A systematic study of energy conservation for extended magnetohydrodynamic (MHD) models that include Hall terms and electron inertia is performed. It is observed that commonly used models do not conserve energy in the ideal limit, i.e., when viscosity and resistivity are neglected. In particular, a term in the momentum equation that is often neglected is seen to be needed for conservation of energy

Background: Group A streptococcal pili are diverse. Results: Mutational analyses identified a specific transpeptidase and lysine residue of the shaft protein required for pilus assembly in a serotype M6 strain. Conclusion: Assembly and cell wall anchoring of the pili are accomplished by concerted actions of transpeptidases. Significance: Our findings lead to predictions of homologous pilus assembly mechanisms in other species.

Asthma–chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) was proposed by the science committees of both Global Initiative for Asthma (GINA) and Global Initiative for Chronic Obstructive Lung Disease (GOLD). However, the definition of ACOS has remained unclear all over the world, and the prevalence rate of ACOS is basically dependent on the patient’s symptoms or the physician’s opinion, based on questionnaire testing. In the current case report, we investigated the prevalence rate of COPD patients with high levels of fractional exhaled nitric oxide (FENO) or immunoglobulin E (IgE) as candidate markers of ACOS in COPD, as a multicenter, cross-sectional study. Outpatients with COPD were enrolled from Tohoku University Hospital, Sendai, Japan, and five hospitals (Tohoku University Hospital, Sendai, Japan; NTT East Tohoku Hospital, Sendai, Japan; Wakayama Medical University Hospital, Kimiidera, Japan; Hiraka General Hospital, Yokote, Japan; Iwate Prefectural Isawa Hospital, Oshu, Japan) with pulmonary physicians from March 1, 2013 to February 28, 2014. When they were estimated using 35 ppb as the cutoff value of FENO, the prevalence rate of ACOS was 16.3% in COPD. When estimated by both FENO and IgE, the high-FENO/high-IgE group was 7.8% in COPD. To the best of our knowledge, this study is the first to detect the prevalence rate of ACOS in COPD populations by using objective biomarkers. The results from the current study should be useful to identify the subgroup requiring early intervention by inhaled corticosteroids/long-acting beta agonist combination in COPD in order to improve the long-term management for ACOS.

Using 30 anesthetized cats, we examined whether oxygen radicals produce airway constriction or hyperresponsiveness. In one group, we administered aerosolized xanthine (0.1%) for 3 min followed by aerosolized xanthine oxidase (XO) (1 U/ml) for 5 min in order to generate oxygen radicals enzymatically in the airways. Pulmonary resistance (RL) instantaneously increased from 14.8 +/- 0.9 to 30.8 +/- 1.4 cm H2O/L/s (p less than 0.01). The increase in RL was significantly depressed by prior administration of polyethylene glycol-superoxide dismutase (PEG-SOD) or polyethylene glycolcatalase (PEG-CAT). In a second group, in order to examine changes in airway responsiveness, we studied acetylcholine (ACh) challenge before and 30, 60, and 120 min after inhalations of xanthine and XO. After xanthine-XO, the airways were hyperresponsive to ACh at 30 and at 60 min (p less than 0.05) but not at 120 min. The geometric means of ACh provocative concentrations that caused an increase in RL of 10 cm H2O/L/s above the baseline value before and 30, 60, and 120 min after xanthine-XO were 0.25, 0.045, 0.073, and 0.15%, respectively. The increase in responsiveness to ACh was significantly correlated with the increase in RL after xanthine-XO inhalation (r = 0.88, p less than 0.05). These data support the concept that oxygen radicals generated by xanthine-XO inhalation may induce bronchoconstriction and airway hyperresponsiveness.

The group A streptococcus (GAS) Streptococcus pyogenes is known to cause self-limiting purulent infections in humans. The role of GAS pili in host cell adhesion and biofilm formation is likely fundamental in early colonization. Pilus genes are found in the FCT (fibronectin-binding protein, collagen-binding protein, and trypsin-resistant antigen) genomic region, which has been classified into nine subtypes based on the diversity of gene content and nucleotide sequence. Several epidemiological studies have indicated that FCT type 1 strains, including serotype M6, produce large amounts of monospecies biofilm in vitro. We examined the direct involvement of pili in biofilm formation by serotype M6 clinical isolates. In the majority of tested strains, deletion of the tee6 gene encoding pilus shaft protein T6 compromised the ability to form biofilm on an abiotic surface. Deletion of the fctX and srtB genes, which encode pilus ancillary protein and class C pilus-associated sortase, respectively, also decreased biofilm formation by a representative strain. Unexpectedly, these mutant strains showed increased bacterial aggregation compared with that of the wild-type strain. When the entire FCT type 1 pilus region was ectopically expressed in serotype M1 strain SF370, biofilm formation was promoted and autoaggregation was inhibited. These findings indicate that assembled FCT type 1 pili contribute to biofilm formation and also function as attenuators of bacterial aggregation. Taken together, our results show the potential role of FCT type 1 pili in the pathogenesis of GAS infections. Bacterial biofilms are organized communities of cell aggregates that are embedded in a matrix of extracellular polymeric substances (9, 13). Biofilm formation is beneficial to bacteria in resistance to the activity of antimicrobial compounds and in persistence against host immune defenses (19). Hence, while many pathogenic bacteria form biofilms, they cause or exacerbate a variety of chronic or recurrent diseases, such as specific forms of recurrent tonsillitis, urinary tract infections, otitis media, and chronic rhino-sinusitis. In addition, biofilm-forming bacteria have a pathogenic role in cystic fibrosis-related lung infections and periodontitis as well as in implant material-related infections.Streptococcus pyogenes (group A streptococci [GAS]) is a human pathogen responsible for a wide variety of diseases ranging from self-limiting purulent infections, such as pharyngitis, tonsillitis, and impetigo, to severe necrotizing fasciitis and autoimmune diseases, including acute rheumatic fever and glomerulonephritis (11). To successfully cause such diverse diseases, firm adherence to epithelial cell surfaces and biofilm formation may be required for colonization in anatomical sites and subsequent disease progression. Indeed, recent studies have reported that GAS produced biofilms in in vitro and in vivo infection models (1,2,7,8,28,31,48,49). Among the many bacterial factors involved in GAS biofilm formation and host cell adherence, pili are pre...