Short-term efficacy of da Vinci robotic surgical system on rectal cancer in 101 patients / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the feasibility and safety of da Vinci robotic surgical system in rectal cancer radical operation, and to summarize its short-term efficacy and clinical experience.</p><p><b>METHODS</b>Data of 101 cases undergoing da Vinci robotic surgical system for rectal cancer radical operation from March 2010 to September 2012 were retrospectively analyzed. Evaluation was focused on operative procedure, complication, recovery and pathology.</p><p><b>RESULTS</b>All the 101 cases underwent operation successfully and safely without conversion to open procedure. Rectal cancer radical operation with da Vinci robotic surgical system included 73 low anterior resections and 28 abdominoperineal resections. The average operative time was (210.3±47.2) min. The average blood lose was (60.5±28.7) ml without transfusion. Lymphadenectomy harvest was 17.3±5.4. Passage of first flatus was (2.7±0.7) d. Distal margin was (5.3±2.3) cm without residual cancer cells. The complication rate was 6.9%, including anastomotic leakage(n=2), perineum incision infection(n=2), pulmonary infection (n=2), urinary retention (n=1). There was no postoperative death. The mean follow-up time was(12.9±8.0) months. No local recurrence was found except 2 cases with distant metastasis.</p><p><b>CONCLUSION</b>Application of da Vinci robotic surgical system in rectal cancer radical operation is safe and patients recover quickly The short-term efficacy is satisfactory.</p>

Robotic-assisted radical gastrectomy using da Vinci robotic system: a report of 41 cases / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the feasibility and safety of da Vinci robotic-assisted radical gastrectomy for gastric cancer.</p><p><b>METHODS</b>Forty-one patients with gastric cancer from Southwest Hospital between March 2010 and December 2011 underwent da Vinci robotic-assisted radical gastrectomy including total gastrectomy(n=12) and distal gastrectomy (n=29).</p><p><b>RESULTS</b>Conversion was required in two patients. One was converted to open surgery, and the other to conventional laparoscopic surgery. The remaining thirty-nine patients underwent da Vinci robotic-assisted radical gastrectomy successfully. The mean operative time was (285±61) min for total gastrectomy, and (225±39) min for distal gastrectomy. The mean blood loss was (180±157) ml in total gastrectomy, and (150±127) ml in distal gastrectomy. The mean number of harvested lymph nodes was 34.2±18.5. The mean time for gastrointestinal function recovery was (3.1±1.2) days. The time to ambulation was (2.7±1.5) days. The time to oral liquid intake was (3.7±1.5) days. Two patients had complication including wound infection and pneumonia. After follow up ranging from 1 to 21 months (median 11 months), 4 patients died from peritoneal metastasis, 1 survived with tumor, and the remaining 36 patients survived without disease.</p><p><b>CONCLUSIONS</b>da Vinci robotic-assisted radical gastrectomy is a feasible and safe surgical procedure with clear operation field, precise dissection, minimal trauma and fast recovery.</p>

Effects of hypoxia-inducible factor-1α on human gastric cancer cell apoptosis under in vitro CO(2) pneumoperitoneum environment / 中华外科杂志

<p><b>OBJECTIVE</b>To study the effect of hypoxia-inducible factor-1α (HIF-1α) on human gastric cancer cells apoptosis in simulated CO2 pneumoperitoneum environment.</p><p><b>METHODS</b>Applied closed box to simulated CO2 pneumoperitoneum environment under the pressure of 0, 5, 10 and 15 mm Hg (1 mm Hg = 0.133 kPa). Compared HIF-1α mRNA and protein expression of MKN-45 cells before and after silencing HIF-1α by RT-PCR and Western blot. Study the changes of bcl-2/bax expression in MKN-45 cells before and after silencing HIF-1α by immunohistochemistry. The apoptosis ratio of MKN-45 was measured by using Annexin V-FITC/PI double labelled staining.</p><p><b>RESULTS</b>In 15 mm Hg group, HIF-1α mRNA and protein expression of MKN-45 cells (1.48 ± 0.22, 1.34 ± 0.09) and HIF-1α protein expression in 10 mm Hg group (1.25 ± 0.10) were significantly higher than those in control group (0.55 ± 0.17, 0.83 ± 0.04) (P < 0.05). But there was no significant differences among 0, 5, 10 mm Hg group and control group in HIF-1α mRNA (P > 0.05); and no obvious difference was found among 0, 5 mm Hg group and the control group in HIF-1α protein expression (P > 0.05). In 15 mm Hg CO2 pressure, bcl-2/bax expression (0.78 ± 0.05) was obviously lower than that in the control group (1.43 ± 0.15) (P < 0.05) and the apoptosis ratio (11.70 ± 0.12) was significantly higher than the control group (0.22 ± 0.07) (P < 0.01) before silencing HIF-1α. But once HIF-1α was silenced, HIF-1α mRNA (0.52 ± 0.11), HIF-1α protein expression (0.92 ± 0.02), bcl-2/bax ratio (1.57 ± 0.04) and apoptosis ratio (0.45 ± 0.11) in MKN-45 were not significantly different between 15 mm Hg group and the control group (P > 0.05).</p><p><b>CONCLUSIONS</b>The apoptosis ratios of MKN-45 under 0, 5, 10 mm Hg CO2 pneumoperitoneum are comparable with that in the control group before the silencing of HIF-1α. The apoptosis ratio of MKN-45 is increased under 15 mm Hg CO2 pneumoperitoneum environment and HIF-1α may be one of the important factor to improve the apoptosis of human gastric cancer cell.</p>

Influence of CD4+ and CD25+ T regulatory cell on mouse bearing gastric tumor in vivo / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the influence of CD4+ CD25+ regulatory T cells(Treg cells) on mouse gastric cancer.</p><p><b>METHODS</b>Treg cell in mouse spleen bearing gastric tumor was tested in different time points. Magic cell sorting(MACS) method was used to purify mouse Treg cells and the Treg cells were injected into mouse bearing gastric tumor with different dosage. After 3 weeks, the tumor size and tumor cell apoptosis rate were measured.</p><p><b>RESULTS</b>Treg existed in normal mouse spleen with a rate of (3.86+/-0.07)%. In tumor model this percentage increased gradually and was (4.12+/-0.13)% after 3 weeks, which was significantly higher than that in control. When Treg cell applied in mouse reached 2.0 x 10(5), the tumor size enlarged significantly(P=0.013) and tumor cell apoptosis rate decreased significantly (P=0.012).</p><p><b>CONCLUSIONS</b>Treg cell is associated with gastric cancer progress in mouse tumor model. Treg cell can promote gastric cancer growth and decrease tumor apoptosis. The anti- Treg GITR can improve anti- tumor effects.</p>

Transcription regulation of 5-Aza-2'-deoxycytidine on maspin gene demethylation in RKO human colorectal cell line / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To detect the methylation status of 5'CpG island in the core promotor of maspin gene in RKO human colorectal cell line,and to explore the transcription regulation of DNA 5'CpG island demethylation on maspin tumor suppressor gene and its effect on the growth of cancer cell.</p><p><b>METHODS</b>The status of 5 'CpG island methylation of maspin gene in RKO human colorectal cell line was analyzed using methylation specific polymerase chain reaction (MSP). After treated with a specific demethylating agent, 5-Aza-2'-deoxycytidine, reverse transcription polymerase chain reaction (RT- PCR) was used to examine maspin gene expression. Cell proliferation was evaluated using MTT assay,distribution of cell cycle and rate of apoptosis were determined using flow cytometry.</p><p><b>RESULTS</b>The 5'CpG island methylation in the core promotor of maspin gene was detected in RKO human colorectal cell line. After treatment with three different concentration of 5-aza-2'-deoxycytidine, the expression of maspin mRNA increased 10.89, 16.91, 23.97 times respectively. MTT array showed the proliferation activity of RKO cell line was obviously reduced after 5-aza-2'-deoxycytidine treatment. The cells were arrested in G(0)/G(1) phase,and the apoptosis rates were 5.17%, 8.71% and 11.23% respectively compared with control group.</p><p><b>CONCLUSION</b>The 5'CpG island methylation is probably responsible for maspin expression silencing in RKO human colorectal cell line, 5-aza-2'-deoxycytidine may effectively cause demethylation and inhibit the growth of tumor cell by reactivating the gene transcription silenced by aberrant hypermethylation.</p>