non-small cell lung cancer.

BACKGROUND: Non-small cell lung cancer (NSCLC) is an aggressive tumor that accounts for a large proportion of cancer-related deaths. Cisplatin (CDDP) has been utilized to treat NSCLC. However, the efficacy of CDDP is usually restrained owing to the development of drug resistance. This study aims to reveal the molecular mechanism of the resistance of NSCLC cells to CDDP. METHODS: The expression levels of circRNA_0072088 (circ_0072088), microRNA-944 (miR-944), and LIM and SH3 protein 1 (LASP1) were measured by quantitative real-time PCR (qRT-PCR) in CDDP-resistant NSCLC tissues and cells. Protein expression was determined by Western blotting in CDDP-resistant NSCLC tissues and cells. The functional effects of circ_0072088, miR-944, and LASP1 on CDDP sensitivity and NSCLC progression were revealed by Cell Counting Kit-8 (CCK-8), flow cytometry, cell colony formation, wound healing, and transwell invasion assays. The binding relationship between miR-944 and circ_0072088 or LASP1 was identified by a dual-luciferase reporter and RNA immunoprecipitation assay. The effects of circ_0072088 knockdown on tumor growth in vivo were analyzed by an in vivo tumor formation assay. RESULTS: Circ_0072088 and LASP1 expression were significantly upregulated, while miR-944 expression was downregulated in CDDP-resistant NSCLC tissues and cells as compared with control groups. Circ_0072088 expression was significantly associated with tumor-node-metastasis stage and tumor size. Functionally, circ_0072088 knockdown improved CDDP sensitivity and repressed NSCLC cell malignancy, whereas miR-944 inhibitor hindered these effects. Mechanistically, circ_0072088 functioned as a sponge for miR-944 and miR-944 targeted LASP1. Circ_0072088 knockdown improved the sensitivity of tumor to CDDP in vivo. CONCLUSION: Circ_0072088 silencing improved CDDP sensitivity and inhibited NSCLC progression by downregulating LASP1 expression through sponging miR-944. These data provide novel insight into the resistance of NSCLC to CDDP.

Analysis of whole-exome data of cfDNA and the tumor tissue of non-small cell lung cancer.

BACKGROUND: Non-small cell lung cancer (NSCLC) has the highest cancer mortality rate in the world, but currently there is no effective method of dynamic monitoring. Gene mutation is an important factor in tumorigenesis and can be detected using high-throughput sequencing technology. This study aimed to analyze the driving genes in the tumor of NSCLC patients by whole exon sequencing, and to compare and analyze the subclones of the tumor at different time points. METHODS: We collected 87 cases of NSCLC tumor tissues, para-cancer tissues, and peripheral blood samples for detecting cell-free DNAs (cfDNAs) from January 2016 to December 2018, and whole-exome sequencing was performed. The gene mutation map of NSCLC was drawn in detail by second-generation sequencing data analysis and new driver genes were found. In addition, we performed a subclonal analysis of tumors from different stages of the same patient to further describe the tumor heterogeneity. RESULTS: We found that the clonal analysis obtained by cfDNA detection was similar to the clonal analysis of the tissue samples, so real-time monitoring of tumor changes can be carried out through monitoring cfDNA. CONCLUSIONS: This study provides evidence for studying the gene mutation information of NSCLC and shows the importance of cfDNA in the analysis of tumor subcloning information.

KCNQ1OT1 lncRNA affects the proliferation, apoptosis, and chemoresistance of small cell lung cancer cells via the JAK2/STAT3 axis.

BACKGROUND: Small cell lung cancer (SCLC) is a devastating and aggressive neuroendocrine carcinoma characterized by high cellular proliferation and early metastatic spread. Numerous studies have demonstrated that long noncoding RNAs (lncRNAs) can regulate tumor generation and development, including in SCLC. The current study aimed to assess the effect of the lncRNA, KCNQ1OT1, on the proliferation, apoptosis, and chemoresistance of SCLC and the potential underlying molecular mechanism. METHODS: Matched chemo-resistant and sensitive cells were applied to RNA isolation and followed by expression profiling by microarray analysis and subsequent quantitative polymerase chain reaction (qPCR) validation. Cell viability and apoptosis were determined by Cell Counting Kit-8 and flow cytometry to examine the chemoresistance and apoptosis of KCNQ1OT1 knockdown with lentivirus-mediated RNA interference. Furthermore, cell proliferation was studied by colony formation, and invasion and migration were tested by Transwell cell invasion and wound-healing assays, respectively. A tumor xenograft model was established to determine the role of KCNQ1OT1 in tumor growth and chemoresistance in response to KCNQ1OT1 knockdown in vivo. Western blot analysis, qPCR, and immunohistochemistry were used to detect the levels of messenger RNA (mRNA) Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway-related markers. RESULTS: Higher expression of KCNQ1OT1 was detected in SCLC chemo-resistant verso chemo-sensitive cells. Knockdown of KCNQ1OT1 inhibited SCLC cell viability and cloning ability, hindered cell migration and invasion, induced apoptosis in vitro, and suppressed tumor growth and chemoresistance in vivo, by activating the JAK2/STAT3 signaling pathway. CONCLUSIONS: This is the first study to indicate that lncRNA KCNQ1OT1 promotes cell proliferation and invasion, and prevents apoptosis of SCLC by activating the JAK2/STAT3 pathway.

A Novel Role of Claudin-5 in Prevention of Mitochondrial Fission Against Ischemic/Hypoxic Stress in Cardiomyocytes.

BACKGROUND: Downregulation of claudin-5 in the heart is associated with the end-stage heart failure. However, the underlying mechanism ofclaudin-5 is unclear. Here we investigated the molecular actions of claudin-5 in perspective of mitochondria in cardiomyocytes to better understand the role of claudin-5 in cardioprotection during ischemia. METHODS: Myocardial ischemia/reperfusion (I/R; 30 min/24 h) and hypoxia/reoxygenation (H/R; 24 h/4 h) were used in this study. Confocal microscopy and transmission electron microscope (TEM) were used to observe mitochondrial morphology. RESULTS: Claudin-5 was detected in murine heart tissue and neonatal rat cardiomyocytes (NRCM). Its protein level was severely decreased after myocardial I/R or H/R. Confocal microscopy showedclaudin-5 presented in the mitochondria of NRCM. H/R-induced claudin-5 downregulation was accompanied by mitochondrial fragmentation. The mitofusin 2 (Mfn2) expressionwas dramatically decreased while the dynamin-related protein (Drp) 1 expression was significantly increased after H/R. The TEM indicatedH/R-induced mitochondrial swelling and fission. Adenoviral claudin-5 overexpression reversed these structural disintegration of mitochondria. The mitochondria-centered intrinsic pathway of apoptosis triggered by H/R and indicated by the cytochrome c and cleaved caspase 3 in the cytoplasm of NRCMs was also reduced by overexpressing claudin-5. Claudin-5 overexpression in mouse heart also significantly decreased cleaved caspase 3 and the infarct size in ischemic heart with improved systolic function. CONCLUSION: We demonstrated for the first time the presence of claudin-5 in the mitochondria in cardiomyocytes and provided the firm evidence for the cardioprotective role of claudin-5 in the preservation of mitochondrial dynamics and cell fate against hypoxia- or ischemia-induced stress.

Stereotactic Body Radiotherapy Versus Surgery for Early-Stage Non-Small-Cell Lung Cancer.

BACKGROUND: Surgery is the gold standard therapy for patients with early-stage non-small-cell lung cancer (NSCLC). However, stereotactic body radiotherapy (SBRT) may provide as an alternative for patients who are medically inoperable or refuse surgical resection. The optimal treatment (SBRT or surgery) for patients with early-stage NSCLC is not clear. METHODS: A systematic search was performed from PubMed, MEDLINE, Embase, and the Cochrane Library. Study heterogeneity and publication bias were estimated. RESULTS: Fourteen cohort studies involving 1438 participants (719 who received SBRT and 719 who received surgery) were included in the meta-analysis. The main bias sources between the two groups, such as age, gender, tumor diameter, forced expiratory volume in 1 s, and Charlson comorbidity index were matched. The surgery was associated with a better overall survival (OS) and long-term distant control (DC) for early-stage NSCLC. The pooled OR and 95% confidence interval (CI) for 1-y, 3-y, 5-y OS, and 5-y DC were 1.56 (1.12-2.15), 1.86 (1.50-2.31), 2.43 (1.80-3.28), and 2.74 (1.12-6.67), respectively. No difference was found between the treatments in the 1-y and 3-y disease-free survival; 1-y, 3-y and 5-y locoregional control; or 1-y and 3-y DC. CONCLUSIONS: Our results found a superior OS and long-term DC for early-stage NSCLC after surgery compared with SBRT after propensity score matching.

[Establishment of A Patient-derived Xenotransplantation Animal Model for Small Cell Lung Cancer and Drug Resistance Model].

BACKGROUND: Small cell lung cancer (SCLC) is characterized by poor differentiation, high malignancy and rapid growth fast, short double time, early and extensive metastatic malignancy. In clinical, chemotherapy is the main treatment method, while resistance to multiple chemotherapy drugs in six to nine months has been a major clinical challenge in SCLC treatment. Therefore, It has important clinical value to building SCLC aninimal model which is similar to patients with SCLC. Animal model of xenotransplantation (PDX) from the patients with small cell lung cancer can well retain the characteristics of primary tumor and is an ideal preclinical animal model. The study is aimed to establish SCLC PDX animal model and induce the chemoresistance model to help to study the mechanism of chemoresistance and individual treatment. METHODS: Fresh surgical excision or puncture specimens from SCLC patients were transplanted into B-NSGTM mice subcutaneous tissues with severe immunodeficiency in one hour after operation the B-NSGTM mice subcutaneous in 1 hour, and inject chemotherapy drugs intraperitoneally after its tumor growed to 400 mm³ with EP which is cisplatin 8 mg/kg eight days and etoposide 5 mg/kg every two days until 8 cycles. Measure the tumor volum and mice weights regularly, then re-engrafted the largest tumor and continue chemotherapy. RESULTS: Nine cases were conducted for B-NSG mice modeling. Three of nine cases could be engrafted to new B-NSG mice at least two generation. The SCLC PDX animal models have been established successfully. After adopting chemotherapy drugs, the chemoresistance PDX models have been established. High homogeneity was found between xenograft tumor and patient's tumor in histopathology, immunohistochemical phenotype (Syn, CD56, Ki67). CONCLUSIONS: The SCLC PDX animal model and the chemoresistance PDX animal model have been successfully constructed, the success rate is 33%, which provides a platform for the clinical research, seeking for biological markers and choosing individual treatment methods of SCLC.

[Effects of minimally invasive versus open esophagectomy on circulating tumor cells in patients with esophageal cancer].

OBJECTIVE: To investigate the effects of minimally invasive esophagectomy (MIE) and open esophagectomy (OE) on the level of circulating tumor cells (CTCs) in patients with esophageal cancer (EC). METHODS: A total of 73 patients with EC undergoing MIE (n=38) or OE (n=35) in our department between October, 2015 and October, 2017 were enrolled, with 10 patients with benign esophagus disease and 10 healthy volunteers as controls. The levels of CTCs in the peripheral blood of the participants were detected using CanPatrolTM technique and analyzed for their association with the operation methods and perioperative complications. RESULTS: CTCs were detected in 60.3% (44/73) of the EC patients but in none of the control subjects. CTC level after the surgery was significantly higher than that during the surgery, and CTC level during the surgery was significantly higher than that before surgery (P<0.001). The preoperative and intra-operative CTC levels were not significantly different between MIE and OE groups (P>0.05), but the postoperative CTC level was significantly lower in MIE group than in OE group, and postoperative increment of CTC level (from the preoperative level) was significantly lower in MIE group than in OE group (P<0.001). The total incidence of postoperative complications was significantly lower in MIE group than in OE group (28.9% vs 54.3%, P=0.023), and in both groups, CTC levels in patients with complications were significantly higher than those in patients without complications (P=0.001 and P=0.005 in MIE and OE groups, respectively). CONCLUSION: MIE may help to reduce the number of peripheral blood CTCs early after the operation, and dynamic monitoring CTCs level assists in evaluation of the prognosis of EC patients. CTC level may serve as an indicator for monitoring the prognosis of EC.

H3K27me3 induces multidrug resistance in small cell lung cancer by affecting HOXA1 DNA methylation via regulation of the lncRNA HOTAIR.

BACKGROUND: The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) serves as a powerful predictor of tumor progression and overall survival in patients. Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC). Moreover, H3 lysine 27 trimethylation (H3K27me3) is catalyzed by enhancer of zeste homolog 2 (EZH2) and plays a critical role in SCLC chemoresistance. However, it is not completely clear whether H3K27me3 affects HOXA1 DNA methylation or whether this effect is mediated by HOTAIR. METHODS: The levels of EZH2 and H3K27me3 were identified in SCLC tissues by immunohistochemical (IHC) staining and in SCLC multidrug-resistant cells by Western blotting. Cell counting kit-8 (CCK-8) and flow cytometry were used to detect and analyze the biological function of H3K27me3. Then, we assessed the role of HOTAIR in the regulation of EZH2 and H3K27me3 by using lentivirus and small interfering RNA. Further, bisulfite sequencing PCR was conducted to detect the methylation levels of HOXA1 DNA. Finally, Western blotting was performed to examine the regulatory role of H3K27me3 in controlling HOTAIR expression in SCLC. RESULTS: In this study, we found that EZH2 and H3K27me3 levels were markedly higher in SCLC tissues and multidrug-resistant SCLC cells. The results indicated that H3K27me3 was related to multidrug resistance. HOTAIR overexpression and knockdown showed that EZH2 and H3K27me3 were regulated by HOTAIR. Moreover, H3K27me3 affected HOXA1 DNA methylation levels. Strikingly, we found that H3K27me3 acted as a negative feedback regulator of HOTAIR. CONCLUSIONS: Our study showed that H3K27me3 affects HOXA1 DNA methylation via HOTAIR regulation, indicating that H3K27me3 may be a potential therapy target for SCLC chemoresistance.

[Establishment of a rabbit model of small diameter vascular graft replacement].

OBJECTIVE: To establish an rabbit model that mimics the hemodynamics of the bypass graft after coronary artery bypass surgery. METHODS: Sixteen New Zealand rabbits were randomly divided into two groups for abdominal aortic artery replacement using a 3-cm-long ePTFE graft with an inner diameter 4 mm through an incision at 1/3 from the middle to the lower part of the abdomen (group A) or in the lower abdomen (group B). The general conditions of the rabbits, operative time, number of collateral vessels that needed to be ligated, rate of massive intraoperative bleeding, fluctuation of vascular anastomosis after surgery, patency rate of the graft on day 7 after the operation were compared between the two groups. RESULTS: The two groups of rabbits had similar body weight, diameter of the abdominal aortic artery, intraoperative bleeding rate and occlusion rate of the vascular graft at 7 days after the procedure. The operative time was longer in group A, but the difference was not statistically significant. In group A, the number of the vascular branches that needed to be ligated was smaller and the rate normal femoral artery pulsation was higher than those in group B. CONCLUSION: It is feasible to establish models of small diameter vascular graft replacement in rabbits, and the patency rate of the graft can be monitored by observation of the general condition and ultrasound examination of the rabbits.

[Investigation of the technique of esophageal stent re-implantation].

OBJECTIVE: To analyze the causes of failure of esophageal stent implantation and explore technical improvement of re-implantation of esophageal stent (RIES). METHODS: According to the conditions of the failed stent implantation, 32 patients who required RIES underwent placement of more appropriate esophageal stents with an improved implantation technique. The patients were followed up for 6 months after the operation to evaluate the effects of RIES. RESULTS: The success rate of the operation was 96.9% in these cases, and the esophageal conditions including stricture and fistula were effectively relieved. During the 6-month follow-up, stent migration occurred in 4 cases (12.5%), and esophageal fistula in the upper edge of the re-implanted stent occurred in 2 cases. No stent loss, bleeding, or stricture was found in these cases. CONCLUSION: The improved technique is effective for stent re-implantation after failed esophageal stent implantation with reduced complications associated with esophageal stenting.