Prevention of early delayed gastric emptying after high-level esophagogastrostomy by "pyloric digital fracture".

OBJECTIVE: This study was designed to evaluate the clinical efficacy of pyloric digital fracture for the prevention of early delayed gastric emptying (DGE) after high-level esophagogastrostomy. METHODS: From January 2004 to March 2009, we sequentially enrolled 78 patients after esophagogastrostomy: 48 patients with pyloric digital fracture (DF group) and 30 patients without any drainage procedure (non-DF group). Intraoperative manometric study was performed in 48 patients of the DF group. Postoperative evaluation was performed, including symptomatic questionnaire, radiographic study, and gastric scintigraphy. RESULTS: Intraoperative manometric study revealed that basal pyloric pressure and peak pressure of pylorus in phase III of the migrating motor complex increased significantly after gastric conduit was made and anastomosed, but decreased appreciably following digital fracture. Compared with the peak pressure of IPPW before digital fracture (88.52 ± 19.88 mmHg), it appreciably decreased following digital fracture (40.45 ± 13.52 mmHg). Occurrences of IPPW (in 10 min) and duration time of each occurrence (s) had similar trends for before and after digital fracture (11.5 ± 4.5 vs. 5.0 ± 3.5 and 7.0 ± 2.0 vs. 3.0 ± 1.0, respectively). Postoperative evaluation demonstrated that early DGE occurred in four patients in the non-DF group (13.3%), and there was no DGE patient in the DF group. There was significant difference regarding gastric scores between the DF group and the non-DF group (10.5 ± 3.4 vs. 16.7 ± 3.8, t = 2.8271, P < 0.05). Gastric scintigraphy revealed that either semi-emptying-time or percent of retention at 4 h of the DF group was significantly lower than that of the non-DF group. CONCLUSION: Pyloric digital fracture can prevent early DGE after high-level esophagogastrostomy efficaciously and conveniently.

An S296R mutation in the human androgen receptor causes activation of the receptor by non-androgenic steroids and stronger inhibition by the nuclear receptor corepressor N-coR.

Mutation of the androgen receptor (AR) is believed to contribute to androgen-independent growth of prostate cancer. In the present study, we examined the functional changes associated with the novel somatic mutation S296R in the N-terminal domain of the AR identified from one recurrent prostate cancer sample. The results indicate that the S296R mutation does not differ obviously from the wild-type AR in its ability to bind the synthetic androgen methyltrienolone, or in its transcriptional activity induced by dihydrotestosterone (DHT) in the absence or presence of the overexpression of coactivators (steroid receptor coactivator-1, transcription intermediary factor-2, cAMP response element-binding protein-binding protein and p300). However, S296R was found to differ from wild-type AR in that its transcriptional activity could be activated by high concentrations (1 micromol/L) of 17beta-oestradiol and progesterone and its transactivity induced by DHT was more obviously inhibited by overexpression of the nuclear receptor corepressor N-coR in CV-1 cells. These findings indicate that a point mutation (S296R) in the N-terminal domain of the AR can decrease the ligand specificity of the AR and alter the interaction between S296R and the corepressor N-coR.

Mutations in the N-terminal Transcriptional Activation Region of Androgen Receptor in the Chinese.

Activation function (AF1) region of N-terminal domain of androgen receptor (AR) is necessary for the transcriptional activation function of AR. The sequences of AF1 in twenty normal chinese were amplified by PCR and determined by direct dsDNA cycle sequencing. Based on this, the mutations in AF1 of AR in patients with androgen insensitivity syndrome(AIS) or prostate cancer(PC) were screened by a combination of single strand conformation polymorphism(SSCP) analysis and direct dsDNA cycle sequencing. The sequences between normal chinese and other races were identical and one point mutation (C966A, Ser296Arg), which had not been reported so far, was identified in a patient with prostate cancer with poor differentiation. That suggests alteration of structure and function in AF1 of N-terminal domain of AR might be relative with PC progression of some patients.