Checklist for One Health Epidemiological Reporting of Evidence (COHERE).

One Health is defined as the intersection and integration of knowledge regarding humans, animals, and the environment, yet as the One Health scientific literature expands, there is considerable heterogeneity of approach and quality of reporting in One Health studies. In addition, many researchers who publish such studies do not include or integrate data from all three domains of human, animal, and environmental health. This points to a critical need to unify guidelines for One Health studies. This report details the Checklist for One Health Epidemiological Reporting of Evidence (COHERE) to guide the design and publication format of future One Health studies. COHERE was developed by a core writing team and international expert review group that represents multiple disciplines, including human medicine, veterinary medicine, public health, allied professionals, clinical laboratory science, epidemiology, the social sciences, ecohealth and environmental health. The twin aims of the COHERE standards are to 1) improve the quality of reporting of observational or interventional epidemiological studies that collect and integrate data from humans, animals and/or vectors, and their environments; and 2) promote the concept that One Health studies should integrate knowledge from these three domains. The 19 standards in the COHERE checklist address descriptions of human populations, animal populations, environmental assessment, spatial and temporal relationships of data from the three domains, integration of analyses and interpretation, and inclusion of expertise in the research team from disciplines related to human health, animal health, and environmental health

Checklist for One Health epidemiological reporting of evidence (COHERE)

One Health is defined as the intersection and integration of knowledge regarding humans, animals, and the environment, yet as the One Health scientific literature expands, there is considerable heterogeneity of approach and quality of reporting in One Health studies. In addition, many researchers who publish such studies do not include or integrate data from all three domains of human, animal, and environmental health. This points to a critical need to unify guidelines for One Health studies. This report details the Checklist for One Health Epidemiological Reporting of Evidence (COHERE) to guide the design and publication format of future One Health studies. COHERE was developed by a core writing team and international expert review group that represents multiple disciplines, including human medicine, veterinary medicine, public health, allied professionals, clinical laboratory science, epidemiology, the social sciences, ecohealth and environmental health. The twin aims of the COHERE standards are to 1) improve the quality of reporting of observational or interventional epidemiological studies that collect and integrate data from humans, animals and/or vectors, and their environments; and 2) promote the concept that One Health studies should integrate knowledge from these three domains. The 19 standards in the COHERE checklist address descriptions of human populations, animal populations, environmental assessment, spatial and temporal relationships of data from the three domains, integration of analyses and interpretation, and inclusion of expertise in the research team from disciplines related to human health, animal health, and environmental health

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions

Characterization of NLRP12 during the Development of Allergic Airway Disease in Mice

Among the 22 members of the nucleotide binding-domain, leucine rich repeat-containing (NLR) family, less than half have been functionally characterized. Of those that have been well studied, most form caspase-1 activating inflammasomes. NLRP12 is a unique NLR that has been shown to attenuate inflammatory pathways in biochemical assays and mediate the lymph node homing of activated skin dendritic cells in contact hypersensitivity responses. Since the mechanism between these two important observations remains elusive, we further evaluated the contribution of NLRP12 to organ specific adaptive immune responses by focusing on the lung, which, like skin, is exposed to both exogenous and endogenous inflammatory agents. In models of allergic airway inflammation induced by either acute ovalbumin (OVA) exposure or chronic house dust mite (HDM) antigen exposure, Nlrp12−/− mice displayed subtle differences in eosinophil and monocyte infiltration into the airways. However, the overall development of allergic airway disease and airway function was not significantly altered by NLRP12 deficiency. Together, the combined data suggest that NLRP12 does not play a vital role in regulating Th2 driven airway inflammation using common model systems that are physiologically relevant to human disease. Thus, the allergic airway inflammation models described here should be appropriate for subsequent studies that seek to decipher the contribution of NLRP12 in mediating the host response to agents associated with asthma exacerbation

Microscopic Theory of Scattering of Weak Electromagnetic Radiation by a Dense Ensemble of Ultracold Atoms

Based on the developed quantum microscopic theory, the interaction of weak electromagnetic radiation with dense ultracold atomic clouds is described in detail. The differential and total cooperative scattering cross sections are calculated for monochromatic radiation as particular examples of application of the general theory. The angular, spectral, and polarization properties of scattered light are determined. The dependence of these quantities on the sample size and concentration of atoms is studied and the influence of collective effects is analyzed

PIK3CA-associated developmental disorders exhibit distinct classes of mutations with variable expression and tissue distribution

Mosaicism is increasingly recognized as a cause of developmental disorders with the advent of next-generation sequencing (NGS). Mosaic mutations of PIK3CA have been associated with the widest spectrum of phenotypes associated with overgrowth and vascular malformations. We performed targeted NGS using 2 independent deep-coverage methods that utilize molecular inversion probes and amplicon sequencing in a cohort of 241 samples from 181 individuals with brain and/or body overgrowth. We identified PIK3CA mutations in 60 individuals. Several other individuals (n = 12) were identified separately to have mutations in PIK3CA by clinical targetedpanel testing (n = 6), whole-exome sequencing (n = 5), or Sanger sequencing (n = 1). Based on the clinical and molecular features, this cohort segregated into three distinct groups: (a) severe focal overgrowth due to low-level but highly activating (hotspot) mutations, (b) predominantly brain overgrowth and less severe somatic overgrowth due to less-activating mutations, and (c) intermediate phenotypes (capillary malformations with overgrowth) with intermediately activating mutations. Sixteen of 29 PIK3CA mutations were novel. We also identified constitutional PIK3CA mutations in 10 patients. Our molecular data, combined with review of the literature, show that PIK3CA-related overgrowth disorders comprise a discontinuous spectrum of disorders that correlate with the severity and distribution of mutations