Down-regulation of long non-coding RNA MEG3 serves as an unfavorable risk factor for survival of patients with breast cancer.

OBJECTIVE: The downregulation of Long non-coding RNA MEG3 (MEG3) has been observed in breast cancer (BC). However, there is no previous study of the relationship between MEG3 and patient prognosis in BC. Accordingly, this study investigated the prognostic values of MEG3 in BC patients. MATERIALS AND METHODS: we performed RT-qPCR to detect the expression of MEG3 in 207 paired BC tissues and adjacent noncancerous tissues. The association of MEG3 expression with clinicopathological factors or prognosis was statistically analyzed. RESULTS: Our findings revealed that the MEG3 expression was significantly decreased in clinical BC tissues compared to adjacent normal tissues (p < 0.01). MEG3 level was significantly associated with differentiation grade (p  = 0.004), TNM stage (p  = 0.011) and lymph nodes metastasis (p  = 0.000). Using Kaplan-Meier analysis, we found that patients with low MEG3 expression had significantly poor overall survival (OS) rate (p  < 0.001) and progression-free survival (PFS)  rate (p  < 0.001). Moreover, multivariate Cox analysis revealed MEG3 expression was an independent poor prognostic factor for both 5-year OS (p  = 0.003) and 5-year PFS (p  = 0.002) in BC patients. CONCLUSIONS: Our results indicated that MEG3 expression was an independent prognostic factor for patients with BC, which may serve as a novel biomarker in BC patients.

Impact of early enteral and parenteral nutrition on prealbumin and high-sensitivity C-reactive protein after gastric surgery.

We investigated the impact of early enteral nutrition (EEN) and parenteral nutrition (PN) on prealbumin (PA) and high-sensitivity C-reactive protein (hs-CRP) in patients after gastric cancer surgery. Sixty-eight selected patients undergoing gastric cancer surgery were randomly divided into the EEN (N = 34) and PN (N = 34) groups. Body weight (BW), serum albumin (ALB), transferrin (TF), PA, hs-CRP, length of hospital stay, cost of postoperative nutritional support, and incidence of complications were compared between groups. On postoperative day 7, the BW, TF, ALB, and PA for both groups were significantly decreased compared with the values obtained on preoperative day 1 (P < 0.01). A significant decrease was observed in TF and PA in the PN group compared with the EEN group (P < 0.01). There was no significant difference in BW and ALB between the two groups (P > 0.05). The hs-CRP level of both groups was significantly higher than on preoperative day 1. There was a significant increase in hs-CRP in the PN group compared with the EEN group (P < 0.01). The anal exhaust time, length of hospital stay, and nutritional support cost were significantly shorter or lower in the EEN group than in the PN group (P < 0.01). There was no significant difference in the incidence of complications between the two groups (P > 0.05). EEN helps regulate the postoperative response of patients after gastric cancer surgery, promotes rehabilitation, and accelerates the recovery of gastrointestinal function. Furthermore, EEN has the advantage of being inexpensive.

Impact of early postoperative enteral nutrition on clinical outcomes in patients with gastric cancer.

The impact of early enteral nutrition (EEN) on clinical outcomes of gastric cancer patients was investigated. Three hundred pa-tients undergoing gastric cancer surgery from July 2010 to May 2014 were randomly divided into experimental and control groups (n = 150/group). Experimental group patients received enteral nutrition in water during the early postoperative period. Control group patients received conventional perioperative treatment. Patients' clinical outcomes, post-operative immune function, and nutritional statuses were compared, which revealed that the postoperative fever duration (80.2 ± 6.0 vs 88.1 ± 8.1 h, P < 0.05), anal exhaust time (78.8 ± 9.3 vs 85.3 ± 8.4 h, P < 0.05), and length of hospitalization (7.73 ± 2.13 vs 9.77 ± 1.76 days, P < 0.01) differed significantly. Treatment costs in thousands of dol-lars were 31.24 ± 3.21 for the experimental group and 35.61 ± 2.32 for the control group; this difference was statistically significant (P < 0.01). The incidence of postoperative complications did not significantly differ between the experimental and control groups [14.0% (21/150) vs 17.3% (26/150), P > 0.05]. At postoperative days 3 and 7, the CD3(+), CD4(+), natural killer cell, albumin, and prealbumin levels and CD4(+)/CD8(+) ra-tio were significantly higher in the experimental group than the control group (all P < 0.05). CD8(+) cell counts were significantly lower in the experimental group than the control group (P < 0.05). Postsurgical oral EEN can improve nutritional status and immune function and promote early recovery of intestinal function in patients with gastric cancer.

Association of MLL3 expression with prognosis in gastric cancer.

Low expression of myeloid/lymphoid or mixed-lineage leukemia 3 (MLL3) is reportedly associated with gastric cancer and tumor progression. The purpose of this study was to examine the expression of MLL3 in tissue samples of patients with gastric cancer and to analyze the relationship between MLL3 protein expression and clinical records. Using immunohistochemical staining and Kaplan-Meier analysis for MLL3 in gastric cancer patients, we found that low expression of MLL3 had a significant relationship with a low survival rate compared to positive MLL3 expression in the patients analyzed (P<0.05). Our data suggest that MLL3 expression plays a vital role in gastric cancer development, and that this protein is an important marker for the prognosis of gastric cancer.

[Clinical and pathological characteristics of Helicobacter pylori-associated chronic gastritis].

To define the clinical and pathological characteristics of Helicobacter pylori-associated gastritis, 173 patients with chronic gastritis, including 99 Hp-positive and 74 Hp-negative patients were studied. We found that there were no significant differences between Hp-positive and Hp-negative patients with regard to clinical symptoms, gastric acid secretion and serum basal gastrin level, whereas the grades of chronic gastritis and active gastritis were markedly higher in Hp-positive patients. 91.2% of patients with active gastritis had evidence of Hp infection. With the increase in Hp density, the proportion of high grades (II and III) gastritis tended to increase, especially the severe active gastritis. In addition, glandular atrophy and intestinal metaplasia in antral mucosa were significantly commoner in Hp-positive patients. There were no significant differences between the two groups in duodenogastric reflux rate, but the reflux rate over moderate degree in Hp-positive patients (19.59%) was somewhat lower that in Hp-negative patients (36.36%) (P = 0.09).

[An urease enzyme linked immunosorbent assay for detection of Helicobacter pylori infection].

A sensitive and specific serological diagnostic test for Helicobacter pylori infection has been developed and validated in 120 patients with dyspeptic symptoms undergoing endoscopy. This test is to use urease, a protein unique to H. pylori, as the basis for the enzyme linked immunosorbent assay (ELISA) that detects serum H. pylori urease antibodies. The ELISA mean optical density (OD) in H. pylori-positive group is higher than that in H. pylori-negative group (0.57 +/- 0.23 vs 0.24 +/- 0.15, P < 0.001), a cut-off 0.3 OD yields a sensitivity of 95% and a specificity of 93%. Serum absorption test showed that Escherichia coli, Klebsiella pneumonia, Proteus mirabilis, Yersinia enterocolotica, Pseudomonas aeruginosa cell lysate do not influence serum H. pylori urease antibody level, though they all have urease except E. coli. The result implied that H. pylori urease can be a good antigen to detect serum H. pylori antibody and it would be useful for epidemiological survey and routine diagnostic approach. Nearly half of the blood donors showed positive result with H. pylori urease antibody. It is suggested that H. pylori infection is quite common in the asymptomatic population.

[Duodenal ulcer disease: Helicobacter pylori and hyperchlorhydria].

Basal and pentagastrin-stimulated gastric acid secretion and basal serum gastrin level were investigated in 55 active duodenal ulcer patients with antral colonization with Helicobacter pylori (HP) and 17 patients without. Our study shows that basal (BAO) and pentagastrin-stimulated gastric acid secretion (MAO and PAO) were significantly higher in HP positive than in HP negative patients with duodenal ulcer disease. There were also a tendency to increase in basal serum gastrin concentration in HP positive patients. We suggest that antral HP increases antral gastrin release and gastric secretion. Increased acid secretion then causes duodenal ulcers by producing a low intraduodenal pH.

[Enzyme-linked immunosorbent assay for the serodiagnosis of Campylobacter pylori infection].

Antibody activities to campylobacter pylori in serum were estimated by an enzyme-linked immunosorbent assay (ELISA) to crude antigens, prepared by sonication of whole organisms obtained from bacterial culture in 100 patients with chronic gastritis. Significantly raised serum IgG antibody activities to C. pylori was found in colonised patients with gastritis, especially in patients with active gastritis. High activities were also found beyond the age of 30. In 6 patients cleared of C. pylori with furazolidone and/or colloidal bismuth subcitrate (De-NoL), serial testing has shown a fall in activity to normal level by 1/2 year in 4 patients. The specificity and sensitivity of the sero-diagnostic assay was 85.3% and 97% respectively. The positive and negative predictive values were 92.8% and 93.5% respectively. The results indicate that such a serodiagnostic assay could be used to screen patients with C. pylori colonisation in epidemiological surveys.

[Comparison of colloidal bismuth subcitrate with ranitidine in healing and relapse of Campylobacter pylori-associated duodenal ulcers].

Eighty patients with Campylobacter pylori-associated duodenal ulcer disease were randomly allocated to receive colloidal bismuth subcitrate (CBS)tablet 120 mg four times a day or ranitidine 150 mg twice daily in a trial comparing the effects of these drugs in short-term healing and post-healing relapse rates of duodenal ulceration. At 8 weeks 88.1% (37/42) of those on CBS and 92.1% (35/38) of those on ranitidine had ulcers healed. The difference is not significant. After ulcer healing, the cumulative rates of relapse, as determined endoscopically, for symptomatic and asymptomatic ulcers were 19.4% (6/31) for CBS and 46.7% (14/30) for ranitidine at 6 months (P less than 0.05) and 41.9% (13/31) for CBS and 73.3% (22/30) for ranitidine at 12 months (P less than 0.05). As campylobacter pylori was cleared in 35 of the 42 patients (83.3%) in the CBS group, while only one of the 38 patients (2.63%) in the ranitidine group (P less than 0.005), it is possible that the clearance of Campylobacter pylori by CBS is instrumental to the reduction of the rate of reulceration.

[Comparison of endoscopy and the milk 99mTc-EHIDA test in assessing duodenogastric reflux].

Duodenogastric reflux was estimated in 101 patients with chronic gastritis by means of endoscopy and milk 99mTc-EHIDA test. 61 patients (60.4%) were deemed to be duodenogastric reflux positive by endoscopy, as compared to 40 patients (39.6%) by milk 99mTc-EHIDA test. These differences are statistically significant (P less than 0.005). The discrepancy arises largely from the error in endoscopic estimation of duodenogastric reflux. In a group of 58 patients who were mild to moderate reflux positive by endoscopy, the assessment made by the milk 99mTc-EHIDA test was reflux positive in only 33 (57%). In other words more than 40% of the endoscopically reflux positive patients did not show reflux with 99mTc activity in the stomach. Measurement of the ratio of 99mTc activity in gastric aspirates to the total 99mTc activity injected intravenously was carried out in 13 patients. A perfect correlation was found between the ratio and the grading of duodenogastric reflux estimated by the milk 99mTc-EHIDA test. This finding suggests that by using the milk 99mTc-EHIDA test, duodenogastric reflux may be monitored semiquantitatively without recourse to a nasogastric tube. Furthermore, 10 patients were evaluated twice by the milk 99mTc-EHIDA test at intervals ranging from 3-14 days. In 8 patients the results were identical. This indicates the good reproducibility of the test. This study demonstrates that milk 99mTc-EHIDA test is a more physiological and more accurate method of studying duodenal contents in the stomach, than endoscopy.

[Effect of antacids on the bioavailability and therapeutic efficacy of cimetidine].

Five patients with duodenal ulcer received cimetidine and after an interval of four days cimetidine with antacid. Cimetidine in serum was analysed with high performance liquid chromatography. There was no significant difference in the values of the pharmacokinetic parameters of cimetidine (Cmax, tmax and AUC) when taking cimetidine alone and cimetidine plus antacid. 53 outpatients with endoscopically proven duodenal ulcer were evaluated in a randomized study, so as to compare the therapeutic effect of cimetidine and aluminum hydroxide gel plus cimetidine. 18 of 26 patient taking cimetidine alone (69.2%) and 19 of 27 patients taking cimetidine plus antacid (70.4%) had their ulcer completely healed after 4 weeks. The overall healing rates after 8 weeks for the groups taking cimetidine alone and cimetidine plus antacid were 80.0% and 92.6% respectively with no significant difference. This study indicates: (1) Simultaneous administration of aluminum hydroxide gel does not alter the bioavailability of cimetidine. (2) Combined administration of aluminum hydroxide gel and cimetidine does not alter the therapeutic effect of cimetidine in patients with duodenal ulcer.

[Clinical characteristics of bile reflux gastritis].

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.

Failure of pancreatic polypeptide release in congenitally obese mice.

Obesity can be reversed in ob/ob mice by parabiosis to lean littermates, by islet transplantation, and by injection of pancreatic polypeptide. These observations suggest that obese mice have functioning satiety centers but lack a circulating satiety factor of pancreatic origin which could be pancreatic polypeptide. This hypothesis has been difficult to test because antisera currently available do not cross-react with rodent pancreatic polypeptide. We have raised an antiserum against the biologically active carboxyl-terminal hexapeptide that measures mouse pancreatic polypeptide specifically. This antiserum has been used to compare circulating and tissue concentrations of pancreatic polypeptide in obese and lean mice. Although pancreatic contents were significantly (p less than 0.01) increased in obese mice (237 +/- 34 pmol/g) compared with lean littermates (107 +/- 20 pmol/g), no postprandial increase in circulating concentrations was observed in obese mice. The hypothesis that obese mice lack a satiety factor of pancreatic origin could be explained by the failure of release of pancreatic polypeptide.