Leuconostoc lactis, often found in fermented dairy products, although considered to have a low pathogenic potential, can cause life-threatening infections in immunocompromised hosts. We herein report a 62-year-old man with a history of alcoholic liver cirrhosis, hepatocellular carcinoma, and diabetes mellitus who developed a very rare case of bacterial meningitis caused by this organism. After we administered antibiotics including ampicillin, he recovered completely within two weeks. This gram-positive coccus (GPC) is sensitive to ampicillin but naturally resistant to vancomycin, while its susceptibility to ceftriaxone has not yet been established. In acute GPC meningitis in immunocompromised hosts, Leuconostoc lactis should therefore be considered as a possible pathogen.Objective Home care is important in patients with heart failure (HF) in order to maintain their quality of life. A biomarker that can be measured noninvasively is needed to optimize the home care of patients with HF. RGD (Arg-Gly-Asp) Peptides clinical trial Urinary angiotensinogen (uAGT) is an indicator of the intrarenal renin-angiotensin system activity, which may be augmented in HF. We hypothesized that uAGT might be a urinary biomarker in HF. Methods We measured uAGT by an enzyme-linked immunosorbent assay and uAGT normalized by urinary creatinine (uCr)-designated uAGT/uCr-at admission and discharge in 45 patients hospitalized for HF. Results We found that both uAGT/uCr [median (interquartile range) 65.5 (17.1-127.7) μg/g Cr at admission; 12.1 (6.0-37.0) μg/g Cr at discharge; p less then 0.01] and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels [5,422 (2,280-9,907) pg/mL at admission; 903 (510-1,729) pg/mL at discharge; p less then 0.01] significantly decreased between admission and discharge along with an improvement in patient's clinical status [New York Heart Association scores 3 (3-4) at admission; 1 (1-1) at discharge; p less then 0.01]. The generalized least squares model revealed that the time course changes in uAGT/uCr also correlated with those in NT-proBNP levels between admission and readmission in five patients readmitted for HF. Conclusion The results indicated that the time course changes in uAGT/uCr correlated with those in the NT-proBNP levels in patients with HF who showed a clinical improvement. Further investigation and development of a kit for the rapid measurement of uAGT are needed to evaluate the clinical utility of uAGT as a biomarker in HF.Objective There is a paucity of information on whether the hepatitis B virus (HBV) vaccine, derived from HBV genotype C, can prevent mother-to-child transmission of HBV genotype D. The aim of this study was to clarify this issue. Methods The subjects consisted of 25 children (8.5±4.1 years old, 7 males, 18 females), born to 17 mothers who were chronically infected with HBV genotype D. Of these, 20 children were inoculated with the genotype C-derived vaccine, one was inoculated with the genotype A-derived vaccine, and one was inoculated with both the A- and C-derived vaccines. Information on the type of vaccine given to the remaining three children was not available. The serum levels of HB surface antigen (HBsAg), antibody to HBsAg (anti-HBs), and antibody to HB core (anti-HBc) of the children, as well as HBV markers of the mothers, were examined. Results All mothers were positive for HBsAg (6,563±11,005 IU/mL), negative for HBeAg, and positive for anti-HBe. HBV-DNA levels (log IU/mL) were 4.3 in one mother. HBsAg and anti-HBc were negative in all children, regardless of the type of vaccine used. Anti-HBs were positive in 13 children and negative in 12. Conclusion All children born to mothers infected with genotype D, including 20 who were inoculated with the genotype C-derived vaccine, were negative for both HBsAg and anti-HBc. These results suggest that the genotype C-derived HB vaccine is effective in preventing mother-to-child transmission from mothers infected with HBV genotype D.Liquid-liquid extraction for the removal of pertechnetate (99TcO4-) and perrhenate (ReO4-) is reported based on using the tripodal extractant N,N,N',N',N″,N″-hexa-n-octylnitrilotriacetamide (HONTA) composed of three amide groups and a tertiary amine. The extraction behaviors were compared with those using alkyldiamideamines (ADAAM(Oct) and ADAAM(EH)), and the commercial amine-type extractant, trioctylamine (TOA). HONTA quantitatively extracted 99TcO4- and ReO4- in the pH range from 1.0 to 2.5 by the co-extraction of protons. The extraction performance of the extractants was improved in the order of HONTA > ADAAM(Oct) > ADAAM(EH) > TOA. 99TcO4- and ReO4- in the extracting phase were successfully stripped using neutral aqueous solutions as the receiving phase, and the extraction ability of HONTA was maintained after five repeated uses. Adiponectin (APN) exhibits different atheroprotective effects, and we have previously reported that APN function is modulated by its binding proteins, E-selectin ligand 1, Mac-2 binding protein, and cystatin C. In the present study, we aimed to identify a novel atheroprotective mechanism of APN via C-C motif chemokine 2 (CCL2). We conducted iMAP -intravascular ultrasound (IVUS) in 111 Japanese male patients with stable angina. The plaque characteristics were determined where "plaque burden" [(EEM CSA - lumen CSA)/(EEM CSA)×100 (%)] ＞50%, and their correlation with serum CCL2 and APN levels was analyzed. Using western blot analysis, the effects of APN on the biological effects of CCL2 were examined in their mutual binding by co-immunoprecipitation assay, the monocyte migration, and the phosphorylation of MAP kinases. In a clinical study, we found that the percentage of plaque in the culprit lesion was correlated positively with serum CCL2 and negatively with serum APN levels, with significance. We identified CCL2 as a novel APN-binding serum protein using immunoprecipitation and western blot analysis. CCL2-induced phosphorylation of MAP kinases and monocyte migration was significantly attenuated by APN in vitro. The opposite association of APN and CCL2 on the percentage of coronary plaque might be caused by their direct interaction and competitive functions on monocyte migration.The opposite association of APN and CCL2 on the percentage of coronary plaque might be caused by their direct interaction and competitive functions on monocyte migration.