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The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Objective: Helicobacter pylori is the major etiologic agent for chronic active gastritis, and it also plays a crucial role in gastric and duodenal ulcer disease, as well as in gastric carcinoma. H. pylori infection has been shown to decrease plasma somatostatin (SST) and increase plasma gastrin concentrations. Ghrelin is a recently discovered peptide produced mostly in the stomach of rodents and humans and is secreted into the bloodstream. There is no data in the literature about the relationship between H. pylori and ghrelin. Design: Thirty-nine age-and BMI-matched H. pylori infection positive and negative women, from whom biopsy specimens were taken during gastric endoscopy, were included in the study. Methods: Total ghrelin was measured by enzyme immunoassay (EIA) in Medistek. All samples were measured in duplicate and averaged; results differing by more than 20% were re-assayed. Two biopsy specimens from antrum, corpus and fundus were obtained. Results: Fifteen of the subjects were H. pylori negative and 24 were H. pylori positive. Age, BMI, lipid profile and insulin sensitivity indices of the groups were similar. Plasma ghrelin levels ð375:92^7:10 vs 370:00^4:14 pmol=l; P . 0:05Þ of H. pylori negative and positive groups did not differ significantly. Conclusion: H. pylori has no effect on plasma ghrelin concentration.

Our rates of eradication were significantly lower when compared to those reported in literature. We believe that advanced age and high H pylori density are negative predictive factors for the rate of H pylori eradication.

Previous study of experimental varicocele models in rats documented HIF-1alpha and VEGF expression combined with angiogenesis in the testis. The results of this study show that varicocele can lead to tissue hypoxia and related pathophysiological events, such as angiogenesis.

Colorectal primary signet ring cell carcinoma (PSRCCR) is a rare entity with a dismal prognosis, mainly because of delayed diagnosis. The objective of this study was to investigate the clinicopathologic features and prognostic factors for PSRCCR. This is a retrospective study including the data of 22 patients with PSRCCR who underwent surgery. Patients were categorized by age, sex, tumor site, and stage. Fifteen patients were male. Median age was 40 years. Sites for metastases were lymph nodes (86.4%), peritoneum (40.9%), and liver (9.1%). Most of the patients (91%) had stage III or IV tumors. The rates of curative and palliative resections performed were equal. Mean overall survival and mean progression-free survival times were found to be 33.3 6 7.1 months (95% confidence interval, 19.4-47.2 months) and 11.8 6 3.5 months (95% confidence interval, 4.9-18.7 months), respectively. It was concluded that site of the tumor, presence of bowel obstruction, peritoneum and lung metastases, adjacent organ infiltration, TNM stage, and efficiency of surgery have significant effects on survival. All in all, these aggressive tumors are generally diagnosed at advanced stages. Depending on the situation, survival is shorter. A high degree of vigilance is required for these patients to avoid the negative impact of late diagnosis on survival.

We aimed to investigate if expressions of survivin and p27 proteins are involved in the development of endometrioid carcinoma, along with whether there are any correlations between these proteins and loss of wild-type PTEN that is found in up to 80% of endometrial carcinomas. We also studied their correlations with classical prognostic factors and survival in endometrial carcinoma. To our knowledge, this is the first time survivin expression is investigated in endometrial hyperplasia along with endometrioid adenocarcinoma. For immunohistochemical analysis, 29 endometrioid adenocarcinoma, 38 endometrial hyperplasia, and 10 proliferative endometrium tissue samples were selected in the pathology archives. Staining of cells was scored as +2 if >50%, +1 if <50%, and negative if none were stained positive. Survivin expression increased from proliferative to hyperplasia to carcinoma cases. PTEN and p27 expressions decreased in hyperplasia and carcinoma cases with respect to proliferative endometrium. All these differences were statistically significant (P < 0.05). PTEN positively correlated to p27 (P < 0.05); however, neither was correlated with survivin. None of these genes were correlated with classical prognostic factors such as grade and myometrial invasion in endometrioid adenocarcinoma. However, mean survival was statistically significantly higher in PTEN-positive cases (46.6 vs 16.4 months) (P < 0.05). Survivin overexpression might be one of the important mechanisms in the development of endometrioid adenocarcinoma along with lost or decreased activity of PTEN and p27. However, survivin seems to exert its role in ways different from those of PTEN or p27 in the development of endometrioid adenocarcinoma. These findings on the role of survivin in endometrioid adenocarcinoma should be confirmed and the pathways through which survivin acts in endometrioid adenocarcinoma studied further with a larger sample size.

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