Control of biofouling by Cordylophora caspia in freshwater using one-off,pulsed and intermittent dosing of chlorine: laboratory evaluation

Cordylophora caspia is a hydrozoan which causes biofouling in power plants and is an increasing problem in UK drinking water treatment works. Thermal control is not usually feasible without a ready source of hot water so laboratory experiments were conducted to assess whether using pulsed doses of chlorine is an alternative solution. C. caspia polyps disintegrated after a single 20 min dose (the length of one backwash cycle in water treatment work filter beds) of 2.5 ppm chlorine. Without further treatment colonies regenerated within 3 days, but repeated dosing with chlorine for 20 min each day inhibited this regeneration. The resistance of surviving colonies to chlorine increased over time, although colony size and polyp regeneration continued to fall. These results suggest pulsed treatment with chlorinated backwashes at 2 ppm could be used to control C. caspia biofouling in rapid gravity filters and this may have relevance to other settings where thermal control is not feasible.     

Polar assembly and scaffolding proteins of the virulence-associated ESX-1 secretory apparatus in mycobacteria

The ESX‐1 secretion system is required for pathogenicity of Mycobacterium tuberculosis (Mtb). Despite considerable research, little is known about the structural components of ESX‐1, or how these proteins are assembled into the active secretion apparatus. Here, we exploit the functionally related ESX‐1 apparatus of Mycobacterium smegmatis (Ms) to show that fluorescently tagged proteins required for ESX‐1 activity consistently localize to the cell pole, identified by time‐lapse fluoro‐microscopy as the non‐septal (old) pole. Deletions in Msesx1 prevented polar localization of tagged proteins, indicating the need for specific protein–protein interactions in polar trafficking. Remarkably, expression of the Mtbesx1 locus in Msesx1 mutants restored polar localization of tagged proteins, indicating establishment of the MtbESX‐1 apparatus in M. smegmatis. This observation illustrates the cross‐species conservation of protein interactions governing assembly of ESX‐1, as well as polar localization. Importantly, we describe novel non‐esx1‐encoded proteins, which affect ESX‐1 activity, which colocalize with ESX‐1, and which are required for ESX‐1 recruitment and assembly. This analysis provides new insights into the molecular assembly of this important determinant of Mtb virulence.     

A longitudinal analysis of regional brain volumes in macaques exposed to x-irradiation in early gestation

Background

Early gestation represents a period of vulnerability to environmental insult that has been associated with adult psychiatric disease. However, little is known about how prenatal perturbation translates into adult brain dysfunction. Here, we use a longitudinal study design to examine the effects of disruption of early gestational neurogenesis on brain volume in the non-human primate.

Methods and Principal Findings

Five Rhesus macaques were exposed to x-irradiation in early gestation (E30–E41), and four control monkeys were sham-irradiated at comparable ages. Whole brain magnetic resonance imaging was performed at 6 months, 12 months, and 3 and 5 years of age. Volumes of whole cerebrum, cortical gray matter, caudate, putamen, and thalamus were estimated using semi-automated segmentation methods and high dimensional brain mapping. Volume reductions spanning all ages were observed in irradiated monkeys in the putamen (15–24%, p = 0.01) and in cortical gray matter (6–15%, p = 0.01). Upon covarying for whole cerebral volume, group differences were reduced to trend levels (putamen: p = 0.07; cortical gray matter: p = 0.08). No group-by-age effects were significant.

Conclusions

Due to the small number of observations, the conclusions drawn from this study must be viewed as tentative. Early gestational irradiation may result in non-uniform reduction of gray matter, mainly affecting the putamen and cerebral cortex. This may be relevant to understanding how early prenatal environmental insult could lead to brain morphological differences in neurodevelopmental diseases.     

Interleukin-1 Receptor–Associated Kinase M–Deficient Mice Demonstrate an Improved Host Defense during Gram-negative Pneumonia

Pneumonia is a common cause of morbidity and mortality and the most frequent source of sepsis. Bacteria that try to invade normally sterile body sites are recognized by innate immune cells through pattern recognition receptors, among which toll-like receptors (TLRs) feature prominently. Interleukin-1 receptor (IL-1R)–associated kinase (IRAK)-M is a proximal inhibitor of TLR signaling expressed by epithelial cells and macrophages in the lung. To determine the role of IRAK-M in host defense against bacterial pneumonia, IRAK-M-deficient (IRAK-M^−/−) and normal wild-type (WT) mice were infected intranasally with Klebsiella pneumoniae. IRAK-M mRNA was upregulated in lungs of WT mice with Klebsiella pneumonia, and the absence of IRAK-M resulted in a strongly improved host defense as reflected by reduced bacterial growth in the lungs, diminished dissemination to distant body sites, less peripheral tissue injury and better survival rates. Although IRAK-M^−/− alveolar macrophages displayed enhanced responsiveness toward intact K. pneumoniae and Klebsiella lipopolysaccharide (LPS) in vitro, IRAK-M^−/− mice did not show increased cytokine or chemokine levels in their lungs after infection in vivo. The extent of lung inflammation was increased in IRAK-M^−/− mice shortly after K. pneumoniae infection, as determined by semiquantitative scoring of specific components of the inflammatory response in lung tissue slides. These data indicate that IRAK-M impairs host defense during pneumonia caused by a common gram-negative respiratory pathogen.