Toshinori Kamisako

The authors wish to make the following corrections to this paper

Gemella is a catalase-negative, facultative anaerobic, Gram-positive coccus that is commensal in humans but can become opportunistic and cause severe infectious diseases, such as infective endocarditis. Few studies have tested the antimicrobial susceptibility of Gemella. We tested its antimicrobial susceptibility to 27 drugs and defined the resistant genes using PCR in 58 Gemella strains, including 52 clinical isolates and six type strains. The type strains and clinical isolates included 22 G. morbillorum, 18 G. haemolysans (GH) group (genetically indistinguishable from G. haemolysans and G. parahaemolysans), 13 G. taiwanensis, three G. sanguinis, and two G. bergeri. No strain was resistant to beta-lactams and vancomycin. In total, 6/22 (27.3%) G. morbillorum strains were erythromycin- and clindamycin-resistant ermB-positive, whereas 4/18 (22.2%) in the GH group, 7/13 (53.8%) G. taiwanensis, and 1/3 (33.3%) of the G. sanguinis strains were erythromycin-non-susceptible mefE- or mefA-positive and clindamycin-susceptible. The MIC₉₀ of minocycline and the ratios of tetM-positive strains varied across the different species—G. morbillorum: 2 µg/mL and 27.3% (6/22); GH group: 8 µg/mL and 27.8% (5/18); G. taiwanensis: 8 µg/mL and 46.2% (6/13), respectively. Levofloxacin resistance was significantly higher in G. taiwanensis (9/13 69.2%) than in G. morbillorum (2/22 9.1%). Levofloxacin resistance was associated with a substitution at serine 83 for leucine, phenylalanine, or tyrosine in GyrA. The mechanisms of resistance to erythromycin and clindamycin differed across Gemella species. In addition, the rate of susceptibility to levofloxacin differed across Gemella sp., and the quinolone resistance mechanism was caused by mutations in GyrA alone.

Background: The quantification of hepatitis B virus (HBV) DNA is used to monitor antiviral treatment for HBV infection. Recently, an HBV-DNA quantification reagent and assay protocol have been developed for the mu TASWako g1 (Fujifilm Wako Pure Chemical Corporation, Osaka, Japan), a fully automated genetic analyzer that uses PCR-capillary electrophoresis. We evaluated the performance of the newly developed mu TASWako HBV-DNA assay using standard and clinical samples. Methods: The performance of mu TASWako HBV-DNA was evaluated using 3rd World Health Organization International Standard for HBV. Thereafter, we evaluated the correlation between the serum HBV DNA concentrations obtained using the mu TASWako HBV-DNA and the Roche Cobas AmpliPrep/COBAS TaqMan HBV test, version 2.0 (CAP/CTM HBV test v.2.0) using 190 serum samples from possible HBV carriers. Results: The limit of detection of the mu TASWako HBV-DNA was 7.1 IU/mL and that of the CAP/CTM HBV test v.2.0 was 14.6 IU/ mL. Seventy-six of the 190 samples yielded values between 1.3 - 7.8 log IU/mL from both assays. The correlation between the results of the assays for these samples was good, with a Deming regression equation of y = 0.929x + 0.041, 95% confidence intervals (CI) for the slope and intercept of 0.892 - 1.12 and -0.474 - 0.110, respectively, and a correlation coefficient r = 0.924. In the low concentration range of 1.3 - 4.0 log IU/mL (n = 64), the Deming regression equation was y = 0.893x + 0.126, and the 95% CIs for the slope and intercept were 0.915 1.342 and -0.930 - 0.025, respectively, and r = 0.809. There was also a close correlation for HBV DNA genotype C (n = 41), with a Deming regression equation of y = 0.975x - 0.048, 95% CIs of the slope and intercept of 0.872 1.183 and -0.591 - 0.188, respectively, and r = 0.950. The correlations of the four HBV DNA level categories (not detected, < LLOQ (< 1.3 log IU/mL), 1.3 - 3.2 log IU/mL, and = 3.3 log IU/mL) between the two assays for the 190 samples was also compared, and the overall concordance rate was 81.6% (155/190), with a. statistic of 0.73 (standard error, 0.040; 95% CI, 0.647 - 0.803). Conclusions: The mu TASWako HBV-DNA has a performance comparable with that of the CAP/CTM HBV test, v.2.0. Thus, mu TASWako HBV-DNA is useful for the monitoring of HBV infection.

Oltipraz, a synthetic dithiolethione, has chemopreventive effect through nuclear factor erythroid 2-related factor 2 (Nrf2) activation. Nrf2 is known to be involved in the development of experimental steatohepatitis in rodents. In this study, to evaluate the effect of oltipraz on lipid and bile acid metabolism, wild-type and Nrf2-null mice were fed the standard diet (containing 4% soybean oil) with or without oltipraz. Based on these results, we examined the effect of oltipraz on the experimental steatohepatitis in high-fat diet (containing 4% soybean oil and 20% lard) fed Nrf2-null mice. Oltipraz induced hepatic mRNA expression of peroxisome proliferator-activated receptor α, carnitine palmityl transferase 1, and bile salt export pump by Nrf2 independent mechanisms. In Nrf2-null mice fed a high-fat diet for 12 weeks, moderate to severe inflammation and fibrosis were observed. Oral administration of oltipraz suppressed the degree of inflammation and fibrosis in Nrf2-null mouse liver fed a high-fat diet. These histopathological findings approximately corresponded to the data of mRNA expression of tumor necrosis factor α, monocyte chemoattractant protein-1, Timp-1, and collagen type 1α1. These results indicated that oltipraz administration ameliorated liver injury by Nrf2 independent manner in a model of steatohepatitis generated by Nrf2-null mice with high-fat diet.

Human chorionic gonadotropin (hCG) is generally quantified in serum, but spot urine samples are also used to assess hCG levels in Japan. The purpose of the present study was to elucidate whether urinary hCG can be used clinically as a substitute for serum hCG. A total of 189 samples of serum and spot urine were collected from patients, including cases of normal pregnancy (NP) -13, abortion (AB) -21, extrauterine pregnancy (EP) 25, and hydatidiform mole (MOL) -7, during medical treatment and comparisons were made concerning serum and urinary hCG levels. The histogram of relative urinary/serum hCG(U-hCG.act/S-hCG) of the samples showed a wide distribution of values, but tended to converge to a narrow distribution by creatinine correction (U-hCG.cor/S-hCG). U-hCG.cor/S-hCG of the AB, EP, and MOL groups decreased 1 day to 14 days or was no earlier than 15 days postoperatively compared to preoperatively. The alteration of serum Intact/Total tended to be similar to that of U-hCG.cor/S-hCG in clinical course. The presented case indicated that U-hCG.act/S-hCG did not correspond to serum hCG levels. Because urinary hCG levels are inconsistent depending on whether spot urine is concentrated or diluted, the levels of hCG in spot urine do not always correlate with serum levels of hCG. Therefore, the data of urinary hCG should be interpreted after creatinine correction. Overall, it is recommended to determine serum hCG levels rather than creatinine corrected urinary hCG levels, considering that the relative urinary/serum hCG was not constant postoperatively.

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Bilirubin has antioxidant properties and is known to have a role in the prevention of cardiovascular disease. Bilirubin is known to be negatively associated with serum parameters related to atherosclerosis. Triglyceride-rich lipoprotein is known to play an important role in the progression of atherosclerosis. The aim of the present study was to elucidate the relationship between serum bilirubin and serum remnant lipoprotein cholesterol (RLP-c). We examined 270 Japanese males (mean age 64.8 years) without liver dysfunction and anemia from the Outpatient Clinic of Kinki University Hospital. Serum bilirubin, cholesterol, LDL cholesterol, HDL cholesterol, triglyceride and RLP-c levels were measured. Serum RLP-c level was significantly lower in patients in the high bilirubin group than those in the low bilirubin group. The findings of this study show that serum bilirubin within physiological levels may affect the serum RLP-c and suggest bilirubin may have a role in preventing atherosclerosis.

Aim: Fish oil rich in n-3 polyunsaturated fatty acids is known to affect hepatic lipid metabolism. Several studies have demonstrated that fish oil may affect the bile acid metabolism as well as lipid metabolism, whereas only scarce data are available. The aim of this study was to investigate the effect of fish oil on the gene expression of the transporters and enzymes related to bile acid as well as lipid metabolism in the liver and small intestine. Methods: Seven-week old male C57BL/6 mice were fed diets enriched in 10% soybean oil or 10% fish oil for 4 weeks. After 4 weeks, blood, liver and small intestine were obtained. Results: Hepatic mRNA expression of lipids (Abcg5/8, multidrug resistance gene product 2) and bile acids transporters (bile salt export pump, multidrug resistance associated protein 2 and 3, organic solute transporter α) was induced in fish oil-fed mice. Hepatic Cyp8b1, Cyp27a1 and bile acid CoA : amino acid N-acyltransferase were increased in fish oil-fed mice compared with soybean-oil fed mice. Besides, intestinal cholesterol (Abcg5/8) and bile acid transporters (multidrug resistance associated protein 2 and organic solute transporter α) were induced in fish oil-fed mice. Conclusion: Fish oil induced the expression of cholesterol and bile acid transporters not only in liver but in intestine. The upregulation of Abcg5/g8 by fish oil is caused by an increase in cellular 27-HOC through Cyp27a1 induction. The hepatic induction of bile acid synthesis through Cyp27a1 may upregulate expression of bile acid transporters in both organs.

The members of 23 laboratories, ten clinical laboratory centers and thirteen hospital laboratories in the Kinki District participated in share their clinical laboratory data. In this joint work, we cross-checked twenty-seven serum values, and all data from the 23 laboratories well accorded; however, several values, such as urea nitrogen, calcium, and albumin needed to be standardized to share the laboratory data.

Background and Aim: To evaluate the importance of cholesterol and bile acid concentrations in the intestinal lumen to cholesterol homeostasis, we investigated the effect of cholesterol‐, bile salt‐ or cholestyramine‐administration on the regulation of intestinal mRNA related to cholesterol and bile acid metabolism.Methods: Male Wistar rats fed on standard laboratory chow (AIN‐93) were allocated into four experimental groups: (i) control group; (ii) cholesterol group (CH), which was fed cholesterol in diet (2% [w/w]) for 14 days; (iii) cholic acid (CA) group, which was fed CA in diet (1% [w/w]) for 14 days; (iv) cholestyramine (CT) group, which was fed CT in diet (5% [w/w]) for 14 days. Blood, liver and small intestine were obtained after 14 days. Serum lipids and bile acids were measured by colorimetric assays, and hepatic and intestinal mRNA relating to lipid and bile acid metabolism was studied by reverse transcription–polymerase chain reaction.Results: Intestinal ABCG8, liver X receptor α, small heterodimer partner (SHP) and sterol regulatory element binding protein 1c (SREBP‐1c) mRNA expressions were markedly increased in the CH group. Intestinal multidrug resistance associated protein (MRP) 2 and MRP3 mRNA expressions were markedly increased in the CA group. In the CT group intestinal MRP2, ABCG5, ABCG8, SHP and SREBP‐1c mRNA expressions were markedly decreased.Conclusion: The bile acid availability in the intestinal lumen alters the expression of various intestinal mRNA relating to not only bile acid metabolism, but also lipid metabolism. Though the mechanism of the intestinal SHP elevation is unclear, cholesterol feeding may affect the intestinal bile acid metabolism via intestinal SHP expression.