Publications by authors named "Aiguo Lu"

32 Publications

High versus low ligation of the inferior mesenteric artery during laparoscopic rectal cancer surgery: A prospective study of surgical and oncological outcomes.

J Surg Oncol 2021 Mar 2. Epub 2021 Mar 2.

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Background And Objectives: There is controversy regarding whether the inferior mesenteric artery (IMA) should be ligated at its origin from the aorta (high ligation, HL) or below the branch of the left colic artery (low ligation, LL) during surgery for rectal cancer.

Methods: This prospective study randomized 95 patients with histologically proven rectal cancer (clinical stages I-III based on the 8th American Joint Committee on Cancer guidelines) to undergo HL (n = 47) or LL with lymph node dissection at the root of the IMA (n = 48).

Results: Only two intraoperative adverse events were observed (two HL patients experienced anastomotic ischemia and underwent extended bowel excision and splenic flexure mobilization). The LL group had a significantly shorter time to first flatus (p < .0001). No significant differences were observed in operative time (p = .14), intraoperative blood loss (p = .21), distance from the upper margin (p = .77), distance from the lower margin (p = .35), harvested lymph nodes (p = .33), or anastomotic leakage (p = .44), 2-year overall survival (p = .97), or 2-year disease-free survival (p = .42).

Conclusion: During laparoscopic low anterior resection, a combination of LL at the IMA and vascular root lymph node dissection may help protect the blood supply of the anastomosis, reduce postoperative complications, and enhance recovery, without compromising radical excision.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jso.26362DOI Listing
March 2021

Artificial Intelligence in Decision-Making for Colorectal Cancer Treatment Strategy: An Observational Study of Implementing Watson for Oncology in a 250-Case Cohort.

Front Oncol 2020 4;10:594182. Epub 2021 Feb 4.

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Background: Personalized and novel evidence-based clinical treatment strategy consulting for colorectal cancer has been available through various artificial intelligence (AI) supporting systems such as Watson for Oncology (WFO) from IBM. However, the potential effects of this supporting tool in cancer care have not been thoroughly explored in real-world studies. This research aims to investigate the concordance between treatment recommendations for colorectal cancer patients made by WFO and a multidisciplinary team (MDT) at a major comprehensive gastrointestinal cancer center.

Methods: In this prospective study, both WFO and the blinded MDT's treatment recommendations were provided concurrently for enrolled colorectal cancers of stages II to IV between March 2017 and January 2018 at Shanghai Minimally Invasive Surgery Center. Concordance was achieved if the cancer team's decisions were listed in the "recommended" or "for consideration" classification in WFO. A review was carried out after 100 cases for all non-concordant patients to explain the inconsistency, and corresponding feedback was given to WFO's database. The concordance of the subsequent cases was analyzed to evaluate both the performance and learning ability of WFO.

Results: Overall, 250 patients met the inclusion criteria and were recruited in the study. Eighty-one were diagnosed with colon cancer and 189 with rectal cancer. The concordances for colon cancer, rectal cancer, or overall were all 91%. The overall rates were 83, 94, and 88% in subgroups of stages II, III, and IV. When categorized by treatment strategy, concordances were 97, 93, 89, 87, and 100% for neoadjuvant, surgery, adjuvant, first line, and second line treatment groups, respectively. After analyzing the main factors causing discordance, relative updates were made in the database accordingly, which led to the concordance curve rising in most groups compared with the initial rates.

Conclusion: Clinical recommendations made by WFO and the cancer team were highly matched for colorectal cancer. Patient age, cancer stage, and the consideration of previous therapy details had a significant influence on concordance. Addressing these perspectives will facilitate the use of the cancer decision-support systems to help oncologists achieve the promise of precision medicine.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fonc.2020.594182DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7899045PMC
February 2021

Pelvic peritoneum closure reduces postoperative complications of laparoscopic abdominoperineal resection: 6-year experience in single center.

Surg Endosc 2021 Jan 21;35(1):406-414. Epub 2020 Feb 21.

Department of General Surgery, Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No. 197, Ruijin Er Road, Shanghai, 200025, China.

Background: To investigate feasibility of laparoscopic abdominoperineal resection with pelvic peritoneum closure (LAPR-PPC) for lower rectal cancer.

Methods: LAPR-PPC has been used for lower rectal cancer in our institution since 2014. In this study, we retrospectively analyzed the data from 86 patients who underwent LAPR-PPC and compared with the data from 96 patients who underwent laparoscopic APR without PPC (LAPR) from January 2013 to December 2018.

Results: The rate of perineal surgical site infection (SSI) (18.75% (18/96) vs. 5.81% (5/86), p < 0.01), delayed (> 4 weeks) perineal healing (12.50% (12/96) vs. 3.49% (3/86), p = 0.027), ileus (7.29% (7/96) vs 1.16% (1/86), p = 0.044), and postoperative perineal hernia (PPH, 5.21% (5/96) vs. 0% (0/86), p = 0.032) were significantly lower in LAPR-PPC group than LAPR group. The patients in LAPR-PPC group had shorter hospitalization time (21.32 ± 11.95 days vs. 13.93 ± 11.51 days, p < 0.01).

Conclusions: PPC procedure enabled the reduction in perineal wound complications, ileus, PPH, and consequently shortened hospitalization time. LAPR-PPC is beneficial for the patients with lower rectal cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00464-020-07414-wDOI Listing
January 2021

A positive feedback loop of β-catenin/CCR2 axis promotes regorafenib resistance in colorectal cancer.

Cell Death Dis 2019 09 9;10(9):643. Epub 2019 Sep 9.

Department of General Surgery, Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200008, China.

Resistance to molecular targeted therapies is a significant challenge for advanced colorectal cancer (CRC). Understanding the underlying mechanisms and developing effective strategies against regorafenib resistance are highly desired in the clinic. Here, we screened the expression of chemokine receptors and identified CC chemokine receptor 2 (CCR2) as a top upregulated gene in regorafenib-resistant cells. CCR2 silencing alleviated drug tolerance in regorafenib-resistant cells, while overexpression of CCR2 enhanced CRC cells resistance to regorafenib. Moreover, CCR2-mediated regorafenib tolerance was demonstrated to be associated with AKT/GSK3β-regulated β-catenin stabilization. In turn, β-catenin modulation is sufficient to trigger the transcriptional activation of CCR2 expression. Clinically, high-CCR2 expression was correlated to shorter overall survival and disease-free survival of patients. A positive correlation between CCR2 and nuclear β-catenin expression was observed in a cohort of CRC tissues. Altogether, these findings suggest β-catenin and CCR2 are part of a positive-feedback loop, which sustains a high CCR2 expression level, conferring CRC cells resistance to regorafenib. Thus, targeting CCR2 may be a useful therapeutic strategy to alleviate regorafenib tolerance to increase the efficacy of CRC treatments.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41419-019-1906-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733926PMC
September 2019

Identification of key genes and pathways involved in microsatellite instability in colorectal cancer.

Mol Med Rep 2019 Mar 11;19(3):2065-2076. Epub 2019 Jan 11.

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.

Microsatellite instability (MSI) has emerged as one of the key biological features of colorectal cancer (CRC). However, controversies remain regarding the association between the MSI status and clinicopathological characteristics of CRC. Therefore, it is crucial to identify potential key genes and pathways associated with MSI in CRC. In the present study, the GSE25071 gene expression profile was retrieved, with thirty‑eight cases of microsatellite stable (MSS), five of MSI‑High (MSI‑H) and three of MSI‑Low (MSI‑L) CRC patients. The differentially expressed genes (DEGs) were analyzed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes pathway enrichment, gene set enrichment analysis (GSEA) and gene co‑expression network analysis. Weighted gene correlation network analysis (WGCNA) was used for the gene modules and correlation of clinical traits. A total of forty‑nine DEGs were identified between MSI‑H and MSS, including six upregulated and forty‑three downregulated DEGs. Only the DEGs of MSI‑H and MSS were subjected to subsequent analysis (limited number of DEGs of MSI‑L and MSS, MSI‑H and MSI‑L). RNA metabolic process, endoplasmic reticulum and chemokine receptor binding were the top ranked terms in GO enrichment. The hub genes of co‑expression network of DEGs included zinc finger protein (ZNF) 813, ZNF426, ZNF611, ZNF320 and ZNF573. The GSEA of MSI‑H and MSS indicated that the mammalian target of rapamycin complex 1 signaling was significantly enriched with a nominal P‑value of 0.038 and normalized enrichment score of 0.446. The WGCNA results showed that the pink module was the top in correlation with MSI status (R2=0.5, P=0.0004). The genes in the pink module were significantly enriched in proteins targeting to endoplasmic reticulum, cytosolic part, structural constituent of ribosome and ribosome pathway. The hub genes identified in the pink module were ribosomal protein L12 (RPL12), RPS3A, RPS9, RPL27A, RPL7, RPL28, RPL14, RPS17, mitochondrial ribosomal protein L16, and G elongation factor, mitochondrial 2. The present study identified key genes and pathways associated with MSI, providing insightful mechanisms.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/mmr.2019.9849DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390070PMC
March 2019

Completely medial access by page-turning approach for laparoscopic right hemi-colectomy: 6-year-experience in single center.

Surg Endosc 2019 03 1;33(3):959-965. Epub 2018 Nov 1.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No. 197, Ruijin Er Road, Shanghai, 200025, China.

Background: To investigate the safety and feasibility of the completely medial access by page-turning approach (CMAP) for laparoscopic right hemi-colectomy.

Methods: In this retrospective study, the data from 72 patients who underwent laparoscopic right hemi-colectomy with CMAP were analyzed and compared with data from 124 patients who underwent the conventional medial approach performed by the same surgical team from September 2011 to March 2017.

Result: Complete mesocolic excision (CME) was achieved in 67 of 72 patients (93.1%) with laparoscopic CMAP. The average operation time, blood loss, and specimen length was 135.9 ± 28.3 min, 63.2 ± 32.2 ml, and 23.9 ± 4.7 cm, respectively. The number of lymph nodes harvested was 20.6 ± 7.7, the time-to-flatus was 2.5 ± 0.8 days, the time-to-fluid intake was 3.2 ± 0.8 days, and the average hospital stay was 8.9 ± 4.7 days. No intra-operative complications occurred in this study. The vessel-related complication and total post-operative complication rate was 2.78% (2/72) and 6.94% (5/72), respectively.

Conclusions: Laparoscopic CMAP was an alternative approach for CME in laparoscopic right hemi-colectomy, which was proved safe and feasible for right colon cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00464-018-6525-1DOI Listing
March 2019

CCL19 suppresses angiogenesis through promoting miR-206 and inhibiting Met/ERK/Elk-1/HIF-1α/VEGF-A pathway in colorectal cancer.

Cell Death Dis 2018 09 24;9(10):974. Epub 2018 Sep 24.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.

The mechanisms underlying the role of chemokines in tumor angiogenesis is still not fully understood. In this study, we detected the influence of CCL19 on colorectal cancer (CRC) angiogenesis. The expression of CCL19 and CD31 in CRC tissues were detected by immunohistochemistry. Human CRC cell lines SW1116 and SW620 stably transfected with CCL19 lentivirus and CCL19 shRNA, and HUVEC stably transfected with CCR7 shRNA were used in our study. Our study showed that CCL19 was significantly low-expressed in CRC tissues and positively related to highly tumor microvessel density. In vitro, we observed that CCL19 high-expressed SW1116 supernatant was able to inhibit proliferation, migration, and sprouting responses of HUVEC, whereas CCL19 low-expressed SW620 supernatant can promote HUVEC angiogenesis. Additionally, we further demonstrated that these functions maybe achieved through promoting miR-206 thus inhibiting Met/ERK/Elk-1/HIF-1α/VEGF-A pathway in a CCR7-dependent manner. Mice angiogenesis model also confirmed that elevated expression of CCL19 inhibit the angiogenesis of CRC in vivo. In summary, our results supported that CCL19 can inhibit CRC angiogenesis through promoting miR-206 thus inhibiting Met/ERK/Elk-1/HIF-1α/VEGF-A pathway. This may be a novel therapeutic option for anti-vascular treatment in CRC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41419-018-1010-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6155262PMC
September 2018

Overexpression of CXCR2 predicts poor prognosis in patients with colorectal cancer.

Oncotarget 2017 Apr;8(17):28442-28454

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.

Colorectal cancer is a heterogeneous disease. Although many risk factors are used to predict colorectal cancer patients' prognosis after surgical resection, new prognostic factors are still needed to be defined to promote predictive efficacy of prognosis and further guide therapies. Herein, we identified the prognostic significance of CXCR2 in colorectal cancer patients. We retrospectively analysed 134 patients with colorectal cancer who underwent minimally invasive surgery between 2010 and 2011. The overall cohort was divided into a training set (n = 78) and a validation set (n = 56). We detected CXCR2 expression using immunohistochemical staining and defined the cut-off value using X-tile program. Next, we analysed the association between CXCR2 expression and clinicopathologic features in training and validation sets. High expression of CXCR2 was associated with Dukes stage (P = 0.018), tumor invasion (P = 0.018) and liver metastasis (P = 0.047). Multivariate COX regression analyses confirmed that high CXCR2 level was an independent prognostic risk factor for both overall survival and disease free survival. Kaplan-Meier survival analysis demonstrated that patients with high expression of CXCR2 had a poor overall survival and disease free survival even in low-risk group (I + II). This indicated that CXCR2 can help to refine individual risk stratification. In addition, we established Nomograms of all significant factors to predict 3- or 5-years overall survival and disease free survival. Moreover, we found the combination of CXCR2 and its ligand CXCL5 had more significant value in predicting the prognosis than single CXCR2 factor.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/oncotarget.16086DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438662PMC
April 2017

Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3β/β-catenin pathways.

Mol Cancer 2017 03 29;16(1):70. Epub 2017 Mar 29.

Shanghai Minimally Invasive Surgery Center, Ruijin hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.

Background: Metastasis is a major cause of death in human colorectal cancer patients. However, the contribution of chemokines in the tumor microenvironment to tumor metastasis is not fully understood.

Methods: Herein, we examinined several chemokines in colorectal cancer patients using chemokine ELISA array. Immunohistochemistry was used to detect expression of CXCL5 in colorectal cancer patients tissues. Human HCT116 and SW480 cell lines stably transfected with CXCL5, shCXCL5 and shCXCR2 lentivirus plasmids were used in our in vitro study. Immunoblot, immunofluorescence and transwell assay were used to examine the molecular biology and morphological changes in these cells. In addition, we used nude mice to detect the influence of CXCL5 on tumor metastasis in vivo.

Results: We found that CXCL5 was overexpressed in tumor tissues and associated with advanced tumor stage as well as poor prognosis in colorectal cancer patients. We also demonstrated that CXCL5 was primarily expressed in the tumor cell cytoplasm and cell membranes, which may indicate that the CXCL5 was predominantly produced by cancer epithelial cells instead of fibroblasts in the tumor mesenchyme. Additionally, overexpression of CXCL5 enhanced the migration and invasion of colorectal cancer cells by inducing the epithelial-mesenchymal transition (EMT) through activation of the ERK/Elk-1/Snail pathway and the AKT/GSK3β/β-catenin pathway in a CXCR2-dependent manner. The silencing of Snail and β-catenin attenuated CXCL5/CXCR2-enhanced cell migration and invasion in vitro. The elevated expression of CXCL5 can also potentiate the metastasis of colorectal cancer cells to the liver in vivo in nude mice intrasplenic injection model.

Conclusion: In conclusion, our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12943-017-0629-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372323PMC
March 2017

An efficient and simple co-culture method for isolating primary human hepatic cells: Potential application for tumor microenvironment research.

Oncol Rep 2016 Oct 28;36(4):2126-34. Epub 2016 Jul 28.

Heart Center, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, P.R. China.

Co-cultivation of non-parenchymal cells (NPCs) and tumor cells from the same donor is important for metastatic cancer research. This study aimed to optimize a protocol for liver NPC isolation. Two novel 3D organotypic co‑culture models for hepatocyte, endothelial cell (EC) and Kupffer cell (KC) isolation were used. Long‑term cell co‑culture, density gradient centrifugation and magnetic‑activated cell sorting (MACS) were established. ECs were isolated from the co‑culture system; the purity of the ECs was 92±1.2%. The island‑like shape of hepatocytes was noted in the 3D co‑culture system, and spindle cells were found in the rest space. Immunofluorescence analysis showed a net structure; the connective tissue was positively stained with VE‑cadherin or CD68, which were ECs and KCs/macrophages. KCs were enriched in this system and separated by using selective adherence to plastic. Clec4f+ KCs consisted of 87±6.3% of these cells. Heterogeneous endothelium populations were detected, including sinusoid ECs, microvascular ECs and hepatic lymphatic vessel epithelial cells. In addition, hepatic progenitor cells were isolated and differentiated into hepatoblasts. Dendritic cells (DCs), invariant natural killer T (iNKT) cells were further separated by density gradient centrifugation and magnetic bead sorting. In the present study, high protein expression levels of desmin and GFAP were observed in the hepatic stellate cells (HSCs). Most of the HSCs were α‑SMA‑positive cells, which underlined the identity of activated HSCs. Intrahepatic human biliary epithelial cells (hBECs) were semi‑purified by centrifugation on a Percoll gradient and were further immunopurified. In conclusion, we provide an efficient long‑term culture method to obtain liver NPCs in sufficient number and purity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/or.2016.4979DOI Listing
October 2016

Plk2 promotes tumor growth and inhibits apoptosis by targeting Fbxw7/Cyclin E in colorectal cancer.

Cancer Lett 2016 10 14;380(2):457-466. Epub 2016 Jul 14.

Department of General Surgery, Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address:

Polo-like kinase 2 (Plk2) and Polo-like kinase 3 (Plk3) have been documented as a tumor suppressor and are lowly expressed in several types of cancer. However, our results showed that Plk3 was lowly expressed, whereas Plk2 expressed highly in tumor tissues. We therefore aimed to explore the mechanisms governing the role of Plk2 in colorectal cancer (CRC). Our investigation demonstrated that Plk2 was an independent prognostic marker in CRC patients. Plk2 promotes tumor growth and inhibits apoptosis of CRC cells in vitro and in vivo. Moreover, Plk2 binds to Fbxw7 and results in its subsequent degradation, which in turn leads to the stabilization of Cyclin E. The pro-tumor activity of Plk2 could be inverted by restoring Fbxw7 expression and depletion of Cyclin E. In addition, the expressions of Fbxw7 and Cyclin E were significantly associated with Plk2 protein levels in CRC tissues. In conclusion, our data show that Plk2 represents an independent prognostic marker and regulates tumor growth and apoptosis by targeting Fbxw7/Cyclin E pathway in CRC, suggesting Plk2 as a potential therapeutic target.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.canlet.2016.07.004DOI Listing
October 2016

CCR4 promotes metastasis via ERK/NF-κB/MMP13 pathway and acts downstream of TNF-α in colorectal cancer.

Oncotarget 2016 Jul;7(30):47637-47649

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Chemokines and chemokine receptors are causally involved in the metastasis of human malignancies. As a crucial chemokine receptor for mediating immune homeostasis, however, the role of CCR4 in colorectal cancer (CRC) remains unknown. In this study, we found that high expression of CCR4 in CRC tissues was correlated with shorter overall survival and disease free survival. In vitro and in vivo experiments revealed that silencing CCR4 attenuated the invasion and metastasis of CRC cells, whereas ectopic overexpression of CCR4 contributed to the forced metastasis of these cells. We further demonstrated that matrix metalloproteinase 13 (MMP13) played an important role in CCR4-mediated cancer cell invasion, which is up-regulated by ERK/NF-κB signaling. Positive correlation between CCR4 and MMP13 expression was also observed in CRC tissues. Moreover, our investigations showed that the level of CCR4 could be induced by TNF-α dependent of NF-κB activation in CRC cells. CCR4 might be implicated in TNF-α-regulated cancer cells metastasis. Combination of CCR4 and TNF-α is a more powerful prognostic marker for CRC patients. These findings suggest that CCR4 facilitates metastasis through ERK/NF-κB/MMP13 signaling and acts as a downstream target of TNF-α. CCR4 inhibition may be a promising therapeutic option for suppressing CRC metastasis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/oncotarget.10256DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5216967PMC
July 2016

Effect of urokinase-type plasminogen activator system in gastric cancer with peritoneal metastasis.

Oncol Lett 2016 Jun 26;11(6):4208-4216. Epub 2016 Apr 26.

Department of Gastroenterological Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.

Peritoneal metastasis is a primary cause of mortality in patients with gastric cancer. Urokinase-type plasminogen activator (uPA) has been demonstrated to be associated with tumor cell metastasis through the degradation of the extracellular matrix. The present study aimed to investigate the mechanisms of the uPA system in gastric cancer with peritoneal metastasis. Expression of uPA, uPA receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1) in four gastric cell lines (AGS, SGC7901, MKN45 and MKN28) was measured by semiquantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay and western blotting. uPA activity was detected using a uPA activity kit. Peritoneal implantation models of rats were established by injecting four gastric cancer cell lines for the selection of the cancer cells with a high planting potential. Biological behaviors, including adhesion, migration and invasion, were determined using a methyl thiazolyl tetrazolium assay. Expression of the uPA system was observed to be highest in the SGC7901 cells among the four gastric cell lines. uPA activity was observed to be highest in the MKN45 cells and lowest in the AGS cells. Furthermore, peritoneal implantation analysis demonstrated that no peritoneal tumors were identified in the AGS cells, whilst the tumor masses observed in the SGC7901 and MKN45 cells were of different sizes. The survival times of the rats injected with the MKN28 and SGC7901 cells were longer than those of the rats injected with the MKN45 cells. Antibodies for uPA, uPAR and PAI-1 in the uPA system had the ability to inhibit the adhesion, migration and invasion of peritoneal metastasis in the gastric cancer cells. The results of the present study demonstrated that the uPA system was positively associated with peritoneal metastasis in gastric cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/ol.2016.4498DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888090PMC
June 2016

Cadherin-12 enhances proliferation in colorectal cancer cells and increases progression by promoting EMT.

Tumour Biol 2016 Jul 14;37(7):9077-88. Epub 2016 Jan 14.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.

Cadherin-12 (CDH12) is a subtype of N-cadherin family. In this study, we investigated the expression of CDH12 and the role of CDH12 in prognosis of colorectal cancer (CRC) patients. In addition, we observed the influence of CDH12 on proliferation and progression of CRC cell lines. By using immunohistochemical staining, we analyzed CRC samples and adjacent non-tumor tissues collected from 78 patients who underwent laparoscopic surgery in Shanghai Minimally Invasive Center, China. Statistical analyses were used to analyze relationship between CDH12 and tumor features. Kaplan-Meier method was used to analyze patients' survival. Proliferation ability of CRC cells was tested by CCK-8 assay, and transwell assays were performed to detect migration and invasion ability. Western blot assay was performed to investigate epithelial-mesenchymal transition (EMT) variants. We found that expression of CDH12 in tumor tissue was higher than in adjacent normal tissue. High expression of CDH12 was associated with tumor invasion depth and predicts poor prognosis of CRC patients. Ectopic/repressing expression of CDH12 increased/decreased the proliferation and migration ability of CRC cells. CDH12 is able to increase cancer cell migration and invasion via promoting EMT by targeting transcriptional factor Snail. These findings may conclude that CDH12 may act as a predictor in CRC patients' prognosis and an oncogene in CRC cell proliferation and migration. CDH12 may influence CRC cell progression through promoting EMT by targeting Snail. In addition, CDH12 is promoted by MCP1 through induction of MCPIP.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s13277-015-4555-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4990612PMC
July 2016

PFDN1, an indicator for colorectal cancer prognosis, enhances tumor cell proliferation and motility through cytoskeletal reorganization.

Med Oncol 2015 Dec 9;32(12):264. Epub 2015 Nov 9.

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Prefoldin (PFDN) subunits have been reported upregulated in various tumor types, while the expression and functions of PFDN1 (PFDN subunit 1) in colorectal cancer (CRC) are not well elucidated. The aim of this study was to investigate the use of PFDN1 as a poor prognosis indicator for CRC and explore the functions of PFDN1 in CRC. The relationship between PFDN1 expression and CRC clinical-pathological statistics was detected on the tissue microarray containing 145 cases of CRC. ShRNA was used to silence PFDN1 expression in SW480 and RKO CRC cells, and these transfected cells were analyzed for changes in proliferation, colony formation, cell cycle, migration, and invasion. Immunofluorescence and immunoblot were used to determine the remodeling of the F-actin and α-tubulin. Finally, tumor growth on nude mice was observed and measured. In this study, we found PFDN1 was upregulated in CRC tissues compared with adjacent normal tissues. Also, PFDN1 expression positively correlated with tumor size and tumor invasion. Moreover, after silencing PFDN1 in SW480 and RKO cells, the proliferation and motility of CRC cells were significantly suppressed. The inhibitory effect of PFDN1 on tumor cell growth and motility was partially due to G2/M cell cycle blockage and cytoskeletal deficiency. Finally, in vivo assay showed that downregulation of PFDN1 inhibited tumor growth on nude mice and PFDN1 expression correlated with higher levels of Ki-67 staining. These findings indicate that PFDN1 was involved in the progression of CRC, and provide new insights into PFDN1 as a potential therapeutic target for CRC treatment.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12032-015-0710-zDOI Listing
December 2015

Survival of Colorectal Cancer in Patients With or Without Inflammatory Bowel Disease: A Meta-Analysis.

Dig Dis Sci 2016 Mar 30;61(3):881-9. Epub 2015 Oct 30.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025, China.

Background: Patients with inflammatory bowel disease (IBD) are at increased risk of colorectal cancer (CRC), but little is known about the influence of IBD on CRC prognosis.

Aims: The aim of this study was to perform a meta-analysis to compare survival in CRC patients with IBD (IBD-CRC) and without IBD.

Methods: An electronic search was conducted via PubMed, Embase, and the Cochrane Library to identify eligible trials until July 2015. We pooled the hazard ratios (HRs) and their 95% confidence intervals (CIs) to quantitatively assess the survival of CRC in patients with or without IBD. In addition, clinicopathological parameters of IBD-CRC versus non-IBD CRC were evaluated.

Results: Twelve studies containing a total of 3472 IBD-CRC patients were eligible according to our selection criteria. Our analysis indicated that CRC patients with IBD had shorter overall survival than those without IBD (HR 1.24, 95% CI 1.19-1.29). IBD-CRC showed a propensity to develop in proximal colon [odds ratio (OR) 2.52, 95% CI 1.35-4.72] and correlated with worse differentiation of tumor (OR 1.59, 95% CI 1.26-1.99) compared to non-IBD CRC. Meta-regression analysis showed that sample size (P = 0.002) could explain 99.01% inter-study heterogeneity.

Conclusion: This meta-analysis found poorer overall survival in CRC patients with IBD than CRC patients without IBD, and further prospective research to confirm these findings is warranted.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10620-015-3940-1DOI Listing
March 2016

The metastasis suppressor, NDRG1, inhibits "stemness" of colorectal cancer via down-regulation of nuclear β-catenin and CD44.

Oncotarget 2015 Oct;6(32):33893-911

Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

N-myc downstream-regulated gene 1 (NDRG1), has been identified as an important metastasis suppressor for colorectal cancer (CRC). In this study, we investigated: (1) the effects of NDRG1 on CRC stemness and tumorigenesis; (2) the molecular mechanisms involved; and (3) the relationship between NDRG1 expression and colorectal cancer prognosis. Our investigation demonstrated that CRC cells with silenced NDRG1 showed more tumorigenic ability and stem cell-like properties, such as: colony and sphere formation, chemoresistance, cell invasion, high expression of CD44, and tumorigenicity in vivo. Moreover, NDRG1 silencing reduced β-catenin expression on the cell membrane, while increasing its nuclear expression. The anti-tumor activity of NDRG1 was demonstrated to be mediated by preventing β-catenin nuclear translocation, as silencing of this latter molecule could reverse the effects of silencing NDRG1 expression. NDRG1 expression was also demonstrated to be negatively correlated to CRC prognosis. In addition, there was a negative correlation between NDRG1 and nuclear β-catenin and also NDRG1 and CD44 expression in clinical CRC specimens. Taken together, our investigation demonstrates that the anti-metastatic activity of NDRG1 in CRC occurs through the down-regulation of nuclear β-catenin and suggests that NDRG1 is a significant therapeutic target.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.18632/oncotarget.5294DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741810PMC
October 2015

Contrasting Sleeve Gastrectomy with Lifestyle Modification Therapy in the Treatment of Polycystic Ovary Syndrome.

J Laparoendosc Adv Surg Tech A 2015 Jun 8;25(6):493-8. Epub 2015 May 8.

2 Department of Gastroenterological Surgery, Shanghai East Hospital, Tongji University School of Medicine , Shanghai, China .

Aims: To explore the feasibility of sleeve gastrectomy (SG) as a treatment for polycystic ovary syndrome (PCOS) and its potential to improve clinical efficacy in PCOS patients with symptoms of oligomenorrhea.

Patients And Methods: Twenty-four obese patients with PCOS underwent laparoscopic SG. Simultaneously, 24 obese patients with PCOS received lifestyle modification therapy (LMT). Follow-ups were conducted at 3-6 months. Weight loss, menstruation, and improvements in hirsutism and metabolic symptoms were compared.

Results: In the SG group, 20 patients were restored to normal menstrual cycles and ovulation at 3-6 months after surgery. Their average androgen levels decreased significantly following surgery (P=.012). Conversely, only 6 patients in the LMT group were restored to normal menstrual cycles and ovulation after receiving 3 months of treatment. Their average preoperative and postoperative androgen levels showed a nonstatistically significant decrease (P>.05). Compared with the LMT group, the SG group showed more pronounced improvements in menstruation. Additionally, body mass and body mass index were significantly reduced in patients in the SG group 3 months after the surgeries, with maximum weight loss observed at approximately 6 months after surgery. Patients who received LMT showed a gradual weight reduction such that body mass decreased significantly after 3 months (P<. 001). Compared with patients in the LMT group, patients in the SG group showed greater weight loss results (P<.0001).

Conclusions: In patients with PCOS, SG resulted in more marked weight loss and better improvements in clinical symptoms compared with LMT.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/lap.2014.0511DOI Listing
June 2015

Plasma 25-hydroxyvitamin D levels and survival of colorectal cancer patients: a meta-analysis.

Eur J Cancer 2015 Apr 4;51(6):786-8. Epub 2015 Mar 4.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address:

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ejca.2015.01.010DOI Listing
April 2015

Lentivirus-mediated knockdown of rhomboid domain containing 1 inhibits colorectal cancer cell growth.

Mol Med Rep 2015 Jul 17;12(1):377-81. Epub 2015 Feb 17.

Department of Gastroenterology, Shanghai East Hospital, Tongji University, Shanghai 200120, P.R. China.

Rhomboid domain containing 1 (RHBDD1), is a member of the rhomboid protease family, which has a pivotal role in the progression of numerous severe malignancies. However, its role in colorectal carcinoma (CRC) remains to be elucidated. In the present study, RHBDD1 was shown to be widely expressed in CRC cell lines. Lentivirus-mediated RNA interference was employed to knockdown RHBDD1 expression in RKO CRC cells. Functional analyses indicated that depletion of RHBDD1 expression resulted in significantly reduced CRC cell proliferation and colony formation, and induced a G0/G1 phase cell cycle arrest. The findings of the present study suggest that RHBDD1 may contribute to CRC tumorigenesis and serve as a potential therapeutic target in human CRC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/mmr.2015.3365DOI Listing
July 2015

CC motif chemokine ligand 19 suppressed colorectal cancer in vivo accompanied by an increase in IL-12 and IFN-γ.

Biomed Pharmacother 2015 Feb 24;69:374-9. Epub 2014 Dec 24.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No. 197 Second Ruijin Road, Shanghai, China. Electronic address:

In this study we investigate the role of CC motif chemokine ligand 19 (CCL19) to colorectal cancer (CRC) in vivo. We injected different dose of recombinant mouse CCL19 (rmCCL19) in the tumor site of the model of transplanted tumor. Result shows that rmCCL19 can suppress CRC tumorigenesis and growth in vivo, and it can also prolong overall survival of mice. Quantitative reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay results showed that the interferon-γ (IFN-γ) and interleukin-12 (IL-12) levels in the tumors and plasma were significantly enhanced after processing with rmCCL19.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2014.12.032DOI Listing
February 2015

Day surgery management model in china: practical experience and initial evaluation.

Int J Clin Exp Med 2014 15;7(11):4471-4. Epub 2014 Nov 15.

Department of General Surgery, Shanghai East Hospital Affiliated to Tongji University 150 Jimo Road, Shanghai 200120, China.

Objectives: Day surgery has been increasingly performed in some major teaching hospitals in China. We aimed to evaluate the current day surgery management model (DSMM) and compare the clinical outcome and health service utility of day surgery with inpatient surgery.

Methods: We reviewed 14482 day surgery cases under the DSMM and 2591 inpatient surgery cases under the non-DSMM between September 2006 and September 2012 in Shanghai East Hospital. The endpoints of interest were hospitalization days, incision infection rate and hospital cost.

Results: Among 14482 day surgery cases, only 52 (0.4%) were converted to hospitalization. The average hospitalization time of the patients was 2-10 hours. None of them had incision infection. Hospital cost of DSMM was less than 50% of non-DSMM (inpatient surgery). The most common postoperative complications were nausea, vomiting and dizziness. Nearly half of patients had mild to moderate pain after surgery.

Conclusions: DSMM optimizes the utilization of healthcare resources by reducing hospital admission, hospital cost and incision infection in China.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276229PMC
December 2014

Tetrandrine induces apoptosis in gallbladder carcinoma in vitro.

Int J Clin Pharmacol Ther 2014 Oct;52(10):900-5

Objective: The aims of this study were to observe the apoptosis effects of tetrandrine on human gallbladder carcinoma cell line (SGC-996), and to explore its related mechanism.

Methods: First, the anti-proliferative activities of tetrandrine on SGC-996 cells were determined by using the MTT assays. Then, cell cycle changes were detected by flow cytometry analysis. The apoptosis of cells was detected by the annexin V/propidium iodide double-staining assay. Detection of mitochondrial membrane potential was used to validate the ability of tetrandrine on inducing apoptosis. Finally, the expressions of the apoptosis-related proteins (caspase-3, PARP, Bcl-2, and Bax) were analyzed by western blot. Statistical analyses were performed using the Student’s t-test for comparison of the results obtained from cells with or without treatment of tetrandrine.

Results: The MTT assay revealed a significant inhibition of cell proliferation in a dose- and time-dependent manner. Cells treated with tetrandrine were arrested at the S phase, according to the flow cytometric analysis. Tetrandrine produced a dose-dependent increase in the apoptotic cell population compared with control cells. Tetrandrine can also affect mitochondrial function by changing the mitochondrial membrane potential. Furthermore, western blot assay demonstrated that the tetrandrine induced apoptosis in SGC-996 cells by regulating the ratio of Bcl-2/Bax and activating the expression of cleaved caspase-3.

Conclusions: The results indicate that tetrandrine may be a potential agent for the treatment of gallbladder carcinoma.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.5414/CP202123DOI Listing
October 2014

Antitumor efficacy of CC motif chemokine ligand 19 in colorectal cancer.

Dig Dis Sci 2014 Sep 5;59(9):2153-62. Epub 2014 Apr 5.

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, No. 197 Second Ruijin Road, Shanghai, China.

Objectives: To investigate the function of CC motif chemokine ligand 19 (CCL19) in colorectal cancer (CRC).

Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blot and immunohistochemistry were performed separately to detect the expression of CCL19 in colorectal carcinoma tissues. The expression of CCL19 and its receptor (CCR7) in CRC cell lines were screened by Western blot. SW620, SW1116 and LoVo cell lines were screened and processed with recombinant human CCL19 (rhCCL19) or si-CCL19 RNA. Cell proliferation assay and transwell assay were performed to evaluate the proliferation, migration and invasion of CRC cells, respectively. And the role of proangiogenesis was checked by endothelial tube formation assay.

Results: qRT-PCR, Western blot and immunohistochemistry revealed that both CCL19 mRNA and protein were obviously expressed in a lower degree in CRC tissues than normal tissues (P < 0.01). The CCL19 expression correlated with tumor size (P = 0.03) and invasion depth (P = 0.04) in a negative manner and CCL19-positive patients had longer lifespans (P < 0.05). SW620 and SW1116 cells were screened as CCL19/CCR7 high-expression cells, while LoVo was selected as CCL19/CCR7 low-expression cell among seven CRC cell lines by Western blot. The proliferation, migration, invasion and proangiogenesis of SW620 and SW1116 cells were distinctly suppressed after they were stimulated by rhCCL19 (P < 0.05), and the data presented dose-dependency. Oppositely, these abilities were significantly enhanced after CCL19 gene was silenced (P < 0.05). However, the effects of rhCCL19 and si-CCL19 RNA on LoVo were not significant (P > 0.05).

Conclusion: Our research findings indicate that CCL19 may play a suppressive role in colorectal tumorigenesis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10620-014-3138-yDOI Listing
September 2014

Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis.

J Transl Med 2013 Nov 15;11:288. Epub 2013 Nov 15.

Shanghai Minimally Invasive Surgery Center, Shanghai Key Laboratory of Gastric Neoplasms, Department of Surgery, Shanghai Institute of Digestive Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, 197 Rui Jin Er Rd, Shanghai 200025, People's Republic of China.

Background: Cadherin 12 (CDH12), which encodes a type II classical cadherin from the cadherin superfamily, may mediate calcium-dependent cell adhesion. It has been demonstrated that CDH12 could play an important role in the invasion and metastasis of salivary adenoid cystic carcinoma. We decided to investigate the relationship between CDH12 expression level and clinicopathologic variables in colorectal carcinoma (CRC) patients and to explore the functions of CDH12 in tumorigenesis in CRC.

Methods: The expression levels of CDH12 in colorectal carcinoma tissues were detected by immunohistochemistry. Real-time PCR and Western Blot were used to screen CDH12 high-expression cell lines. CCK-8 assay was used to detect the proliferation ability of CRC cells being transfected by shRNAs against CDH12. The wound assay and transwell assay were performed to test migration and invasion ability. The importance of CDH12 in cell-cell junctions was detected by cell adhesion assay and cell aggregation assay. Endothelial tube formation assay was used to test the influence of CDH12 on angiogenesis.

Results: Statistical analysis of clinical cases revealed that the positive rate of CDH12 was higher in the CRC tumor tissues compared with the adjacent non-tumor tissues. The expression levels of CDH12 in CRC patients are significantly correlated with invasion depth. Consistently, the ability of proliferation, migration and invasion were suppressed when CDH12 was decreased in CRC cells transfected with shRNAs. Cell adhesion assay and cell aggregation assay presented that tumor cells tend to disperse with the lack of CDH12. Endothelial tube formation assay showed that down-regulation of CDH12 could obviously inhibit the process of angiogenesis, implying that CDH12 may play an important role in tumor metastasis

Conclusion: Our results showed that CDH12 promotes proliferation, migration, invasion, adhesion and angiogenesis, suggesting that CDH12 may be an oncogene in colorectal cancer. CDH12 is expected to become a new diagnostic and prognostic marker and a novel target of the treatment of colorectal cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1479-5876-11-288DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3879717PMC
November 2013

TXNDC9 expression in colorectal cancer cells and its influence on colorectal cancer prognosis.

Cancer Invest 2012 Dec;30(10):721-6

Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai, China.

In this study, we analyzed the protein expression of thioredoxin domain containing 9 (TXNDC9) in 116 colorectal cancer (CRC) cases. Among them, 97 were positive in CRC tissues and 60 were positive in normal mucosa. TXNDC9 expression in CRC was correlated with the extent of tumor invasion and the tumor size. TXNDC9-negative patients had longer lifespans. In vitro assays showed the significant suppression of CRC cell proliferation (P < .01) compared with two control groups; the number of invaded cells also decreased (P < .01). These findings suggest that TXNDC9 gene may function in cancer development and may be an effective target for inhibiting the growth and metastasis of CRC cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3109/07357907.2012.732160DOI Listing
December 2012

Surgical treatment for xanthogranulomatous cholecystitis: a report of 74 cases.

Surg Laparosc Endosc Percutan Tech 2009 Jun;19(3):231-3

Department of Surgery, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine, Shanghai Minimally Invasive Surgery Centre, Shanghai, PR China.

Aims: To be more aware of the presence of xanthogranulomatous cholecystitis (XGC) and find a better surgical measure of its treatment.

Methods: Data from 74 cases of XGC treated between May 1996 and May 2008 at our hospital were retrospectively analyzed and reported here. Laparoscopic and laparotomy group were compared with respect to operative time, postoperative hospital stay, postoperative complication, etc.

Results: In the 74 cases, 47 underwent laparoscopic surgery, the rest 27 underwent laparotomy surgery. The mean operative time of laparotomy and laparoscopic cases were 113.9 minutes and 69.4 minutes, respectively, which shows statistically significant difference between the 2 groups (P<0.01). The postoperative hospital stay of the laparotomy and laparoscopic group is 18.3 days and 8.66 days, respectively (P<0.01). The converting rate of the laparoscopic group is 10.6%.

Conclusions: Surgical treatment remains the most effective and feasible option for XGC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/SLE.0b013e3181a822f8DOI Listing
June 2009

Effect of endoscopic thyroidectomy via anterior chest wall approach on treatment of benign thyroid tumors.

J Laparoendosc Adv Surg Tech A 2009 Apr;19(2):149-52

Shanghai Minimally Invasive Surgery Center, Surgery Department, Shanghai Ruijin Hospital affiliated with Shanghai JiaoTong University Medical School, Shanghai, China.

Objective: The aim of this study was to evaluate the inflammatory response and acid-base equilibrium index, as well as other clinical facts of the endoscopic thyroidectomy via the anterior chest wall approach.

Methods: Thirty-nine patients who received thyroidectomy in our surgical center during September 2007 and January 2008 were included in this study. Twenty of the patients underwent an endoscopic surgery, and the remaining 19 received conventional surgery. These patients' data were compared within and between treatment groups with respect to clinical facts and inflammatory evaluations. Arterial blood gas data and electrolyte data were analyzed within the endoscopic group.

Results: Endoscopic thyroidectomy group showed shorter operative time, compared to that of the conventional thyroidectomy group, although the difference didn't reach statistical significance. No significant difference regarding postoperative hospital stay was observed between two groups. Postoperative day 1 shows much higher values of interleukin-6 and tumor necrosis factor than that measured preoperative or postoperative day 3 in both groups. C-reactive protein appeared to be significantly increased postoperatively in both groups, although no difference between the two groups was found. Although blood cortisol significantly increased in both groups postoperatively, the data of endoscopic group postoperative day 1 was lower than the same day of the conventional group. Arterial blood gas analysis showed that both PCO2 and TCO2 were statistically different between preoperation and 30 minutes after insufflation. No insufflation complication was observed.

Conclusion: Compared with conventional thyroid surgery, endoscopic thyroidectomy via the anterior chest wall approach presented with no significant difference in respect of both clinical facts and laboratory outcomes.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/lap.2008.0296DOI Listing
April 2009

Duodenal perforations after endoscopic retrograde cholangiopancreatography: experience and management.

J Laparoendosc Adv Surg Tech A 2008 Oct;18(5):691-5

Department of General Surgery, Shanghai Minimally Invasive Surgery Center, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China.

Objective: The aim of this study was to summary the experiences and lessons from periduodenal perforations related to endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic sphincterotomy (EST).

Methods: A retrospective review from 2004 to 2007 identified 9 patients (0.37%) of periduodenal perforation related to ERCP/EST. Charts were reviewed for the following parameters: clinical presentation of patients, ERCP findings, diagnostic methods, treatment (surgical or conservative procedures), complications, and outcome.

Results: Nine patients who had periampullary perforations received ERCP/EST for common bile duct stones. Cannulation was considered difficult in 7 of 9 patients, and the precut technique was used. The diagnosis was made due to subcutaneous emphysema or peritonitis, and 3 patients received emergent operations (e.g., external biliary or retroperitoneal drainage), and 1 patient had a reoperation for a retroperitoneal sealed abscess. Their median length of hospital stay was 50 days. The other 6 were treated conservatively with nasal-duodenal and nasal-biliary drainage. Their median length of hospital stay was 13 days. There was no mortality.

Conclusions: The precut technical may be a risk factor of duodenal perforation. Early diagnosis of duodenal perforation is essential for an optimum outcome, and subcutaneous emphysema may be a sensitive sign. Although the management of perforation after ERCP/EST is still controversial, a selective management is proposed, based on the features of classification type. Nevertheless, duodenal and biliary drainage is essential in both surgical and conservative therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/lap.2008.0020DOI Listing
October 2008