No abstract

The cell envelope of Salmonella and related organisms contains a complex lipopolysaccharide composed of an inner core and an outer region containing the specific surface 0-antigens. The following structure has been postulated for the polysaccharide of S. typhimurium:' Abe Abe-Gal-Man-Rha-Gal-Man-Rha-[GNAc-Glu-Gal-Glu-(Hep, P04, Ethanolamine, KDO)] Lipid A Gal +_ 0-Antigenic Side Chains-* (Core Biosynthesis of the core proceeds by successive transfer of monosaccharide residues from nucleotide sugars to the incomplete lipopolysaccharide.1 The origin of the repeating oligosaccharide units of the0-antigenic side chains is less well understood. We previously described the incorporation of galactose, mannose, and rhamnose into 0-antigen repeating units in a mutant of S. typhimurium deficient in GDP-mannose.2 Similar results have also been:described by Nikaido and Nikaido3 with a mutant of S. typhimurium lacking TDP-rhamnose and by Robbins4 with wild-type S. anatum. However, in these experiments the nature of the intermediate reactions was not established. Anderson et al.5 have presented evidence for a lipid-linked disaccharide intermediate in the biosynthesis of cell-wall glycopeptide in Staphylococcus aureus and Micrococcus lysodeikticus, and our data suggest that analogous intermediates are

To clarify what kind of risk factors predict incident fractures in patients treated with bisphosphonates, the authors investigated the relationship between baseline characteristics and incident vertebral fracture in Japanese osteoporosis patients undergoing bisphosphonate treatment. This was a multi-center follow-up study conducted at three centers, in which a total of 251 Japanese patients with osteoporosis (mean age 70.5 years) from the three centers were followed for 3.2 ± 2.0 years. Baseline data, including pre-existing fractures, bone mineral density in the lumbar spine (LBMD), bone metabolic markers, urinary pentosidine, and plasma homocysteine, were evaluated. Changes in LBMD, bone turnover markers, and incident fractures after the treatment were followed. Sixty-one patients developed incident vertebral fractures; this group of patients was older and had lower LBMD, a higher prevalent vertebral fracture number, and higher homocysteine and pentosidine levels than patients who did not develop incident vertebral fractures. Changes in LBMD, urinary N-terminal telopeptides of type I collagen (NTX), and bone-derived alkaline phosphatase showed no significant association with the occurrence of vertebral fractures. Cox's proportional hazard model demonstrated that age, prevalent fracture, pentosidine, and homocysteine were independent predictors of the incident vertebral fracture rate under bisphosphonate treatment. Higher baseline levels of pentosidine and homocysteine in osteoporosis patients are potential risk factors for incident vertebral fractures when these patients are treated with bisphosphonates. Further clarification is needed to explain why such patients have higher fracture susceptibility.

Hormone replacement therapy (HRT) plays a large part in maintaining and improving the quality of life (QOL) of postmenopausal women. Despite this obvious role, the use of HRT has stagnated in Japan as well as the United States, since the interim report of the HRT trial of Women's Health Initiative study was published in 2002. The Japan Society of Obstetrics and Gynecology and Japan Society for Menopause and Women's Health formulated the Guidelines for Hormone Replacement Therapy in 2009, which was subsequently revised in 2012, with the aim of organizing perceptions about HRT and allowing people to provide or receive HRT with a sense of security. Later on, in light of changes in indications for HRT and attitudes toward its impact on cancer risks, amendments were made again in 2017. With the establishment of the 2017 guidelines, practitioners in Japan are able to address various issues related to HRT with more appropriate judgment. Moreover, the practice of reliable, safe and effective HRT is expected to promote further efforts toward improvement or maintenance of QOL in patients.

These results showed that hypercholesterolemia has an inverse effect on bone loss independent of cytokines presumed to mediate bone loss.