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Objective To investigate the efficacy and limitation of endoscopic ultrasonography (EUS) on the diagnosis of gastrointestinal submucosal tumor (SMT) prior to endoscopic resection.Methods Data of 211 patients,who were confirmed as gastrointestinal SMT before operation and received endoscopic resection for gastrointestinal submucosal tumor at Department of Gastroenterology,Shanghai Ruijin Hospital from January 2016 to December 2018 were analyzed.The value and limitation of EUS for SMT were investigated according to the final pathology.Results For the lesion distribution,66 were in esophagus,108 in stomach,2 in duodenum and 35 in rectum.The accuracy of tumor origin by EUS was 99.5％ (210/211).The accuracy of tumor nature by EUS was 75.8％ (160/211).For the lesions originated from different locations,the diagnostic accuracy for lesion originated from esophageal mucosa/submucosa,esophageal muscularis propria,gastric mucosa/submucosa,gastric muscularis propria,duodenal submucosa,rectal mucosa/submucosa by EUS were 90.0％ (54/60),83.3％ (5/6),31.0％ (13/42),89.4％ (59/66),50.0％(1/2),82.9％ (29/35),respectively.With respect to hypoechoic lesions,leiomyoma,leiomyoma/gastrointestinal stromal tumor,and neuroendocrine tumor were the predominant type of tumor originated from esophageal mucosa,gastrointestinal muscularis propria and rectal mucosa/submucosal,respectively.Conclusion Although EUS is indispensible for the diagnosis of gastrointestinal submucosal tumor,it plays a limited role in the differential diagnosis of various lesions originated from gastric mucosa and submucosa.Since part of the submucosal tumors may be potential for malignant development,an diagnosis made by EUS should be more careful.
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Objective To explore the mechanism of vitamin D in the genesis of irritable bowel syndrome (IBS).Methods A total of 50 newborn Sprague Dawley (SD) rats were divided into three model groups and two control groups (saline control group and normal control group).The model was induced by dilute acetic acid enema.After rats were weaned,the rats of three IBS model groups were fed with normal diet,vitamin D deficient diet and vitamin D sufficient diet,respectively.The visceral sensitivity of the rats was assessed by the colorectal distention experiment.The intestinal tissues of rats was taken for histological score,and the intestinal mast cell (MC) was also counted.The mRNA level of vitamin D receptor (VDR) in colon tissues of rats was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR).T test or rank sum test was performed for statistical analysis.Results When the water volume of balloon was 0.5 mL and 1.0 mL,the abdominal withdrawal reflex (AWR) scores of male rats of the vitamin D deficient model group were 2.67±0.33 and 3.60±0.28,which were higher than those of normal vitamin D model group (1.93±0.15 and 3.20±0.18),and the differences were statistically significant (t=4.491 and 2.683,both P＜0.05).When the water volume of balloon was 1.0 mL and 1.5 mL,the AWR scores of female rats of the vitamin D sufficient model group were 3.00 (3.00,3.00) and 3.33 (3.33,3.67),which were lower than those of normal vitamin D model group (3.67,3.33 to 4.00;and 4.00,4.00 to 4.00),and the differences were statistically significant (Z=-2.362 and-2.390,both P＜0.05).There was no statistically significant difference in histological scores of intestinal mucosal tissues of ileum distal segment and sigmoid between the model groups with different vitamin D concentration and saline control group as well as normal control group (all P＞0.05).The number of MC in the mucosal tissue of the sigmoid colon of female rats in IBS model group was 41.00± 19.80,which was higher than that in normal control group (12.40 ± 5.35),and the difference was statistically significant (t=3.118,P=0.030).The number of MC in the mucosal tissue of ileum of the female rats in vitamin D deficiency model group was 16.00 ± 3.71,which was higher than that in normal vitamin D model group (7.30± 2.66),and the difference was statistically significant (t =4.263,P =0.003).The VDR mRNA level in the colon tissues of male model rats of normal vitamin D model group was 1.48±0.33,which was higher than that of saline control group and normal control group (0.97± 0.21 and 1.00±0.21;t=2.590 and 2.482,both P＜0.05).The VDR mRNA levels in colon tissues of female rats of vitamin D deficient model group was 1.90 ± 0.66,which was higher than that of normal control group (1.00 ± 0.14),and the difference was statistically significant (t =2.649,P =0.038).Conclusions Vitamin D may affect visceral hypersensitivity in IBS,and MC may involve in vitamin D induced visceral hypersensitivity.
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Objective To investigate the role of mucosal mast cells infiltration and degranulation with nerve growth factor (NGF)in development of visceral hypersensitivity in Sprague-Dawley (SD)rats. Methods The model of visceral hypersensitivity of irritable bowel syndrome (IBS)was established in 19 neonate SD rats with intestinal stimulation (rectalballon distention)on 8th,10th and 12th postnatal days. The other 19 neonate SD rats without colonic distention were assigned to the control group.After rats grew up (six to eight weeks old),the visceral sensitivity was tested by abdominal withdrawal reflex (AWR)in 10 rats of each group.Mast cell infiltration and degranulation were observed with toluidine blue staining in colon tissue slides.The NGF level of intestinal tissues was detected by enzyme-linked immunosorbent assay (ELISA)methods in the left nine rats of each group.The culture system of dorsal root ganglias (DRG)from the neonatal rats was set up.The changes of electrophysilogical characters of DRG stimulated with NGF (100 ng/mL)for four days were recorded with patch-clamp.Paired t test was performed for comparison between groups.Results The results of AWR indicated that neonatal colonic stimulation could significantly increase visceral sensitivity after growing up.Under 20,40 and 60 mmHg (1 mmHg=0.133 kPa)distention pressure,visceral sensitivity scores of visceral hypersensitivity rats and rats of control group were 1 .00±0.50 vs 1 .67 ±0.50,1 .89 ±0.31 vs 2.89 ±0.34 and 2.89 ±0.33 vs 3.89±0.33,the differences were statistically significant (t=-2.83,-6.00 and -6.00,all P <0.05 ). The results of master cells staining in tissue slides showed colonic master cells infiltration was obvious in rats with visceral hypersensitivity,and part of mast cells were degranulation.The result of ELISA demonstrated that NGF level of visceral hypersensitivity rats was significantly higher than that of control group ((11.07±3.06)pg/mg vs (2.38 ±1.88)pg/mg,t =-6.93,P <0.05).The results of electrophysilogical tests of primary cultured DRG indicated that compared with blank control growp,the action potential threshold of neuron in NGF 100 ng/mL group significantly decreased ((-18.0±2.1 )mV vs (-29.0 ± 2.5 )mV,t = 12.26,P <0.05)and discharge frequency increased ((5 .0± 1 .4 )/800 ms vs (12.0 ± 3.2)/800 ms,t=-8.40,P <0.05 ).Meanwhile,neuron voltage-gated K+ current density remarkably decreased,most were sustained delayed rectifier K+ current (I K )decreasing ((279.0 ±48.0)pA/pF vs (203.0±39.0)pA/pF,t=6.18,P <0.05).Conclusion Colonic stimulation in neonatal rats could cause intestinal master cells infiltration and degranulation,which induced changes of neuron electrophysilogical characters and resulted in visceral hypersensitivity after growing up.
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Objective To screen the difference of gene expression in dorsal root ganglia (DRG)of inflammatory visceral hypersensitivity rats and to explore the role of voltage gated calcium channel (VGCC) in inflammatory visceral hypersensitivity. Methods Total 180 male Sprague-Dawley rats were in this study,the weight varied from 200 gram to 300 gram. 2,4,6-trinitrobenzenesulfonic acid (TNBS) model group was maken by 2. 0% TNBS slowly injection,the dosage was 100mg per kilogram. The normal control group was only injected with same volume of 0. 9% sodium chloride solution. After the model had been maken for four days,gene expression profiles of L6-S2 DRGs were tested by rat cDNA microarray chips. And the result was verified by RT-PCR and Western blot. The changes of intracellular Ca2+ and the voltage gated calcium currents were recorded by patch-clamp.The special Ca2+ channel blockers were given by intrathecal injection,and then the changes of visceral sensitivity were observed. The visceral sensitivity was measured by abdominal withdrawal reflex (AWR). Results There were significant changes of 172 genes expression in L6-S2 DRGs of TNBS model rats,which included Ca2+ channel,membrane receptor and intracellular second messenger. Of those,L-type Ca2+ channel (Cav1. 2) and R-type Ca2+ channel (Cav2. 3) were significantly up-regulated. The results of gene microarray chips were further confirmed by RT-PCR and Western blot.The intracellular Ca2+ testing indicated that there was no statistical significant of resting intracellular Ca2+ in colonic special sensory neuron between TNBS group and normal control group (P＞0. 05);while the evoked transients [Ca2+] significantly increased compared with normal control group (P＜0. 05). The whole cell patch clamp recording showed that the L-type and R-type calcium current were significantly increased in colonic primary sensory neurons of TNBS group compared with normal control group (P＜0. 05). The inflammatory visceral hypersensitivity was significantly reduced by intrathecal injection of nimodipine and SNX-482 (P＜0. 05). Conclusion The up-regulation of Cav1. 2and Cav2. 3 play an important role in inflammatory visceral hyperalgesia,which may be the possible potential therapeutic targets for visceral inflammatory hyperalgesia.
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Objective To investigate the effect of small interfering RNA (siRNA) mediated silencing of △Np73 on 5-FU chemotherapy sensitivity in SW620 colocancer cells and provide new treatment approach for the colon cancer.Methods siRNAs were transfected into SW620 colon cancer cells.The expression of △Np73 was observed.Cell viability of colon cancer cells were measured by MTr assay and cell apoptosis was assessed with flow cytometry after treatment of control siRNA or △Np73 siRNA or combined with 5-FU,respectively.The tumorigenesis was assessed by injecting △Np73 siRNA or control siRNA transfeeted SW620 colon cancer cells into nude mice,followed by treatment with 5-FU in the tumors.Results △Np73 siRNA was able to strongly inhibit △Np73 expression,however,it did not inhibit the growth of cells.Combination treatment with △Np73 siRNA and 5-FU produced significant higher apoptotic cell(42.9%) as compared with those with 5-FU treatment(18.9%) alone or those with △Np73 siRNA(8.8%) alone.The treatment with 5-FU in the xenngrafts derived from △Np73 siRNA transfected SW620 cells in nude mice can inhibitor tumor growth significantly (t=15.32,P<0.05).Conclusion △Np73siRNAs can specifically repress the expression of △Np73.Thus it sensitizess the cells to 5-FU chemotherapy in colon cancer.
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Objective To investigate the effects of EEF1 A2 on growth and proliferation of the human pancreatic cancer cell line SW1990. MethodsThe EEF1 A2 gene was introduced into pancreatic cancer cell line SW1990 by adenovirus vector. The effects of EEF1 A2 on the growth of human pancreatic cancer cell were measured by MTT. Cell cycle was detected by flow cytometry and cell growth rate was examined by soft agar cloning formation test. ResultsAfter EEF1A2 induction, the expression of EEFA1 A 2 mRNA in pancreatic cancer cell line SW1990 increased, value of A750 at 72 h was 1. 2996 ±0. 2091, number of cells was 81250, cloning efficiency at 14 d was 82%, all of these parameters were significantly higher than those in the groups of blank adenoviras vector and PBS groups (P <0.05 ) ; the percentage of G1 phase cell was 28.5%, which was significantly lower than those in the groups of blank adenovirus vector and PBS groups; the percentage of Sphase ceil was 60.9%, which was significantly higher than those in the groups of blank adenovirus vector and PBS groups (P < 0.05 ). ConclusionsEEF1 A2 gene significantly enhanced cell growth and proliferation in human pancreatic cancer in vitro.
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Objective To describe the clinical and pathological features and survival of juvenile patients with pancreatic carcinoma ( age ≤ 40 years old ) and to explore whether pancreatic carcinoma in young patients was a particular subtype. Methods As a case control study, the clinical data and follow-up data of sporadic 29 cases diagnosed as juvenile pancreatic carcinoma in Ruijin hospital from January, 2000 to December, 2007 were analyzed and compared with randomly selected 89 cases of senile eases (age≥ 61 years old) with pancreatic carcinoma. Results The percentage of juvenile pancreatic carcinoma was 3.6% (29/811 ) and the male/female ratio was 2.5: 1. The incidence rate of abdominal pain was significantly higher in the juvenile patients than in the senile patients (72.4% vs 48.3% , P < 0.05 ) ;the incidence of malnutrition was significantly lower in juvenile patients than that in senile patients ( 13.8% vs 38.0%, P <0.05 ) ;and the rate of patients with advanced stage disease ( Ⅲ～Ⅳ ) was significantly higher in juvenile patients than in senile patients (69.0% vs 55. 1%, P < 0.05). The percentage of radical operation in juvenile patients was not statistically different from that in senile patients ( 34.5% vs 30.34%, P > 0.05 ), and analysis using the Kaplan-Meier method and log-rank test revealed no significant difference in overall survival between the two groups ( median survival time : 7.0 vs 8.0 months, P > 0.05 ). Conclusions The age onset of the pancreatic carcinoma tended to be younger. The predominant clinical manifestations of juvenile pancreatic carcinoma were abdominal pain or back pain. Juvenile pancreatic carcinoma may be a particular subtype of pancreatic cancer.