Clinical application of laparoendoscopic single-site surgery for colorectal cancer: a randomized controlled trial.
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer
PROVIDER: 2701750 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
Similar Datasets
Project description:Interventions: group A:Closure of pelvic floor peritoneum;group B:No closure of pelvic floor peritoneum
Primary outcome(s): Intraoperative conditions: operation time, closure of the pelvic floor peritoneal suture time, intraoperative blood loss;Postoperative complications: perineal incision infection, abdominal infection, abdominal bleeding or perineal incision bleeding, radioactive enteritis, intestinal fistula, vaginal fistula, bladder fistula obstruction, recurrent intestinal obstruction requiring surgical intervention, and the incidence of perineal hernia, parastomal hernia, reoperation 
Study Design: Randomized parallel controlled trial
| 2663460 | ecrin-mdr-crc
Project description:Cartilage destruction in osteoarthritis (OA) results from disturbed chondrocyte metabolism. Here, we used microarrays to show that TGF alpha and CCL2 are simultaneously upregulated in a rat model of OA and cooperate to drive cartilage degradation. The goals of the experiments included here were to a) characterize gene expression in knee joint articular chondrocytes at various stages of development of OA (2 and 8 weeks after surgical induction of OA), and b) to establish trends in gene expression among groups of genes related to the TGF alpha-EGFR axis, over time, in OA. The model chosen to study these results has been previously validated (Appleton, CT et al, 2007, Arthritis Rheum) and used to describe similar gene expression results at a different time point (4 weeks) after induction of OA. The rat model of OA involves surgical destabilization of the knee joint, followed by forced low-intensity mobilization over several weeks; a sham surgery is used as the control (representing a healthy non-OA knee joint) wherein a surgical incision is made but not structural (i.e. ligamentous) modification is made to the joint. Altogether, our data indicate that TGF and CCL2 cooperate to drive cartilage degradation in osteoarthritis. A total of 12 samples were analyzed. 3 replicates were used per condition: OA surgery at 2 weeks, OA surgery at 8 weeks, Sham (control) surgery at 2 weeks and Sham surgery at 8 weeks. Expression of OA samples was assessed relaitve to Sham (control) expression levels.
2012-11-15 | E-GEOD-42295 | biostudies-arrayexpress
Project description:Cartilage destruction in osteoarthritis (OA) results from disturbed chondrocyte metabolism. Here, we used microarrays to show that TGF alpha and CCL2 are simultaneously upregulated in a rat model of OA and cooperate to drive cartilage degradation. The goals of the experiments included here were to a) characterize gene expression in knee joint articular chondrocytes at various stages of development of OA (2 and 8 weeks after surgical induction of OA), and b) to establish trends in gene expression among groups of genes related to the TGF alpha-EGFR axis, over time, in OA. The model chosen to study these results has been previously validated (Appleton, CT et al, 2007, Arthritis Rheum) and used to describe similar gene expression results at a different time point (4 weeks) after induction of OA. The rat model of OA involves surgical destabilization of the knee joint, followed by forced low-intensity mobilization over several weeks; a sham surgery is used as the control (representing a healthy non-OA knee joint) wherein a surgical incision is made but not structural (i.e. ligamentous) modification is made to the joint. Altogether, our data indicate that TGF and CCL2 cooperate to drive cartilage degradation in osteoarthritis.
2012-11-15 | GSE42295 | GEO
Project description:Interventions: experimental group:SMA-guided lymph node dissection;control group:SMV-guided lymphatic dissection
Primary outcome(s): Operation time;Amount of bleeding;Conversion rate of laparotomy;Number of lymph nodes obtained;First anal exhaust time;First time out of bed;Drainage flow of drainage tube;indwelling time of drainage tube;Incidence of postoperative short-term complications;Rate of re-hospitalization 30 days after surgery;Rate of mortality 30 days after surgery;Local recurrence rate;Median disease-free survival time;Median overall survival time
Study Design: Case-Control study
| 40635 | ecrin-mdr-crc
Project description:Longitudinal RNASeq of rat plantar surgical incision model
| PRJNA777619 | ENA
Project description:Two female pigs weighing 40-55 kg were used. Each animal had four 4-cm midline caudal abdominal incisions created with the test devices. The test devices were monopolar electrosurgery (Electrocautery Pencil, ConMed, Utica NY) and Harmonic blade (HK105, Ethicon Endo-Surgery, Cincinnati OH). Each animal had two Harmonic Blade incisions and two Electrosurgery incisions for a total of 8 incisions. The incisions were created by marking the site on the ventral aspect of the abdomen and identified by level from cranial to caudal, as incision A, B, C and D respectively. The incision was started with a scalpel blade through the skin (epidermis and dermis). Each incision was deepened through the subcutaneous tissues down to the linea alba using the Harmonic at power level 5 for cutting tissue and power level 3 for coagulating bleeders, or electrosurgery set at 40 Watts for cutting and Blend 2/Spray for coagulation. The linea alba was not incised. Closure of the incision was accomplished by apposing the skin with 3-0 nylon in a simple interrupted pattern. Dermabond was then applied to seal the epidermis. No bandages were applied to the incisions. After three days, incision sites were removed en bloc from the abdominal wall. The tissue block was sliced perpendicular to the surgically incision to create slabs 4-6 mm thick. The slab was trimmed to remove the skin from the top and muscle from the bottom of the sample. The side walls were trimmed to approximately 4 mm from the surgical incision leaving a rectangular block of subcutaneous fatty tissue. Four to six samples were taken from each incision. Animals were then euthanized. Samples for genomics and proteomics analysis were placed in sterile DNAse-, RNAse-, protein-free Eppendorf tubes, flash frozen in liquid nitrogen, held on dry ice throughout tissue collection, and then stored at -80 C. Tissue samples were also collected in 10% neutral buffered formalin for histopathology analysis.
2014-04-15 | PXD000038 | Pride
Project description:Samples were prospectively collected from patients with histologically normal surgical resection margins. 96 tissue samples (histologically normal margins, oral carcinoma and adjacent normal tissues) from 24 patients comprised the training set. Our study design was guided by the hypothesis that the expression of genes present in oral squamous cell carcinoma (OSCC) but not in healthy oral tissues would be indicative of recurrence in advance of histological alteration. We used meta-analysis of five published microarray data sets (GEO accession GDS2520, Kuriakose et al. 2004; GDS1584, Toruner et al. 2004; GSE6791, Pyeon et al. 2007; GSE9844, Ye et al. 2008; and GSE10121, Sticht et al. 2008), in conjunction with the current training set, to identify genes reliably over-expressed in OSCC. This reduced gene set was used to train a risk model to predict recurrence based on over-expression of a subset of these genes in histologically normal surgical resection margins. Validation of the risk signature was performed using quantitative real-time reverse-transcription PCR in an independent set of 136 samples from an independent cohort of 30 patients.
2011-08-03 | GSE31056 | GEO
Project description:Transcriptomic analyses of dorsal spinal cord after surgical incision.
| PRJNA412076 | ENA
Project description:Samples were prospectively collected from patients with histologically normal surgical resection margins. 96 tissue samples (histologically normal margins, oral carcinoma and adjacent normal tissues) from 24 patients comprised the training set. Our study design was guided by the hypothesis that the expression of genes present in oral squamous cell carcinoma (OSCC) but not in healthy oral tissues would be indicative of recurrence in advance of histological alteration. We used meta-analysis of five published microarray data sets (GEO accession GDS2520, Kuriakose et al. 2004; GDS1584, Toruner et al. 2004; GSE6791, Pyeon et al. 2007; GSE9844, Ye et al. 2008; and GSE10121, Sticht et al. 2008), in conjunction with the current training set, to identify genes reliably over-expressed in OSCC. This reduced gene set was used to train a risk model to predict recurrence based on over-expression of a subset of these genes in histologically normal surgical resection margins. Validation of the risk signature was performed using quantitative real-time reverse-transcription PCR in an independent set of 136 samples from an independent cohort of 30 patients. This was a case-only design involving a training set of 23 tumors and 73 margins from 24 patients with squamous cell carcinoma of the tongue.
2011-08-02 | E-GEOD-31056 | biostudies-arrayexpress
Project description:Background: CrohnM-bM-^@M-^Ys disease is presently an incurable inflammatory bowel disease. Fistulae are extensions of the intestinal tract that may form connections with other organs. These are a common complication of CrohnM-bM-^@M-^Ys disease affecting up to 50% of patients with the most common including perianal and rectovaginal fistulae. The dysregulated growth observed in fistulae shares several major characteristics seen in the development of tumours. These similarities include epithelial-to-mesenchymal transition (EMT), invasive cell growth, increased extracellular matrix production and remodelling, up-regulated local expression of growth factors such as IGF-1 and the down-regulation of apoptosis pathways. Although several susceptibility loci have been described within CrohnM-bM-^@M-^Ys disease there is no individual gene or mutation that identifies susceptibility or the subsequent formation of fistulae within all people. Copy-number variation (CNV) is one mechanism that may explain much of this genetic complexity. CNV may be caused by a variety of mechanisms such as cycles of chromosomal breakage/fusion/bridging that are typical within chronically inflamed tissue. Interestingly CNV shows locus-specific mutation rates between individuals higher than that of SNPs and has been associated with complex Mendelian traits including disease susceptibility. In this current study we performed array comparative genomic hybridisation (aCGH) analysis of active fistulae resected from patients as part of a previous surgical intervention. As the control for comparison we employed tissue taken from the same patient within the same surgery at an uninvolved site of the gastrointestinal tract. This matched control was employed to better investigate CNV specific to the fistula tissue of each individual avoiding complications associated with the large number of CNV present within the healthy population. Major question addressed by the work: What are the differences in genetic copy-number within localised intestinal fistula tissue of individuals with CrohnM-bM-^@M-^Ys disease compared to healthy intestinal tissue from the same individual? Samples were selected from patients presenting with CrohnM-bM-^@M-^Ys Disease fistulae at Eastern Health Department of Gastroenterology and Hepatology (Arnold Street, Box Hill, Victoria, Australia). The 8 samples used in this study were formalin-fixed paraffin-embedded (FFPE) specimens following a surgical intervention to remove fistula tissue. To focus on changes within the individual patient we used tissue taken from the same surgery at an uninvolved region of the intestine as the matched control for CNV analysis.
2014-07-01 | E-GEOD-44275 | biostudies-arrayexpress