Genome evolution and plasticity of <em>Serratia marcescens</em>:an important multidrug resistant nosocomial pathogen

Serratia marcescens is an important nosocomial pathogen that can cause an array of infections, most notably of the urinary tract and bloodstream. Naturally, it is found in many environmental niches, and is capable of infecting plants and animals. The emergence and spread of multidrug-resistant strains producing extended-spectrum or metallo beta-lactamases now pose a threat to public health worldwide. Here we report the complete genome sequences of two carefully selected S. marcescens strains, a multidrug-resistant clinical isolate (strain SM39) and an insect isolate (strain Db11). Our comparative analyses reveal the core genome of S. marcescens and define the potential metabolic capacity, virulence, and multidrug resistance of this species. We show a remarkable intraspecies genetic diversity, both at the sequence level and with regards genome flexibility, which may reflect the diversity of niches inhabited by members of this species. A broader analysis with other Serratia species identifies a set of approximately 3,000 genes that characterize the genus. Within this apparent genetic diversity, we identified many genes implicated in the high virulence potential and antibiotic resistance of SM39, including the metallo beta-lactamase and multiple other drug resistance determinants carried on plasmid pSMC1. We further show that pSMC1 is most closely related to plasmids circulating in Pseudomonas species. Our data will provide a valuable basis for future studies on S. marcescens and new insights into the genetic mechanisms that underlie the emergence of pathogens highly resistant to multiple antimicrobial agents

The corrected blood urea nitrogen predicts the developmental quotient of extremely low-birth-weight infants at the corrected age of 36 months

Elsevier, Ken, Nagaya ; Shinya, Tanaka ; Hiroyuki, Kitajima ; Masanori, Fujimura, Early Human Development, 83(5), 2007, 285-291. authorBackground : Currently, there are no nutritional indices to predict cognitive function in extremely low-birth-weight (ELBW) infants. Objective : To assess the neonatal blood urea nitrogen (BUN) values in ELBW infants according to their cognitive function at the corrected age of 36 months. Methods : This was a retrospective study that assessed the neonatal factors affecting the developmental outcome in two groups “developmental quotient (DQ) ≥ 80” and “DQ < 80”, the groups were divided based on the DQ at the corrected age of 36 months. Between 1996 and 1999, 178 ELBW infants born at < 28 weeks of gestation were admitted to our neonatal intensive care unit (NICU), of these, 32 died. Of the surviving 146 infants, 37 infants without any exclusion criteria (that would affect the cognitive function and BUN) except the nutritional factor, were assessed. Area under the curve (AUC) of corrected BUN (CBUN: BUN × 0.5/serum creatinine) from 28 to 84 days of life was used as an index of protein intake. Results : No significant differences were observed between the two groups with regard to the gestational age, birth weight, Z score of birth weight, and sex. However, compared to 15 infants with DQ < 80, 22 infants with DQ ≥ 80 had significantly shorter duration of artificial ventilation and O2 supplementation, a higher Apgar score at 5 min, and a higher AUC of CBUN. On multiple regression analysis, DQ ≥ 80 was observed to be significantly correlated with the AUC of CBUN (Odd's ratio 1.03, 95% confidence interval: 1.002–1.06). Conclusion : The CBUN level would provide an estimate of adequate protein intake and the subsequent development of an ELBW infant

【周産期医学必修知識】 新生児 胎児,新生児の免疫とその異常

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Platyspondylic lethal dysplasia torrance type with a heterozygous mutation in the triple helical domain of COL2A1 in two sibs from phenotypically normal parents.

AuthorHeterozygous COL2A1 mutations create a group of skeletal dysplasias collectively termed type II collagenopathies. Sporadic cases of type II collagenopathies are almost exclusively caused by de novo mutations. Very few cases with intrafamilial recurrence due to germinal mosaicism have been known. We report here on a family in which a severe form of skeletal dysplasia was recurrent in two sibs whose phenotype was most consistent with platyspondylic lethal skeletal dysplasia Torrance type (PLSD-T). A COL2A1 analysis showed that the two sibs had a heterozygous mutation in the triple helical region of COL2A1, c.3545G>A (p.G1182A) in exon 50. The parents did not consent to a molecular analysis; however, the presence of the same mutation in the two sibs is proof of germinal mosaicism in one of the parents. PLSD-T has been believed to arise from a heterozygous dominant negative mutation in the C-propeptide region of COL2A1. However, our observation suggests that the phenotype is also caused by a mutation in the C-terminal triple helical region of COL2A1

Biliary atresia and stool: its consistency and fat content, another potentially useful clinical information

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