Characteristic systemic cytokine responses in children with human bocavirus‐positive lower respiratory tract infection

To investigate systemic cytokine responses in human bocavirus (HBoV)‐associated lower respiratory tract infection, serum cytokine profiles were analyzed in HBoV positive‐children (n = 14) using multiplex immunoassay. Concentrations of TNF‐α, IL‐2, IL‐5 and IL‐8 on admission were significantly different from those of respiratory syncytial virus‐positive children (n = 28). This unique cytokine response might partly explain some characteristic clinical features of HBoV‐associated respiratory infection.     

Stabilization and Augmentation of Circulating AIM in Mice by Synthesized IgM-Fc

Owing to rapid and drastic changes in lifestyle and eating habits in modern society, obesity and obesity-associated diseases are among the most important public health problems. Hence, the development of therapeutic approaches to regulate obesity is strongly desired. In view of previous work showing that apoptosis inhibitor of macrophage (AIM) blocks lipid storage in adipocytes, thereby preventing obesity caused by a high-fat diet, we here explored a strategy to augment circulating AIM levels. We synthesized the Fc portion of the soluble human immunoglobulin (Ig)M heavy chain and found that it formed a pentamer containing IgJ as natural IgM does, and effectively associated with AIM in vitro. When we injected the synthesized Fc intravenously into mice lacking circulating IgM, it associated with endogenous mouse AIM, protecting AIM from renal excretion and preserving the circulating AIM levels. As the synthesized Fc lacked the antigen-recognizing variable region, it provoked no undesired immune response. In addition, a challenge with the Fc-human AIM complex in wild-type mice, which exhibited normal levels of circulating IgM and AIM, successfully maintained the levels of the human AIM in mouse blood. We also observed that the human AIM was effectively incorporated into adipocytes in visceral fat tissue, suggesting its functionality against obesity. Thus, our findings reveal potent strategies to safely increase AIM levels, which could form the basis for developing novel therapies for obesity.     

Factor Structure of the Japanese Version of the Edinburgh Postnatal Depression Scale in the Postpartum Period

Background

The Edinburgh Postnatal Depression Scale (EPDS) is a widely used screening tool for postpartum depression (PPD). Although the reliability and validity of EPDS in Japanese has been confirmed and the prevalence of PPD is found to be about the same as Western countries, the factor structure of the Japanese version of EPDS has not been elucidated yet.

Methods

690 Japanese mothers completed all items of the EPDS at 1 month postpartum. We divided them randomly into two sample sets. The first sample set (n = 345) was used for exploratory factor analysis, and the second sample set was used (n = 345) for confirmatory factor analysis.

Results

The result of exploratory factor analysis indicated a three-factor model consisting of anxiety, depression and anhedonia. The results of confirmatory factor analysis suggested that the anxiety and anhedonia factors existed for EPDS in a sample of Japanese women at 1 month postpartum. The depression factor varies by the models of acceptable fit.

Conclusions

We examined EPDS scores. As a result, “anxiety” and “anhedonia” exist for EPDS among postpartum women in Japan as already reported in Western countries. Cross-cultural research is needed for future research.     

Cell Wall-Anchored Nuclease of Streptococcus sanguinis Contributes to Escape from Neutrophil Extracellular Trap-Mediated Bacteriocidal Activity

Streptococcus sanguinis, a member of the commensal mitis group of streptococci, is a primary colonizer of the tooth surface, and has been implicated in infectious complications including bacteremia and infective endocarditis. During disease progression, S. sanguinis may utilize various cell surface molecules to evade the host immune system to survive in blood. In the present study, we discovered a novel cell surface nuclease with a cell-wall anchor domain, termed SWAN (streptococcal wall-anchored nuclease), and investigated its contribution to bacterial resistance against the bacteriocidal activity of neutrophil extracellular traps (NETs). Recombinant SWAN protein (rSWAN) digested multiple forms of DNA including NET DNA and human RNA, which required both Mg²⁺ and Ca²⁺ for optimum activity. Furthermore, DNase activity of S. sanguinis was detected around growing colonies on agar plates containing DNA. In-frame deletion of the swan gene mostly reduced that activity. These findings indicated that SWAN is a major nuclease displayed on the surface, which was further confirmed by immuno-detection of SWAN in the cell wall fraction. The sensitivity of S. sanguinis to NET killing was reduced by swan gene deletion. Moreover, heterologous expression of the swan gene rendered a Lactococcus lactis strain more resistant to NET killing. Our results suggest that the SWAN nuclease on the bacterial surface contributes to survival in the potential situation of S. sanguinis encountering NETs during the course of disease progression.     

Accounting for Biomass Carbon Stock Change Due to Wildfire in Temperate Forest Landscapes in Australia

Carbon stock change due to forest management and disturbance must be accounted for in UNFCCC national inventory reports and for signatories to the Kyoto Protocol. Impacts of disturbance on greenhouse gas (GHG) inventories are important for many countries with large forest estates prone to wildfires. Our objective was to measure changes in carbon stocks due to short-term combustion and to simulate longer-term carbon stock dynamics resulting from redistribution among biomass components following wildfire. We studied the impacts of a wildfire in 2009 that burnt temperate forest of tall, wet eucalypts in south-eastern Australia. Biomass combusted ranged from 40 to 58 tC ha⁻¹, which represented 6–7% and 9–14% in low- and high-severity fire, respectively, of the pre-fire total biomass carbon stock. Pre-fire total stock ranged from 400 to 1040 tC ha⁻¹ depending on forest age and disturbance history. An estimated 3.9 TgC was emitted from the 2009 fire within the forest region, representing 8.5% of total biomass carbon stock across the landscape. Carbon losses from combustion were large over hours to days during the wildfire, but from an ecosystem dynamics perspective, the proportion of total carbon stock combusted was relatively small. Furthermore, more than half the stock losses from combustion were derived from biomass components with short lifetimes. Most biomass remained on-site, although redistributed from living to dead components. Decomposition of these components and new regeneration constituted the greatest changes in carbon stocks over ensuing decades. A critical issue for carbon accounting policy arises because the timeframes of ecological processes of carbon stock change are longer than the periods for reporting GHG inventories for national emissions reductions targets. Carbon accounts should be comprehensive of all stock changes, but reporting against targets should be based on human-induced changes in carbon stocks to incentivise mitigation activities.     

Involvement of proteinase-activated receptor-2 in mast cell tryptase-induced barrier dysfunction in bovine aortic endothelial cells

We report here a direct modulation by mast cell tryptase of endothelial barrier function through activation of proteinase-activated receptor-2 (PAR-2). In cultured bovine aortic endothelial cells (BAECs), tryptase, trypsin and PAR-2 activating peptide impaired the barrier function as determined by the permeability of protein-conjugated Evans blue. The tryptase-induced barrier dysfunction was completely blocked by U73122, and partially reversed by xestospongin C, calphostin C or Y27632. The intracellular Ca(2+) was elevated by tryptase. It was notable that ioxaglate, a contrast material that degranulates mast cells, markedly increased the permeability when applied to BAECs in combination with mast cells, an action that was blocked by nafamostat, a potent tryptase inhibitor. Immunofluorescence analysis showed that actin stress fibre formation and disruption of VE-cadherin were observed after exposure to tryptase or ioxaglate in combination with mast cells. Therefore, it is suggested that mast cell tryptase impairs endothelial barrier function through activation of endothelial PAR-2 in a manner dependent on the phospholipase C activity.     

Mammalian DNA mismatch repair protects cells from UVB-induced DNA damage by facilitating apoptosis and p53 activation

DNA mismatch repair (MMR) is integral to the maintenance of genomic stability and more recently has been demonstrated to affect apoptosis and cell cycle arrest in response to a variety of adducts induced by exogenous agents. Comparing Msh2-null and wildtype mouse embryonic fibroblasts (MEFs), both primary and transformed, we show that Msh2 deficiency results in increased survival post-UVB, and that UVB-induced apoptosis is significantly reduced in Msh2-deficient cells. Furthermore, p53 phosphorylation at serine 15 is delayed or diminished in Msh2-deficient cells, suggesting that Msh2 may act upstream of p53 in a post-UVB apoptosis or growth arrest response pathway. Taken together, these data suggest that MMR heterodimers containing Msh2 may function as a sensor of UVB-induced DNA damage and influence the initiation of UVB-induced apoptosis, thus implicating MMR in protecting against UV-induced tumorigenesis.