Surveillance colonoscopy after endoscopic resection of colorectal adenomas is a crucial step in colorectal cancer screening. After identifying the patients at risk,a tailored follow-up colonoscopy surveillance strategy should be formulated. The follow up colonoscopy time interval after endoscopic resection of colorectal adenomas should be scheduled on the basis of past history,family history,and results of initial high quality colonoscopy examination. By reviewing the American and European guidelines for surveillance after polypectomy,a follow-up colonoscopy time interval schedule matched with the risk stratification is suggested for discussion.

Objective To evaluate the effect of delayed preconditioning with morphine on ischemic cerebral injury in mice and the role of classical protein kinase C (cPKC).Methods Forty male BALB/C mice,weighing 20-22 g,were randomly divided into 4 groups (n =10 each):sham operation group (group S),ischemic cerebral injury group (group ICI),morphine preconditioning group (group MP) and cPKC inhibitor Go6983 group (group G).Ischemia was induced by middle cerebral artery occlusion (MCAO).In S group,the middle cerebralartery was only exposed but not occluded.In MP group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO.In G group,morphine 10 mg/kg was injected intraperitoneally 24 h before MCAO and 5 μl Go6983 (6nmol) was injected into the left lateral cerebral ventricle immediately before MCAO.The neurologic deficit was evaluated and scored according to neurological disability status scale in a blind nanner 6 h after MCAO.The animals were sacrificed and brains were immediately removed for measurement of the brain edema and infarct volume.Apoptotic rate was calculated.Results Compared with S group,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly increased in ICI,MP and G groups (P ＜ 0.01).Compared with group ICI,the neurologic deficit scores,infarct volume,brain edema and apoptotic rate were significantly decreased in group MP (P ＜ 0.01),and no significant change was found in the parameters mentioned above in group G (P ＞ 0.05).Conclusion Delayed preconditioning with morphine can reduce ischemic cerebral injury in mice and activation of classical cPKC signaling pathway is involved in the mechanism.

Objective To analyze the miss rates of colorectal adenomas during colonoscopy as well as risk factors influencing the adenoma miss rates and to take corresponding measures. Methods A total of 432 patients who underwent index and follow-up colonoscopy in 18 months were randomized and investigated. The results of two colonoscopies were compared and the missed adenomas were defined as the adenomas de-tected only during the second colonoscopy. Miss rates were calculated according to patient-based methods. Chi-square test was used to analyze the relative factors influencing the adenoma miss rate of per-patient. Then the meaningful factors were chosen into the logistic regression model for multiple factors analysis. Results Of 432 patients,116(26. 9%)had missed adenomas on first colonoscopy. Single factor analysis found that the size of adenoma( χ2 = 89. 686,P = 0. 000),the shape of adenoma( χ2 = 68. 488,P = 0. 000),the location of adenoma(χ2 = 77. 055,P = 0. 000)and adenoma tissue types(χ2 = 417. 000,P = 0. 000)were the risk factors for miss rates of colorectal adenomas. Number of polyps(χ2 = 8. 450,P= 0. 038),the organi-zation type of polyp(χ2 = 10. 718,P= 0. 013)and proficiency of colonoscopists(χ2 = 56. 069,P= 0. 000), the quality of bowel preparation(χ2 = 39. 195,P = 0. 000),insertion time(χ2 = 13. 133,P = 0. 001)were also the risk factors for miss rates of colorectal adenomas. Logistic regression analysis showed that the bigger the adenoma size,the less missed adenomas(OR= 0. 341,95%CI:0. 173-0. 671). Also,the longer insertion time took,the lower the adenoma miss rate(OR = 0. 987,95% CI:0. 981-0. 994). Per-patient miss rates were lower for high-risk adenomas compared with low-risk adenomas(OR = 0. 324,95%CI:0. 154-0. 680). Adenomas happening in multiple parts of bowel easily leads to missing(OR= 3. 791,95%CI:1. 505-9. 546). Conclusion The missed diagnosis of adenomas is not only significantly associated with features of missed adenomas,but also with skills of colonoscopists,insertion time,and bowel preparation. The key is high-quality index colonoscopy to avoid adenomas missing.

Inflammatory orofacial pain, in which substance P (SP) plays an important role, is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs). SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms, including glial fibrillary acidic protein (GFAP) activation, phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways, and cytokine upregulation. However, in the TG, the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown. In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process. In the present study, complete Freund's adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo. SP was administered to SGC cultures in vitro to confirm the effect of SP. Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist), U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2), and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia. In addition, SP promoted SGC activation, which was proven by increased GFAP, p-MAPKs, IL-1β and TNF-α in SGCs under inflammatory conditions. Moreover, the increase in IL-1β and TNF-α was suppressed by L703, 606, U0126 and SB203580 in vivo and in vitro. These present findings suggested that SP, released from TG neurons, activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs, contributing to inflammatory orofacial pain associated with peripheral sensitization.