Mifepristone combined with ethacridine lactate for third-trimester stillbirth induction: a 5-year experience from Shanghai.

OBJECTIVE: To review and analyze the efficacy and safety of mifepristone combined with ethacridine lactate for induction of stillbirth in the third trimester. METHODS: All patients with stillbirth in late pregnancy (≥ 28 weeks) in a university-affiliated maternity center from October 2016 to September 2021 were included in this study. After exclusion, patients were divided into ethacridine lactate and non-ethacridine lactate groups according to induction methods. Logistic regression was conducted to identify the risks of complications. RESULTS: We identified 122 patients that experienced stillbirth (5' Apgar score = 0) in third-trimester from the 5-year total deliveries in the hospital, among whom 39 stillbirths that resulted from termination of pregnancy for severe fetal anomalies and 1 stillbirth that was in twin pregnancy were excluded. Thus, 82 cases with stillbirths (dead before induction) were included in the analyses. In the 82 cases, 49 (59.76%) accepted intra-amniotic ethacridine lactate induction with 47 (95.92%, 47/49) successfully induced. No statistical difference was observed in induction failure rate between ethacridine dosage groups of < 75mg and ≥ 75mg (0/25, vs. 2/24, respectively; P > 0.05). The ethacridine lactate induction group showed no increased risks in complications (6.12%, 3/49), compared with non-ethacridine lactate group (12.12%, 4/33) (P = 0.35, OR, 0.47, 95%CI, 0.10 to 2.27). CONCLUSION: Mifepristone combined with ethacridine lactate is a safe and low-risk induction method for patients with stillbirth in the third trimester.

Diagnostic classification of endosonography for differentiating colorectal ulcerative diseases: A new statistical method.

AIM: To establish a classification method for differential diagnosis of colorectal ulcerative diseases, especially Crohn's disease (CD), primary intestinal lymphoma (PIL) and intestinal tuberculosis (ITB). METHODS: We searched the in-patient medical record database for confirmed cases of CD, PIL and ITB from 2008 to 2015 at our center, collected data on endoscopic ultrasound (EUS) from randomly-chosen patients who formed the training set, conducted univariate logistic regression analysis to summarize EUS features of CD, PIL and ITB, and created a diagnostic classification method. All cases found to have colorectal ulcers using EUS were obtained from the endoscopy database and formed the test set. We then removed the cases which were easily diagnosed, and the remaining cases formed the perplexing test set. We re-diagnosed the cases in the three sets using the classification method, determined EUS diagnostic accuracies, and adjusted the classification accordingly. Finally, the re-diagnosing and accuracy-calculating steps were repeated. RESULTS: In total, 272 CD, 60 PIL and 39 ITB cases were diagnosed from 2008 to 2015 based on the in-patient database, and 200 CD, 30 PIL and 20 ITB cases were randomly chosen to form the training set. The EUS features were summarized as follows: CD: Thickened submucosa with a slightly high echo level and visible layer; PIL: Absent layer and diffuse hypoechoic mass; and ITB: Thickened mucosa with a high or slightly high echo level and visible layer. The test set consisted of 77 CD, 30 PIL, 23 ITB and 140 cases of other diseases obtained from the endoscopy database. Seventy-four cases were excluded to form the perplexing test set. After adjustment of the classification, EUS diagnostic accuracies for CD, PIL and ITB were 83.6% (209/250), 97.2% (243/250) and 85.6% (214/250) in the training set, were 89.3% (241/270), 97.8% (264/270) and 84.1% (227/270) in the test set, and were 86.7% (170/196), 98.0% (192/196) and 85.2% (167/196) in the perplexing set, respectively. CONCLUSION: The EUS features of CD, PIL and ITB are different. The diagnostic classification method is reliable in the differential diagnosis of colorectal ulcerative diseases.

[Effect of transforming growth factor alpha on the expression of cyclin E and cyclin D1 in gastric carcinoma cells].

OBJECTIVE: To explore the effect of transforming growth factor alpha (TGFalpha) on the expression of cyclin E and D1 in gastric carcinoma cells. METHODS: Human gastric adenocarcinoma SGC7901 cells were cultured routinely and synchronized at G(0)/G(1) phase in serum-free RPMI-1640. The percentage of the cells at G(0)/G(1) phase was detected by propidium iodide staining and flow cytometry (FCM), and the synchronized cells were cultured in RPMI-1640 supplemented with 2.5% calf serum and treated with 10, 30, and 50 microg/L TGFalpha for 5 h. The expression of cyclin E and D1 in SGC7901 cells was detected by immunofluorescent staining and FCM. RESULTS: The percentage of the cells at G(0)/G(1) phase increased from 54% in routine culture to 72% in the serum-free RPMI-1640 culture. TGFalpha treatment of the cells synchronized at G(0)/G(1) phase induced significant increment of cyclin E and D1 expressions (P<0.001), and at the dose of TGFalpha of 50 microg/L, their expressions increased by 25.18% and 27.52%, respectively (P<0.001). CONCLUSION: TGFalpha can increase the expression of cyclin E and D1 in gastric carcinoma cells to promote their cell cycle progress.

[Effect of Helicobacter pylori infection on gastric mucosal cell proliferation in Mongolian gerbils].

OBJECTIVE: To explore the mechanism that Helicobacter pylori (H. pylori) infection can induce adenocarcinoma in Mongolian gerbil model with long-term H. pylori infection. METHODS: Mongolian gerbil model with long-term H. pylori infection was established by inoculation H. pylori NCTC 11637 strain, and immunohistochemical straining and in situ hybridization were employed to observe changes in gastric mucosal cell proliferation due to H. pylori infection. RESULTS: Mongolian gerbil model with long-term H. pylori infection was successfully established. Immunohistochemical staining of 5'-bromodeoxyuridine (BrdU) and proliferating cell nuclei antigen (PCNA) showed that H. pylori infection induced the increase in gastric mucosal cell proliferation (P<0.05), and in situ hybridization of epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) revealed elevated expressions of EGF mRNA and EGFR mRNA with time passage after H. pylori infection (P<0.05). CONCLUSION: H. pylori inoculation can induce abnormality in gastric mucosal cell proliferation, which is instrumental for the progression from chronic gastritis to glandular atrophy, intestinal metaplasis and ultimately to atypical hyperplasia. The abnormal expressions of EGF and EGFR may be the key element for abnormality of gastric mucosal cell proliferation.

Gastrin, somatostatin, G and D cells of gastric ulcer in rats.

AIM: To investigate the relationship among gastrin, somatostatin, G and D cells in gastric ulcer and in its healing process in rats. METHODS: Fourty-nine Wistar rats were divided into 7 groups. The gastric ulcer model was induced by acetic acid successfully. The gastrin and the somatostatin in rat plasma, gastric fluid and antral tissue were measured by radioimmunoassay(RIA). G and D cells in antral mucosa were analyzed with polyclonal antibody of gastrin and somatostatin by immunohistochemical method and Quantimet 500 image analysis system. RESULTS: In gastric ulcer, the level of gastrin in plasma, gastric fluid, and antral tissue increased, that of somatostatin declined, and the disorder gradually recovered to the normal level in the healing process. Immunohistochemical technique of G and D cells in antral mucosa demonstrated that the number of G cells increased and that of D cells decreased, both areas of G and D cells declined, the ratio of number and area of G/D increased in gastric ulcer, and the disorder gradually recovered in the healing process. CONCLUSION: In gastric ulcer, the increased gastrin secreted by G cells, the declined somatostatin secreted by D cells, and the disordered G/D cell ratio can lead to gastrointestinal dysfunction.

Overexpression of cyclin E in Mongolian gerbil with Helicobacter pylori-induced gastric precancerosis.

AIM: To explore dysregulation of cyclin E in malignancies, and to further investigate the role of cyclin E in Helicobacter pylori (H. pylori)-induced gastric precancerosis. METHODS: Four-week-old specific pathogen-free male Mongolian gerbils were employed in the study. 0.5 mL 1 x 10(8) cfu x L(-1) suspension of H.pylori NTCC11637 in Brucella broth was inoculated orally into each of 20 Mongolian gerbils, and a further 20 gerbils were inoculated with Brucella broth as controls. 10 of the infected gerbils and 10 of the non-infected control gerbils were sacrificed at 25, 45 wk after infection. The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonal antibody to cyclin E in Mongolian gerbil of H. pylori-induced gastric precancerosis. RESULTS: H. pylori was constantly detected in all infected animals throughout the study. At 25 wk after infection of H. pylori, ulcers were observed in the antral and body of stomach (n=6). Histological examination showed that all animals developed severe inflammation and multifocal lymphoid follicles appeared in the lamina propria and submucosa of gastric antrum. At 45 wk after infection of H. pylori, severe atrophic gastritis (n=10), intestinal metaplasia (n=8) and dysplasia (n=6) could be observed. Cyclin E mRNA levels were significantly more at 25 wk after infection of H. pylori (1.27+/-0.26), and at 45 wk after infection of H. pylori (1.82+/-0.39) than control-animals (0.59+/-0.20, P<0.01) cyclin E mRNA levels were evaluated by 2.2-fold at 25 wk (P<0.01) and 3.1-fold at 45 wk (P<0.01) precancerosis induced by H. pylori, when compared with control gastric epithelium of Mongolian gerbil. Immunohistochemical staining revealed exclusive nuclear staining of cyclin E. Furthermore, there was a sequential increase in cyclin E positive cells from normal epithelium to precancerosis. CONCLUSION: Overexpression of cyclin E occurs relatively early in gastric tumorigenesis in this model.