Association between being breastfed in infancy and adult colorectal cancer risk among Japanese men and women.

It has been postulated that being breastfed in infancy affects not only health status in childhood but also disease risk in adulthood. To investigate the association of being breastfed with the risks of adult colorectal cancer and benign tumor, we conducted a case-control study including 1190 colorectal cancer and 1585 benign tumor cases and 5301 controls, admitted to a single hospital in Miyagi Prefecture, Japan, between 1997 and 2013. History of having been breastfed was assessed using a self-administered questionnaire, and odds ratios (ORs) were estimated using unconditional logistic regression. There was no association between being breastfed and colorectal cancer risk (breastfed versus formula-only fed, OR = 1.21; 95% CI 0.87-1.67). There was also no association with the risk of benign tumor (OR = 1.04). On the other hand, analyses stratified by sex and birth year found heterogeneous associations. Women born after 1950 who had been breastfed tended to have increased risks of colorectal cancer (OR = 1.58) and benign tumor (OR = 1.51) relative to those who had been formula-only fed, although not statistically significant. In men born after 1950, being breastfed was associated with a significantly decreased risk of benign tumor (OR = 0.57; 95% CI 0.33-0.98).

[Pancreatic groove carcinoma in a young adult].

A 26-year-old woman was admitted to our hospital with jaundice. Under a diagnosis of biliary and duodenal stenosis due to so called "groove pancreatitis", prednisolone (30 mg/day, 2 weeks) was administered. But these stenosis did not improve after the treatment, and pancreaticoduodenectomy was performed. Histologically, poorly differentiated adenocarcinoma was found in the "groove" between the duodenum and the pancreatic head. We should be kept of "pancreatic groove carcinoma" in mind when making a diagnosis of "groove pancreatitis".

Inhibition of heme oxygenase ameliorates sepsis-induced liver dysfunction in rats.

PURPOSE: The disintegration of heme produces carbon monoxide (CO), a known vasodilator, which is catalyzed by heme oxygenase (HO). This study aimed to clarify the effect of HO inhibition on septic rat livers using two types of HO inhibitors; Sn-protoporphyrin (Sn-PP) and Zn-protoporphyrin (Zn-PP). METHODS: Sepsis was induced in male Sprague-Dawley rats by cecal ligation and puncture (CLP). Either NaOH or HO inhibitors were injected intraperitoneally; first 18 h prior to CLP, then immediately after CLP. The animals were killed 12 and 24 h after CLP and the liver tissue and plasma were harvested. RESULTS: Using Northern blotting, we found that mRNA of the stress-inducible isozyme, HO-1, was dramatically induced 12 h after CLP. Administering the HO inhibitors, Sn-PP and Zn-PP (5 micromol/kg), induced a significant inhibition of the elevation of aspartate aminotransferase plasma levels, the elevation of cyclic guanosine monophosphete (cGMP) in the liver tissue, and the increase in the sinusoidal space ratio, 24 h after CLP. Both Sn-PP and Zn-PP decreased the mortality rate 24 h after CLP compared with normal saline. CONCLUSIONS: CO produced by excessively induced HO-1 after CLP promotes an immoderate dilation of the sinusoidal space through the up-regulation of cGMP, resulting in liver dysfunction. Therefore, administering HO inhibitors at appropriate doses could be beneficial for the amelioration of sepsis-induced liver dysfunction.

Changes of hepatic sinusoids in experimental septicemia of rats are correlated with the production of nitrogen monoxide. A morphometrical and immunohistochemical study.

BACKGROUND/AIMS: Two types of experimental septic models were prepared to morphologically and histometrically analyze the changes in the hepatic sinusoid. Furthermore, the local expression of nitrogen monoxide synthetase was analyzed by immunohistochemical and immune electron microscopical studies for the purpose of investigating the involvement of nitrogen monoxide in these changes. METHODOLOGY: Using Sprague-Dawley strain male rats, two types of experimental septic models were prepared. These were a bacterial peritonitis model induced by a cecal ligation and puncture method, and a peritonitis model after intraperitoneal administration of endotoxin at 10 mg/kg. Serum alanine aminotransferase and endotoxin were measured in due order. The liver tissues were sampled and examined by usual light microscopical and electron microscopical analyses. The sites of the portal and central vein regions were randomly selected, and the sinusoidal cavity/liver volume ratio was estimated by the point counting method under high magnification. In addition, the expressions of nitrogen monoxide synthetase were investigated in the collected samples of the liver, lung and aortic wall. RESULTS: According to the histometrical analysis of the sinusoid, the sinusoidal cavity volume ratio at 6 hours after the onset increased from 0.0690 +/- 0.0147 to 0.089 +/- 0.004 in the central vein region. The ratio rapidly increased from 0.058 +/- 0.009 to 0.093 +/- 0.008 in the portal region from 6 to 12 hours after the onset. The values of serum alanine aminotransferase and endotoxin were significantly increased from 6 to 12 hours after the onset of peritonitis. The inducible nitrogen monoxide synthetase was observed in the alveolar macrophages, monocytes, and hepatic Kupffer cells from 6 to 12 hours after the onset of peritonitis. CONCLUSIONS: These results demonstrated that the sinusoidal cavity became dilated in the sepsis model and at the same time nitrogen monoxide synthetase was expressed in the sinusoidal wall-composing cells. There is a possibility that the action of nitrogen monoxide is involved in the changes in the volume of the sinusoidal cavity, suggesting the involvement of nitrogen monoxide derived from sinusoidal wall-composing cells in the hepatic dysfunction caused by sepsis in addition to nitrogen monoxide generation from Kupffer cells.