No abstract

Because of its features of easy use, accuracy, and generalizability, mE-PASS is a candidate for a nation-wide survey.

Macrophage infiltration into colon cancer and amphoterin expression in cancer cells was examined in 42 human colon cancers invading the subserosa. The mean number of infiltrating macrophages was significantly higher in Dukes’ B cases than in Dukes’ C cases (p = 0.0065). Tumors with few infiltrating macrophages (macrophage depletion) were significantly more frequent in Dukes’ C cases than in Dukes’ B cases (p = 0.0014). No Dukes’ C cases with relevant macrophage infiltration showed macrophage-cancer cell contact, whereas 5 Dukes’ B cases showed such contact (p < 0.0001). In human colon cancer cells implanted in the cecum of nude mice, KM12SM (highly metastatic) tumors yielded less macrophage infiltration and more liver metastases than KM12C (low risk of metastasis) tumors (14 ± 3 vs. 78 ± 32 and 24 ± 6 vs. 5 ± 3 per liver, respectively). Amphoterin expression was detected at high frequency in both Dukes’ B and C cases (p = 0.0684). In macrophage-depleted cases, amphoterin expression was significantly higher than that in non-depleted cases (p = 0.0015). To confirm biological effects of amphoterin on macrophages, an infiltration assay using the cell-layered Boyden chamber was done. Infiltration of PMA-treated U937 monocytes through the KM12SM cell layer was increased by pretreatment of KM12SM cells with amphoterin antisense S-oligodeoxynucleotide exposure. Moreover, extracted amphoterin inhibited PMA-U937 monocyte infiltration in a dose-dependent manner. Thus, amphoterin may play an important role in the inhibition of macrophage infiltration into colon cancer.

Objective: Acute mesenteric ischemia is potentially fatal, but prognostic factors have not yet been established. This study was undertaken to elucidate them. Methods: This is a retrospective cohort study, consisting of 110 patients who had been treated in the past 5 years, from 26 national hospitals in Japan. Results: The overall in-hospital mortality rate was 51%. Logistic regression analysis demonstrated two independent prognostic factors, electrocardiogram scale with an odds ratio of 1.7 (95% CI 1.2–2.4) and shock index of 11 (95% CI 1.5–80). A stepwise analysis gave a prediction equation for in-hospital mortality (R) using these variables and age score. We further modified this equation to a simpler scoring system (S) using the same variables. Both R and S showed a good discriminatory ability as determined by areas under the receiver-operating characteristic curve (0.83, 95% CI: 0.74–0.91 for R; 0.82, 95% CI 0.74–0.91 for S). The observed mortality rates increased as the R or S increased (19% at R <0.25, 41% at 0.25 ≤ R <0.6, 85% at R ≥0.6; 19% at S ≤2, 37% at S of 3 or 4, 91% at S ≥5). Conclusion: The new prediction rules can be used at any hospital and may be promising tools for medical decision-making, informed consent and reviewing quality of care.

No abstract

The influence of ranitidine and cysteamlne on intestinal metaplasia was examined in 7‐month‐old male Crj: CD (SD) rats. At the age of 5 weeks, the animals were treated with 10 Gy doses of X‐rays at 3‐day intervals up to a total of 20 Gy in the gastric region, and 6 months after irradiation, the rats received either ranitidine (0.02% in diet) or cysteamine (0.1% in drinking water) for 2 months. The incidence and number of intestinal metaplasia with alkaline phosphatase‐positive foci in rats given X‐rays and cysteamlne (group 4) were significantly low compared with those in rats given X‐rays and ranitidine (group 3) (p<0.01). In both the pyloric and the fundic gland mucosae, the average numbers of type C metaplasia (intestinal crypts with Paneth cells) and total numbers of metaplastic foci in rats of group 3 were much higher than those in group 4 (P<0.05). The present results showed that the occurrence of intestinal metaplasia was significantly increased after administration of ranitidine and decreased by cysteamine. ACTA PATHOL JPN 38 : 1285‐1296, 1988.

BackgroundSpontaneous regression (SR) of colorectal cancer (CRC) is extremely rare, and only few cases have been reported. Although it is not yet clarified, a plausible mechanism for SR of CRC is an immunological event.Case presentationIn this report, we present the case of SR of primary CRC in a 78-year-old man. Preoperative colonoscopy was performed, and a type 2 tumor measuring 30 mm in diameter in the transverse colon was detected. The biopsy revealed a poorly differentiated adenocarcinoma. Colectomy was performed 2 months after initial colonoscopy. During the surgery, only a 10-mm ulcer harboring a polypoid lesion measuring 8.5 mm was detected in the resected tissue; no other masses or carcinoma cells were seen on histological examination. Afterwards, the biopsy specimens were reanalyzed, and immunohistological analysis verified this as adenocarcinoma with stroma-infiltrating lymphocytes. Further analysis revealed a loss of two mismatch repair proteins, suggesting sporadic high-frequency microsatellite instability (MSI-H).ConclusionAccording to previous literature, a common site of SR in CRC is the proximal colon, which is a feature of MSI-H CRC. However, our report showed a rare case of SR of CRC, which was in the transverse colon, with MSI-H present. This report indicates a relationship between immunological features of MSI-H and the occurrence of SR of CRC. A better understanding of this phenomenon and the mechanisms involved will have significant preventive and therapeutic implications for CRC, including anti-PD-1 immune checkpoint inhibitor therapy.

Double gallbladder is a rare congenital biliary anomaly, but an accessory gallbladder arising from the left hepatic duct is a more remarkably rare congenital anomaly. We report a case of double gallbladder with adenocarcinoma and gallstones, which was preoperatively diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) and then confirmed by open laparotomy. A review of the literature is presented.