Predictors Of Babesia Microti Infection In Ixodes Scapularis Ticks In New England, Usa

Babesia microti is the primary etiological agent of human babesiosis (Vannier & Krause). Although it shares the same tick vector and mammal reservoirs as B. burgdorferi, the causative agent of Lyme disease, the geographic extent of B. microti is limited to a subset of the range of B. burgdorferi (Diuk-Wasser et al.). Despite the slower spread of B. microti, it is equally prevalent in ticks in certain areas where both B. burgdorferi and B. microti have been endemic for long periods. The slower rate of B. microti expansion as compared to B. burgdorferi has been attributed to a lower efficiency of transmission for B. microti (Dunn et al.), however, this alone does not explain the similar prevalence of both microbes in areas long endemic to both pathogens. This study assesses the relative importance of ecological conditions and pathogen interactions in B. microti and B. burgdorferi prevalence in I. scapularis nymphs from a sample of 1514 nymph-stage ticks collected at 35 sites in eastern Connecticut, western Rhode Island, and southern Massachusetts. Our results show that the odds of a tick testing positive for B. microti is not associated to the density of nymphal ticks or the prevalence of B. burgdorferi at the site level, but it is associated with the presence of B. burgdorferi in the individual tick and the geographic location of the tick. None of the covariates tested showed a strong association with the odds of a tick testing positive for B. burgdorferi

Remotely sensed and modelled pasture biomass, land condition and the potential to improve grazing-management decision tools across the Australian rangelands

This report assesses the potential for expanding on current capacity to monitor land condition using remotely sensed fractional cover products to improve biomass estimation, animal productivity, pasture growth models and grazing decision tools (e.g. safe carrying capacity) across the Australian rangelands. We focus on northern Australia and include relevant research and implementation from southern Australia where appropriate

Introduction: meeting the challenges of Workplace English Communication in the 21st century

Open access article. Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) applies[Abstract not available]Ye

Conserved Subcortical and Divergent Cortical Expression of Proteins Encoded by Orthologs of the Autism Risk Gene MET

Met receptor tyrosine kinase signaling regulates the growth and development of axons and may contribute to the wiring of cortical and limbic circuits in the rodent forebrain. Whether the orthologous MET receptor functions similarly in the developing primate forebrain is not known but is of considerable interest considering the association of variant MET alleles with social and communication phenotypes in autism. To begin addressing this question, we compared Met/MET protein expression in the developing mouse and rhesus macaque forebrain. There was a strong temporal conservation of expression during the time of rapid axon development and the onset of robust synapse formation. Expression patterns of Met/MET in limbic-related structures were almost identical between species. In marked contrast, there was highly divergent expression in the neocortex. In mouse, Met was broadly distributed throughout neocortex. In the macaque, robust MET expression was largely restricted to the posterior cingulate, inferior temporal, posterior parietal, and visual cortices, including face processing regions. The pattern is consistent with the importance of vision in the social repertoire of the primate. Collectively, these data suggest a conserved developmental function of the MET receptor in wiring together limbic and neocortical circuits that facilitate species-appropriate responses, including social behavior

Neuronal activity disrupts myelinated axon integrity in the absence of NKCC1b

Through a genetic screen in zebrafish, we identified a mutant with disruption to myelin in both the CNS and PNS caused by a mutation in a previously uncharacterized gene, slc12a2b, predicted to encode a Na+, K+, and Cl− (NKCC) cotransporter, NKCC1b. slc12a2b/NKCC1b mutants exhibited a severe and progressive pathology in the PNS, characterized by dysmyelination and swelling of the periaxonal space at the axon–myelin interface. Cell-type–specific loss of slc12a2b/NKCC1b in either neurons or myelinating Schwann cells recapitulated these pathologies. Given that NKCC1 is critical for ion homeostasis, we asked whether the disruption to myelinated axons in slc12a2b/NKCC1b mutants is affected by neuronal activity. Strikingly, we found that blocking neuronal activity completely prevented and could even rescue the pathology in slc12a2b/NKCC1b mutants. Together, our data indicate that NKCC1b is required to maintain neuronal activity–related solute homeostasis at the axon–myelin interface, and the integrity of myelinated axons

Broad targeting of resistance to apoptosis in cancer

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer

Political transition and emergent forest-conservation issues in Myanmar.

Political and economic transitions have had substantial impacts on forest conservation. Where transitions are underway or anticipated, historical precedent and methods for systematically assessing future trends should be used to anticipate likely threats to forest conservation and design appropriate and prescient policy measures to counteract them. Myanmar is transitioning from an authoritarian, centralized state with a highly regulated economy to a more decentralized and economically liberal democracy and is working to end a long-running civil war. With these transitions in mind, we used a horizon-scanning approach to assess the 40 emerging issues most affecting Myanmar's forests, including internal conflict, land-tenure insecurity, large-scale agricultural development, demise of state timber enterprises, shortfalls in government revenue and capacity, and opening of new deforestation frontiers with new roads, mines, and hydroelectric dams. Averting these threats will require, for example, overhauling governance models, building capacity, improving infrastructure- and energy-project planning, and reforming land-tenure and environmental-protection laws. Although challenges to conservation in Myanmar are daunting, the political transition offers an opportunity for conservationists and researchers to help shape a future that enhances Myanmar's social, economic, and environmental potential while learning and applying lessons from other countries. Our approach and results are relevant to other countries undergoing similar transitions