Complete genome sequence of Selenomonas species strain TAMA-11512, isolated from blood culture of a septic patient.

We report the complete sequence of Selenomonas species strain TAMA-11512, isolated from the blood culture of a septic patient. The phylogeny and average nucleotide identity show that the strain TAMA-11512 is considered a novel bacterial species in Selenomonas genus.

Disseminated tuberculosis following invasive procedures for peripancreatic lymph node tuberculosis with portal vein obstruction: a case report.

Peripancreatic tuberculous lymphadenopathy can mimic pancreatic cancer on imaging. There have only a few reports on varices from portal vein obstruction due to abdominal tuberculous lymphadenopathy. Iatrogenic disseminated tuberculosis is also rare. Herein, we present a rare case of peripancreatic tuberculous lymphadenopathy with ruptured duodenal varices due to portal vein obstruction. The patient presented to our hospital with hematemesis. Computed tomography revealed a peripancreatic mass. Duodenal varices rupture from portal vein obstruction due to pancreatic cancer were initially suspected. The patient underwent portal vein stenting for portal vein obstruction and endoscopic ultrasound-guided fine-needle aspiration for diagnosis, which revealed granulomas indicative of tuberculosis. The patient was discharged once because fine-needle aspiration did not lead to a definitive diagnosis of tuberculosis. Subsequently, he developed disseminated tuberculosis. Peripancreatic tuberculous lymphadenopathy can cause ectopic varices with portal vein obstruction. Tuberculosis should also be included in the differential diagnosis in the case of portal vein obstruction, to facilitate early treatment and avoid unnecessary surgery. Furthermore, fine-needle aspiration or portal vein stenting for tuberculous lesions can cause disseminated tuberculosis. Since a diagnosis might not be made until after several fine-needle aspirations have been conducted, careful follow-up is necessary after the procedure for such lesions.

Islet amyloid with macrophage migration correlates with augmented ß-cell deficits in type 2 diabetic patients.

AIMS: Islet amyloid is a hallmark in type 2 diabetic subjects, but its implication in clinical features and development of islet pathology is still unclear. METHODS: From 118 autopsy cases with type 2 diabetes, 26 cases with islet amyloid deposition (DA+) were selected. Twenty diabetic subjects without obvious amyloid deposition (DA-) matched for the age and diabetes duration and 20 non-diabetic subjects (ND) served for comparison. We examined the severity of amyloid deposition and its relationships with population of endocrine cells, expression of cell damage markers or macrophage infiltration. Correlation of clinical profile with islet pathology was also sought on the subset of the investigated patients. RESULTS: ß-Cell volume density was nearly 40% less in DA+ and 20% less in DA- when compared to ND. Severity of amyloid deposition correlated with reduced volume densities of ß-cell and α-cell, and increased body mass index (BMI), but not with duration of diabetes, age or HbA1c. Amyloid-rich islets contained an increased number of macrophages mixed with ß-cells with oxidative stress-related DNA damage, characterized by γH2AX expression, and suppressed (pro)insulin mRNA expression. CONCLUSIONS: In Japanese type 2 diabetic patients, islet amyloid was more common with severe ß-cell loss and high BMI, associated with macrophage infiltration.