[Clinical study of different bowel preparations on changes of gut flora in patients undergoing colorectal resection].

OBJECTIVE: To compare the impact of traditional and fast bowel preparation on the changes of gut flora in the patients following colorectal resection. METHODS: Sixty patients undergoing colorectal resection from March 2010 to March 2011 in the Nanfang Hospital were randomly divided into the control group(n=27, 3 days of bowel preparation) and the experimental group(n=33, 1 day of bowel preparation). Fresh feces were collected before bowel preparation and on the first defecation after surgery. The postoperative changes in gut flora and septic complications were observed. RESULTS: Gut flora disturbance was found in both groups. The postoperative population of Bifidobacterium and Lactobacillus decreased significantly(P<0.05), and the decrease was more significant in the experimental group compared to the control group(P<0.05), while E.coli and Staphylococcus were much higher than the preoperative level(P<0.05), which was more significant in the control group. The incidence of postoperative infection was 9.1%(3/33) in the experimental group, which was significantly lower than 29.6%(8/27) in the control group(P<0.05). CONCLUSION: Fast bowel preparation is effective in reducing gut flora disturbance and the incidence of postoperative infection.

Screening peptides binding specifically to colorectal cancer cells from a phage random peptide library.

The aim of this study was to screen for polypeptides binding specifically to LoVo human colorectal cancer cells using a phage-displayed peptide library as a targeting vector for colorectal cancer therapy. Human normal colorectal mucous epithelial cells were applied as absorber cells for subtraction biopanning with a c7c phage display peptide library. Positive phage clones were identified by enzyme-linked immunosorbent assay and immunofluorescence detection; amino acid sequences were deduced by DNA sequencing. After 3 rounds of screening, 5 of 20 phage clones screened positive, showing specific binding to LoVo cells and a conserved RPM motif. Specific peptides against colorectal cancer cells could be obtained from a phage display peptide library and may be used as potential vectors for targeting therapy for colorectal cancer.

[MicroRNA-221 promotes colon carcinoma cell proliferation in vitro by inhibiting CDKN1C/p57 expression].

OBJECTIVE: To investigate the regulatory effect of microRNA-221 (MIR221) on CDKN1C/p57 expression in colon carcinoma cells in vitro. METHODS: Caco2 cells were treated with or without anti-p57-siRNA prior to the addition of pre-MIR221 or anti-MIR221. The MIR221 expression pattern was detected by real-time RT-PCR, and the mRNA and protein levels of CDKN1C/p57 expression were detected using semi-quantitative RT-PCR and Western blotting. Caco2 cell proliferation following the treatment was detected with MTT assay. CDKN1C/p57 3'-UTR fragment was amplified by PCR from the genome DNA of human colon and inserted into a luciferase reporter plasmid. The luciferase reporter plasmid construct was then transfected into Caco2 cells along with pre-MIR221 or anti-MIR221, and the luciferase activity in the transfected cells was detected. RESULTS: MIR221-specific inhibitor significantly up-regulated CDKN1C/p57 protein expression in Caco2 cells (P<0.01). Anti-MIR221 could markedly inhibit Caco2 cell proliferation, and the inhibitory effect was obviously abolished by pretreatment with anti-p57-siRNA, suggesting that the inhibition was mediated by CDKN1C/p57 (P<0.01). A significant increase of luciferase activity was detected in Caco2 cells co-transfected with the luciferase reporter plasmid construct and anti-MIR221 (P<0.01). CONCLUSIONS: MIR221 can interact with the target site on the 3'-UTR of CDKN1C/p57 mRNA to inhibit CDKN1C/p57 expression by post-transcriptional gene silencing to promote colon carcinoma cell proliferation, suggesting the value of MIR221 as a potential target for treatment of colon carcinoma.

[MicroRNA-221 controls CDKN1C/P57 expression in human colorectal carcinoma].

OBJECTIVE: To investigate the expression of microRNA-221 (miR-221) and CDKN1C/P57 in colorectal carcinoma (CRC) and adjacent non-cancerous tissues. The effect of miR-221-specific inhibitor on cell proliferation and apoptosis in CRC cells was also assessed. METHODS: The expression of miR-221 was detected by real-time RT-PCR. CDKN1C/P57 mRNA and corresponding protein expression pattern were detected by semi-quantitative RT-PCR and Western-blot. The specific 2'-methoxy-modified RNA oligonucleotide of miR-221(miRNA inhibitor,anti-miR-221) was designed, synthesized and transfected into Caco2 cell by liposome. Finally, the status of CRC cell proliferation and apoptosis were detected by MTT assay and flow cytometry. RESULTS: The expression of miR-221 was significantly up-regulated in CRC tissues as compared to the adjacent non-cancerous tissues(2.041±1.401 vs. 0.806±0.341, P<0.01). There was no significant difference in CDKN1C/P57 mRNA expression between CRC and non-cancerous tissues, whereas CDKN1C/P57 protein markedly decreased in CRC (3.019±1.708 vs. 0.972±0.316, P<0.01). miR-221-specific inhibitor significantly enhanced CDKN1C/P57 protein expression, inhibited proliferation of CRC cells and induced apoptosis of CRC cells(P<0.01). CONCLUSIONS: miR-221 inhibits CDKN1C/P57 expression by post-transcriptional gene silencing to promote CRC development and progression. miR-221-specific inhibitor potentially inhibits the growth of CRC cells. Therefore, it may be a new target for the biologic therapy for CRC.

[Effect of miR-221-specific inhibitor on the proliferation and apoptosis of human colorectal carcinoma cells].

OBJECTIVE: To investigate miRNA-221 expression in human colorectal carcinoma (CRC) cells and the effects of miR-221-specific inhibitor on the proliferation and apoptosis of CRC cells. METHODS: Four human CRC cell lines (HT-29, Lovo, SW-480, and CaCO2) were examined for miRNA-221 expression using real-time Q-PCR. The specific 2,-methoxy-modified RNA oligonucleotides of miR-221 (anti-miR-221) were synthesized and transfected into Caco2 cells via liposome, and the changes in the expression of miR-221 in the cells were detected by real-time Q-PCR. The proliferation and apoptosis of the transfected CRC cells were detected using MTT assay and flow cytometry. RESULTS: The 4 human CRC cells showed significantly upregulated expression of miR-221 compare with HUVECs (P<0.01). The miR-221-specific inhibitor, anti-miR-221, significantly inhibited the expression of miR-221 in Caco2 cells and suppressed the cell proliferation, causing also obvious cell apoptosis (P<0.01). CONCLUSION: The miR-221-specific inhibitor shows potent inhibitory effect on the growth of CRC cells, suggesting its value as a potential anti-tumor candidate for treatment of CRC.

MicroRNA-221 inhibits CDKN1C/p57 expression in human colorectal carcinoma.

AIM: To investigate the regulatory effect of microRNA-221 (miR-221) on CDKN1C/p57 expression in colorectal carcinoma (CRC). METHODS: Thirty four CRC and adjacent non-tumorous tissue samples were collected individually. Total RNA and protein were isolatedand from these samples and four human CRC-derived cell lines (including HT-29, Lovo, SW-480 and Caco2). MiR-221 expression was examined using real-time RT-PCR. CRC cells were treated with or without anti-p57-siRNA prior to the addition of pre-miR-221 or anti-miR-221. The mRNA and protein levels of CDKN1C/p57 were examined using semi-quantitative RT-PCR and Western blot, respectively. CRC cell proliferation and apoptosis were assessed using MTT assay and flow cytometry, respectively. The CDKN1C/p57 3'-UTR fragment was amplified using PCR from the genomic DNA of human colon cells and inserted into a luciferase reporter construct. The reporter construct was then transfected into CRC cells together with pre-miR-221 or anti-miR-221, and the luciferase activity in the transfected cells was examined. RESULTS: MiR-221 expression was significantly up-regulated in 90% of CRC samples compared to that in the adjacent non-tumorous tissue, and the expression level was positively correlated to an advanced TNM stage and local invasion. There was no significant difference in CDKN1C/p57 mRNA expression between CRC and corresponding non-tumorous tissues, whereas CDKN1C/p57 protein expression was markedly decreased in the CRC samples. A significant inverse correlation between miR-221 and CDKN1C/p57 expression was found in CRC cells. Moreover, a miR-221-specific inhibitor significantly increased CDKN1C/p57 protein expression in CRC cells. Anti-miR-221 markedly inhibited CRC cell proliferation and induced apoptosis. This inhibitory effect was abolished by pretreatment with anti-p57-siRNA, suggesting that the inhibition was mediated by CDKN1C/p57. A significant increase of the luciferase activity was observed in CRC cells co-transfected with the luciferase reporter construct and anti-miR-221. CONCLUSION: MiR-221 binds to the target site in the 3'-UTR of the CDKN1C/p57 mRNA to inhibit CDKN1C/p57 expression by post-transcriptional gene silencing to promote CRC occurrence and progress, therefore serving as a potential therapeutic target for the prevention and treatment of CRC.

[Effects of FOLFOX4 neoadjuvant chemotherapy on the non-tumoral liver in patients with metastatic colorectal carcinoma].

OBJECTIVE: To investigate the effect of FOLFOX4 neoadjuvant chemotherapy on the non-tumoral liver in patients with metastatic colorectal carcinoma. METHODS: A large series of surgically resected liver metastases(n=42) was selected and the morphological changes were examined by light and electron microscope. The mRNA and protein levels of connective tissue growth factor (CTGF) expression were detected by semi-quantitative RT-PCR and Western blotting analysis. RESULTS: Twelve (63.2%) of the 19 post-chemotherapy liver resection specimens had sinusoidal dilatation and hemorrhage. In contrast, 23 livers treated by surgery alone remained normal. Neoadjuvant chemotherapy could significantly enhance the mRNA and protein levels of CTGF expression in hepatic stellate cells. CONCLUSION: Systemic FOLFOX4 neoadjuvant chemotherapy in metastatic colorectal carcinoma frequently causes morphological injuries involving hepatic microvasculature and induces CTGF expression in hepatic stellate cells to participate in hepatic fibrosis.

[Expression of R-spondin1 in intestinal epithelium of mice with intestinal ischemia-reperfusion injury].

OBJECTIVE: To investigate the expression of R-spondin1 (RSpo1) in the intestinal epithelium of mice with intestinal ischemia-reperfusion injury and explore its significance. METHODS: Fifty normal male Kunming mice were randomized into sham-operated group (n=10) and intestinal ischemia-reperfusion injury group (n=40), and in the latter group, the mice were subjected to 20-min intestinal mesenteric artery occlusion followed by reperfusion for 6, 12, 24, or 48 h. Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to detect intestinal RSpo1 expression of the mice. RESULTS: The results of RT-PCR and ELISA showed that RSpo1 expression was significantly decreased in mice at 6 h of reperfusion following the intestinal ischemia (P<0.05), and increased gradually with prolonged repersuion time, reaching the peak level at 24 h (P<0.05). The expression underwent rapid decrease afterwards to a significantly lower level than that in the control group at 48 h (P<0.05). CONCLUSION: Intestinal ischemia-reperfusion injury may inhibit expression of RSpo1 in the early stage, and enhance its expression in the middle stage. RSpo1 can promote proliferation and differentiation of intestinal epithelial stem cells and plays an important role in the repair intestinal mucosal damage.

[Dynamic observation of intestinal epithelial stem cells of small intestine during the injured-repaired progress induced by 5-FU].

OBJECTIVE: To investigate the dynamic changes of intestinal epithelial stem cells during the injured-repaired progress induced by 5-FU. METHODS: Fifty adult C57BL/6J mice were enrolled in this study, 40 of them were intraperitoneally injected with 5-FU (30 mg per kg of body weigh) for five days, and 10 of them intraperitoneally injected with PBS as control. At day 1, 3, 5, 7 after treatment, the mice were killed and middle intestine was taken. Pathology was examined by HE staining. Musashi-1 (msi-1) expression was detected by immunohistochemical technique. The percentage of Rho low staining cells was detected by flow cytometry. RESULTS: After treatment with 5-FU, the intestinal mucosa was damaged. The Rho low staining cells were increasing, and at day 1 after treatment, the percentage of Rho low staining cells reached the highest level (P<0.01). The number of cells expressing msi-1 did not change significantly (P>0.05), but the percentage of positive msi-1 cells increased significantly (P<0.01). There was positive correlation between the percentage of Rhodamine 123 low staining cells and positive msi-1 cells in each group (r=0.867, P<0.01). CONCLUSIONS: The Rho low staining cells may contain rich intestinal epithelial stem cells. The intestinal epithelial stem cells expressing msi-1 can regenerate the damage of intestinal mucosa induced by 5-FU.

[Screening peptides binding specifically to large intestinal cancer LoVo cells from phage random peptide library].

OBJECTIVE: To screen the polypeptides specifically binding to human large intestinal cancer LoVo cells from a phage-displayed peptide library for potential use as targeting vectors for large intestinal cancer therapy. METHODS: With the LoVo cells as the target cells and human normal large intestinal mucosal epithelial cells as the absorber cells for subtraction biopanning from a c7c phage-display peptide library, the positive phage clones were identified by enzyme-linked immunosorbent assay (ELISA) and immunofluorescence detection. The amino acid sequences of the identified peptides were deduced by DNA sequencing. RESULTS: After 3 rounds of screening, 5 positive phage clones showing specific binding to LoVo cells and containing conserved motif RPMP were obtained from the 20 randomly selected clones. CONCLUSION: Specific peptide against large intestinal cancer cells can be obtained from a phage-display peptide library for use as potential vectors for targeting therapy of large intestinal cancer.

[Expression of proliferating cell nuclear antigen in severely damaged small intestinal mucosa due to high-dose 5-FU exposure].

OBJECTIVE: To detect the expression of proliferating cell nuclear antigen (PCNA) in severely damaged intestinal mucosa due to high-dose 5-FU exposure. METHODS: Thirty-two adult C57BL/6J mice were subjected to daily intraperitoneal high-dose 5-FU injection at 150 mg/kg for 5 consecutive days, and on days 1, 3, and 5, the mice were sacrificed to obtain the small intestinal tissue for HE straining and immunohistochemistry for detecting PCNA expression. Another 8 mice with intraperitoneal PBS injection served as the control group. RESULTS: High-dose 5-FU exposure of the mice resulted in severe intestinal mucous damage, with complete destruction of the villi and crypts and significantly increased cells positive for PCNA expression (P<0.01). CONCLUSION: High-dose 5-FU treatment can significantly increase the PCNA index, and the cells expressing PCNA can be closely associated with regeneration of the severely damaged mucosa due to the exposure.

[L-arginine reduces intestinal epithelial cell apoptosis in rats with severe abdominal infection].

OBJECTIVE: To explore the effect of L-arginine (L-Arg) on intestinal mucosal cell apoptosis in rats with severe abdominal infection. METHODS: Eighteen Wistar rats were randomized into 3 groups, namely the CLP group (n=6) in which the rats were subjected to cecal ligation plus puncture (CLP) to induce severe abdominal infection, L-Arg group (n=6) where the rats received 300 mg/kg peritoneal L-Arg injection following CLP establishment, and the control group (n=6) where the rats underwent ventrotomy only. Intestinal epithelial apoptotic cells were quantified in each group using TUNEL assay 24 h after the operation. RESULTS: Compared with the control group, the rats in CLP and L-Arg groups showed significantly increased number of apoptotic cells in the intestinal epithelium 24 h after the operation (P<0.001). The apoptotic index (AI) in the L-Arg group (18.1-/+2.2) was significantly lower than that in CLP group (20.8-/+2.3, P=0.038). CONCLUSION: Severe abdominal infection results in increased apoptosis of the intestinal epithelial cells in rats, and L-Arg treatment may reduce the cell apoptosis.

[A study of expression of Tcf-4 in the small intestine mucosa crypt during severe abdominal infection].

OBJECTIVE: To explore the expression of T cell factor 4(Tcf-4) in the process of severe abdominal infection in rats. METHODS: Forty healthy adult Wistar rats were randomly divided into control group (celiotomy only) and groups of 12, 24, 48 hours after establishment of abdominal infection. The latter groups included rats receiving cecal ligation and puncture (CLP) to establish the severe abdominal infection. Each group consisted of 10 rats. Immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the number of Tcf-4-positive cells and expression of Tcf-4 mRNA in the crypts of the mucosa of the small intestine. RESULTS: It showed that the expression of Tcf-4 in the mucosal crypts of the small intestine in control group was weak but the number of cells with positive Tcf-4 expression was increased in crypts of small intestinal mucosa 12 hours after CLP, reaching its peak level at 24 hours, and remained higher than control group at 48 hours (all P<0.01). The transcription level of Tcf-4 was associated with the stages of the severe abdominal infection. RT-PCR showed that Tcf-4 mRNA was upregulated rapidly 12 hours after CLP (0.21+/-0.01, P<0.01), and it reached peak level after 24 hours (0.28+/-0.02, P<0.01), decreased slowly but still obviously higher (0.20+/-0.01, P<0.05) than that of control group (0.19+/-0.01). CONCLUSION: The expression of Tcf-4 is induced by severe abdominal infection. The results suggest that Tcf-4 might be related with the proliferation and differentiation of intestinal stem cell during severe abdominal infection, and plays an important role in damage and repair of enteric mucosa.

[Effect of L-Arginine on intestinal mucosal injury of rats with severe abdominal infection].

OBJECTIVE: To investigate the effect of L-Arginine on intestinal mucosal injury of rats with severe abdominal infection. METHODS: Rats received cecal ligation and puncture (CLP) to reproduce sepsis model. A total of 18 Wistar rats were divided into two groups randomly (each n=9): L-Arginine group and model group. Three hundred mg/kg of L-Arginine was injected into the abdomen in rats of L- Arginine group after CLP. Model group received equal volume of normal saline. Blood sample was harvested and the serum levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) were determined at 24 hours after operation in both groups. The histopathological change of intestinal mucosa was observed under light microscope and mucosa damage index was determined. RESULTS: The intestinal mucosal damage was observed both in model group and L- Arginine group after CLP, but the injury was milder in L- Arginine group. There was significant difference in mucosa injury index between L-Arginine group and model group (3.4+/-0.6 vs. 4.1+/-0.5, P<0.05). The serum level of NO [(76.1+/-26.2) micromol/L vs. (87.3+/-16.7) micromol/L, P>0.05] and iNOS [(30.6+/-7.4) U/L vs(44.4+/-6.6) U/L, P<0.01] in L-Arginine group were lower than those in model group. CONCLUSION: L-Arginine could protect against intestinal mucosal injury and depress the serum level of iNOS in severe abdominal infection of rats.

[Intestinal mucosal pathology in rats with severe abdominal infection].

OBJECTIVE: To observe the pathological changes of the intestinal mucosa in rats with severe abdominal infection. METHOD: A total of 60 SD rats were divided randomly into control group and experimental group (n=30), and in the latter group, the rats underwent cecal ligation and puncture (CLP) while those in the former had only laparotomy. The jejunum and ileum were sampled on postoperative days 1, 2 and 4 for optical and electron microscopic observations. The positivity rate of blood bacterial culture and plasma level of endotoxin were determined in the rats. RESULTS: No abnormal changes were observed with either optical and electron microscope in the small intestinal mucous membrane of rats in the control group, but in rats of the experimental group, microscopic examination revealed interstitial edema, vascular engorgement and neutrophil infiltration in the small intestine mucous membrane and the submucosa, and electron microscopy demonstrated loose and disorderly arrangement of the microvilli of the intestinal epithelium. Plasma endotoxin level in rats in the experimental group was 5- to 12-fold higher than that in the control group. The positivity rates of blood bacterial culture were 20%, 30% and 10% on postoperative days 1, 2 and 4 respectively in the experimental group, but were all zero in the control group. CONCLUSION: Pathologic lesions in the intestinal mucosa occur during the early stage of severe abdominal infection in rats as the result of bacteria and endotoxin translocation.

[Effect of ethyl pyruvate on peroxidation injury of intestinal mucosa in rats with severe abdominal infection].

OBJECTIVE: To investigate the preventive effect of ethyl pyruvate (EP) on peroxidation injury to intestinal mucosa in rats with severe abdominal infection. METHODS: Thirty-six SD rats were divided randomly into three groups (n=30 in each group): control group (laparotomy only), infection group [cecal ligation and puncture (CLP) was performed to reproduce severe abdominal infection model] and EP group (CLP plus 40 mg/kg EP subcutaneous injection, once per 8 hours). The changes in intestinal mucosa pathologic score were observed, and malondialdehyde (MDA) and myeloperoxidase (MPO) activities in intestinal tissue, and serum MDA levels were determined at postoperative 24 and 48 hours. RESULTS: Inflammation of small intestine mucosa was more severe in the infection group than in EP group, and the pathologic scores were lower in EP group than those of the infection group at post-CLP 24 and 48 hours (all P<0.05). There was a significant positive correlation between the intestinal and plasma MDA in the infection group (r=0.867, P<0.05). The MDA and MPO levels in intestinal tissue and serum were higher in the infection group than in EP group and control group (all P<0.05). CONCLUSION: With severe intraperitoneal infection in rats, the intestinal mucosa is damaged by the reactive oxygen species. EP could ameliorate the injury of intestinal mucosa by attenuating the injurious effects of the reactive oxygen species.

[Beta-catenin expression in intestinal mucosa of rats with severe abdominal infection].

OBJECTIVE: To investigate the expression of beta-catenin in the intestinal mucosa of rats with severe abdominal infection. METHODS: Forty healthy adult Wistar rats were randomly divided into a control group (n=10, with celiotomy only) and 3 abdominal infection groups (n=10) sacrificed at 12, 24, 48 h after cecal ligation plus puncture for inducing severe abdominal infection, respectively. Immunohistochemistry and RT-PCR were performed to detect beta-catenin expression in the crypt of the small intestine during severe abdominal infection and in normal conditions. RESULTS: Rats with severe abdominal infection showed stronger beta-catenin expression in the crypt of the small intestine than normal rats, and the transcription level of beta-catenin was associated with the stages of severe abdominal infection. RT-PCR showed that beta-catenin mRNA increased rapidly 12 h after the infection (0.74-/+0.10 vs 0.52-/+0.06, P<0.01), reaching the peak level at 24 h (0.90-/+0.09, P<0.01), followed then by gradual decrease but remained still obviously higher than the control level at 24 h (0.80-/+0.09, P<0.01). CONCLUSIONS: Severe abdominal infection may induce beta-catenin expression which might be related with the proliferation and differentiation of intestinal stem cells in such condition and play an important role in intestinal mucosa damage and repair.

[Expression of proliferating cell nuclear antigen of the intestinal mucosa during critical intraperitoneal infection].

OBJECTIVE: To explore the expression and significance of proliferating cell nuclear antigen (PCNA) in intestinal epithelial cells during critical intraperitoneal infection. METHODS: A total of 60 SD rats were divided randomly to two groups: control group and infection group (30 rats in each group). Cecal ligation and puncture (CLP) was done in the infection group, and laparotomy only in the control group. Immunohistochemical technique was applied for assaying PCNA index of the jejunum and ileum samples on postoperative day 1, day 2 and day 4. RESULTS: The inflammatory reaction of small intestine mucous membrane was severer in the infection group than the control group. Compared with the control group, the PCNA indexes on day 1 and day 2 in the infection group were higher significantly (both P<0.01). The highest PCNA index was seen on postoperative day 1 in the infection group, then it lowered gradually (both P<0.01). CONCLUSION: The PCNA index of intestinal epithelial cells is elevated during the early period of critical intraperitoneal infection. The findings indicate that PCNA index is related with the injury and repair of intestinal mucosa during critical intraperitoneal infection.

[Surgical approach for carcinoma in the gastric cardia].

OBJECTIVE: To explore the optimal surgical approach for carcinoma in the gastric cardia. METHODS: A total of 157 patients with carcinoma in the gastric cardia were assigned into 2 groups according to the surgical approaches adopted, namely transabdominal (57 patients) and transthoracic approaches (100 patients), and the therapeutic effects of the two approaches were compared. RESULTS: In the transabdominal group, the average volume of intraoperative blood transfusion was 164.91+/-36.83 ml, average operative time 219.04+/-10.72 min and average hospital stay 14.39+/-1.39 d, with an average number of 6.04+/-2.84 lymph nodes removed. In the transthoracic group, the 4 parameters were 575.50+/-40.12 ml, 286.40+/-7.94 min, 20.32+/-0.81 d, and 3.62+/-2.56 respectively. None of the cases developed pleural effusion in the former group, which had a tumor recurrence rate of 22.80% within the follow-up period for 3 to 60 months. In contrast, 15 cases had pleural effusion in the latter group with a tumor recurrence rate of 41.00%. There was a significant difference between the two groups in terms of the therapeutic effects. CONCLUSION: Transabdominal approach is the better alternative to transthoracic one for operation of carcinoma in the gastric cardia.

[Prognosis of rectal cancer in relation to the selection of the surgical approaches].

OBJECTIVE: To investigate the prognostic significance of surgical approach selection in patients with rectal cancer. METHODS: A retrospective analysis of the relation of surgical approach selection to the prognosis was conducted in 112 cases of rectal cancer between July 2000 to June 2002. RESULTS: In this group of cases, local resection of the tumor was performed in 10 cases, Dixon operation in 75 cases and Miles operation in 27 cases. A total of 106 patients survived the operations with 10 had tumor recurrence (a recurrence rate of 8.93 %). All the 10 patients receiving local resection of the tumor survived without episodes of tumor recurrence or metastasis. After the operations, 101 patients (90.18 %) retained normal sexual function and 109 (97.32 %) were with normal urinary function. CONCLUSION: The postoperative quality of life of the patients with rectal cancer very much relies on the selection of adequate surgical procedures.