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We compared antimicrobial susceptibility patterns of 206 group B streptococcal (GBS) strains isolated from pregnant women and six from neonates/infants with invasive infection during the two periods 1985-1986 and 1999-2000. All strains in both periods were susceptible to the penicillins, cephalosporins and carbapenem tested. Seven (3%) isolates were resistant to erythromycin and three (1%) were resistant to clindamycin. There were no significant differences between the two study periods in the incidence of GBS resistant to the 14 antibiotics tested. These results showed that penicillins are still the first choice to prevent vertical transmission of GBS in Japan.

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The worldwide incidence of obesity has accelerated during the last decade. Obesity is caused by excessive accumulation of white adipose tissue, often as the result of ingesting calories in excess of daily requirements ( 1, 2 ). In investigations of disease outcome, excess adipose tissue is defi ned by using the body mass index (BMI), which is calculated as weight (kg)/height (m 2 ). A BMI of 25.0-25.9 kg/m 2 corresponds to an overweight condition, whereas obesity is defi ned as a BMI of 30 kg/m 2 or greater ( 3, 4 ). Adipose depots in mammals are distributed throughout the body and include the fat surrounding the heart and the subcutaneous, retroperitoneal, and mesenteric fat. The amount of mesenteric fat is thought to be correlated most strongly with morbidity rate in obesity ( 5 ). Therefore, investigating the system regulating adipocytes in the mesenteric fat may yield insight into target molecules for treating or preventing obesity-related diseases.Both humans and animals vary in their body-weight responses to high-fat diets (HFDs). When animals are fed HFDs, most of them increase in body weight, with higher levels of adiposity than occur when standard chow is fed. However, a few subjects fed HFDs show less weight gain than do control animals fed standard chow or obesity-prone (diet-induced obesity, DIO) animals. These animals that do not become obese even when fed HFDs are categorized as being "diet resistant" (DR) ( 6, 7 ). To investigate the characteristics of genes expressed in the mesenteric fat tissues, we Abstract A high-fat diet (HFD) is a well-known contributing factor in the development of obesity. Most rats fed HFDs become obese. Those that avoid obesity when fed HFDs are considered diet resistant (DR). We performed a microarray screen to identify genes specifi c to the mesenteric fat of DR rats and revealed high expression of guanylin and guanylyl cyclase C (GC-C) in some subjects. Our histologic studies revealed that the cellular source of guanylin and GC-C is macrophages. Therefore, we developed double-transgenic (Tg) rats overexpressing guanylin and GC-C in macrophages and found that they were resistant to the effects of HFDs. In the mesenteric fat of HFD-fed Tg rats, Fas and perilipin mRNAs were downregulated, and those of genes involved in fatty acid oxidation were upregulated, compared with the levels in HFD-fed wild-type rats. In vitro studies demonstrated that lipid accumulation was markedly inhibited in adipocytes cocultured with macrophages expressing guanylin and GC-C and that this inhibition was reduced after treatment with guanylin-and GC-C-specifi c siRNAs. Our results suggest that the macrophagic guanylin-GC-C system contributes to the altered expression of genes involved in lipid metabolism, leading to resistance to obesity.

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Levels of antibody to serotype VIII group B Streptococcus (GBS) were surveyed in serum samples from 583 pregnant women, from 461 neonates born to these women, and from 4 mother-and-neonate pairs with early-onset serotype VIII sepsis. Colonization by serotype VIII GBS was associated with significantly higher serum concentrations of serotype-specific antibodies (geometric mean [GM], 5.53 mg/mL), compared with both noncolonization (1.53 mg/ mL) and colonization with other serotypes (2.19 mg/mL). There was excellent correlation between antibody levels in mothers and those in their neonates. The prevalence of positive antibody levels, when arbitrarily defined, according to antibody levels in neonatal sepsis (GM, 0.49 mg/mL) as 11.0 mg/mL, was 58% of all pregnant women and 85% of the women colonized by serotype VIII. This high serotype prevalence may explain, at least in part, why serotype VIII causes early-onset neonatal disease at rates lower than those which would be expected on the basis of its prevalence in mothers in Japan who are colonized by GBS.Group B Streptococcus (GBS) is an important pathogen that causes neonatal sepsis and meningitis, with high mortality and morbidity [1]. Although many factors influence the rate of vertical transmission, one of the most important is the concentration of specific serum IgG antibodies to the different capsular polysaccharides (CPSs) of GBS [2][3][4][5][6][7]. A low concentration of serotype III CPS-specific antibody in maternal serum is associated with susceptibility to serotype III infection in neonates [2,3]. Similar correlations have been reported for serotypes Ia, Ib, II,.In Japan, serotypes VI and VIII have been increasingly recognized among isolates from pregnant women since the early 1980s. At present, serotype VIII accounts for 36% of all GBS serotypes [8]. Compared with the carrier rate in pregnant women, the frequency of isolation of serotype VIII in earlyonset neonatal infection is low. In a nationwide surveillance of neonatal GBS infection from 1993 to 1997, the most frequent serotype among 43 strains examined was serotype III (28%), followed by serotypes VI (19%), II (12%), and V (12%) [9]. However, only 2 neonates (5%) had serotype VIII invasive disease [9]. The reason for the discrepancy is not obvious. We hypothesized that the rarity of serotype VIII GBS disease in Japanese neonates may be due to a high prevalence of serotypespecific antibodies in maternal serum that protect the neonates against invasive disease. To address this issue, we investigated the distribution of IgG antibody to serotype VIII GBS in maternal and neonatal serum samples, using an ELISA. Subjects, Materials, and MethodsSubjects. The subjects included pregnant women ( ) n p 583 attending Nishi-Kobe Medical Center from June 1999 to May 2000 and, subsequently, their neonates ( ). We excluded pregnant n p 461 women with multiplets. There were no neonates with invasive GBS infection during this study period. We also analyzed levels of antibody to serotype VIII in 4 mother-and-neonate pairs...

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