The Structure and Evolution of Beta-Rhizobial Symbiotic Genes Deduced from Their Complete Genomes

Abstract Nitrogen-fixing Rhizobia were discovered more than 100 years ago. They are classified into two clades, Alphaand Beta-rhizobia. Their symbiotic function is remarkable, but its origin and evolution has been confusing from a phylogenetic perspective.

In this study, we make use of 33 publicly available complete genome sequences downloaded from NCBI, which consist of bacteria and archaea, and focus on 10 strains, constructing symbiotic structural maps for them based on their genomes and previous gene annotations. Phylogenies of the symbiosisessential genes nodA and nifH were examined.

Although large incongruities with some hypotheses from previous studies were detected by the present study, we support the general concept that Beta-rhizobia were the original symbionts of legumes, but that their symbotic genes originated from a common ancestor to the Alpha-rhizobia.

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The Lysosome -A Central Hub for Cellular Function and Dysfunction

During the last decades our knowledge of the versatile tasks of the lysosome has increased tremendously. Several ground breaking discoveries, have positioned the lysosome as one of the central organelles for normal physiological function and in disease.

In this short overview we exemplify some of the recent achievements in our understanding of lysosomal function during nutrient sensing, cell death, exocytosis and cholesterol homeostasis as well as lysosomal malfunction during disease.

Outlined are also several of the gaps in our knowledge and challenges that need to be addressed in the future.

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Impacts of Interleukin-17 Neutralization on the Inflammatory Response in a Healing Ligament

In this study, we sought to improve ligament healing by modulating the inflammatory response after acute injury through the neutralization of Interleukin-17 (IL-17), which we hypothesized would decrease inflammatory cell infiltration and cytokine production.

Administration of an Interleukin-17 neutralizing antibody (IL-17 NA) immediately following a rat medial collateral ligament (MCL) transection resulted in alterations in inflammatory cell populations and cytokine expression within the healing ligament, but did not reduce inflammation.

Specifically, treatment resulted in a decrease in M2 (antiinflammatory) macrophages, an increase in T cells, and an increase in the levels of IL-2, IL-6, and IL-12 in the MCL 7 days post injury.

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Lymphoid Seeding in the Thymus: A New Function for Ephb2 and Ephb3

like B lymphocytes that differentiate in the bone marrow (BM), T lymphocytes need the special 3D epithelial microenvironment of the thymus to develop properly, in which they establish intimate interactions with Thymic Epithelial Cells.

Thus, whereas B lymphocytes derive from haematopoietic progenitor cells in the BM, T cells need more- or-less committed lymphoid progenitors to colonize the adult thymus through blood vessels because this organ lacks auto-renewing progenitor cells.

Mechanisms involved in the selective migration of BM progenitor cells have been largely associated with attracting chemokines and molecules involved in lymphoid cell migration through vascular endothelia, such as integrins and selectins.

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Primary Immunization among Children in Malaysia: Reasons for Incomplete Vaccination

Incomplete primary immunization against vaccine preventable diseases is a significant public health problem. This study aimed to identify population at-risk for incomplete immunization and their associated factors.

Data on immunization module from the National Health and Morbidity Survey (NHMS) 2016 was analyzed. This survey was conducted as a nation-wide community based survey using stratified random sampling design.

Immunization history of children aged 12 to 23 months from the randomly selected addresses were taken from their mothers by face-to-face interview using mobile device.

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Smad7 as a Target for Immunomodulation Strategy in Inflammatory Bowel Diseases

Inflammatory bowel diseases (IBD) are chronic inflammatory pathologies of the gut, characterized by a relapsing-remitting course.

Although IBD pathogenesis is not fully understood, epidemiological and experimental data suggest that multiple environmental factors can, in genetically predisposed individuals, trigger an excessive immune response directed against the antigens of the normal intestinal microflora, which eventually leads to the tissue damage. Defects in the physiological mechanisms/factors of counter-regulation contribute to amplify and sustain such a detrimental response.

For instance, in inflamed tissue of IBD patients there is diminished activity of the immunesuppressive cytokine transforming growth factor (TGF)-β1, due to elevated levels of Smad7, an intracellular inhibitor of TGF-β1 signaling.

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Rebound from Inhibition: Self-Correction against Neurodegeneration?

Neural networks play a critical role in establishing constraints on excitability in the central nervous system. Several recent studies have suggested that network dysfunction in the brain and spinal cord are compromised following insult by a neurodegenerative trigger and might precede eventual neuronal loss and neurological impairment.

Early intervention of network excitability and plasticity might therefore be critical in resetting hyperexcitability and preventing later neuronal damage.

Here, the behavior of neurons that generate burst firing upon recovery from inhibitory input or intrinsic membrane hyperpolarization (rebound neurons) is examined in the context of neural networks that underlie rhythmic activity observed in areas of the brain and spinal cord that are vulnerable to neurodegeneration.

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