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Legitimate and Health Response to COVID-19 in the Arabic Nations around the world.
psychosis.Emerging infectious diseases (EIDs) are increasingly recognized as a threat to both biodiversity and human health (Scheele et al., 2019; Wells et al., 2020). But pathogens cannot been seen as unique entities; their intraspecific genetic variability represented in variants, strains, antigenic types or genetic lineages may cause different impacts at the population level (Nelson and Holmes, 2007; Greenspan et al., 2018). The global spread of pathogens has been largely facilitated by globalization of transport, which particularly intensified during the last century (O'Hanlon et al., 2018). check details As seen with SARS-CoV-2, air travel can rapidly spread a pathogen globally (Wells et al., 2020). Furthermore, after initial introduction subsequent translocations of a pathogen may cause the contact of different variants facilitating the rise of novel genotypes that may have higher pathogenicity or transmissibility (Nelson and Holmes, 2007; Greenspan et al., 2018). Chytridiomycosis is an EID caused by the fungus Batrachochytrium dendrobatidis (Bd), that infects amphibian skin causing population declines to extinction in susceptible species. Now a wildlife pandemic, Bd has been recognized as the single pathogen causing the greatest loss of biodiversity on Earth (Scheele et al., 2019). Recent advances in genetics have made novel tools for pathogen detection and characterization more accessible and reliable (Boyle et al., 2004; Byrne et al., 2019). In this issue of Molecular Ecology Resources, Ghosh et al. (2021) report the development of a new genotyping qPCR assay targeting mitochondrial DNA (mtDNA) of Bd, and based on noninvasive swab samples (Figure 1), discriminate between the two most globally widespread and pathogenic genetic lineages of Bd. Having a better understanding of how the genetic diversity of a pathogen is distributed is crucial to understand their spread patterns and develop timely mitigation strategies.Four major medical societies involved with hydroxychloroquine (HCQ) therapy concur on the need for common principles and cooperation to minimize the risk of ocular toxicity. At a daily dosage of ≤5 mg/kg/day actual body weight, the risk of retinal toxicity from HCQ is less then 2% for usage up to 10 years. Widespread adoption of more sensitive testing techniques, such as optical coherence tomography and automated visual fields, by eye care providers will allow the detection of early toxicity and thus preserve the patient's visual function. Baseline testing is advised to rule out confounding disease when a patient is started on HCQ. Annual screening with sensitive tests should begin no more than 5 years after treatment initiation. Providers should be sensitive to the medical value of HCQ, and not stop the drug for uncertain indications. It is important to note that effective communication among prescribing physicians, patients, and eye care providers will optimize the utility and safety of HCQ.
The search for high-risk factors in stage II colon cancer (CC) is ongoing and several high-risk factors for stage II CC have been identified; however, the effects of tumour sidedness on prognosis are not clear. This study aims to determine whether tumour sidedness could be identified as another high-risk factor for stage II CC.

We retrospectively analysed 189 patients with stage II CC and compared clinicopathological findings and long-term outcomes between the patients with right colonic cancer (RCC) and with left colonic cancer (LCC). Prognostic factors for survival were determined using univariate and Cox proportional regression analyses.

A total of 72 patients were diagnosed with RCC and 117 patients were diagnosed with LCC. Patients with RCC were significantly older (P < 0.001), and the number of harvested lymph nodes was greater in the RCC group (RCC 25 versus LCC 19; P = 0.003). The overall survival (OS) was worse in the RCC group than the OS in the LCC group (5-year survival rate - RCC 81.3% versus LCC 90.4%; P = 0.025). Cox proportional regression analysis showed that tumour sidedness was an independent prognostic factor for both OS (hazard ratio (HR) 3.78, 95% confidence interval (CI) 1.61-8.85, P = 0.022) and DFS (HR 2.58, 95% CI 1.33-4.99, P = 0.005).

Patients with RCC have more negative prognostic factors and worse long-term outcomes than those with LCC in stage II CC. Tumour sidedness is a high-risk factor in stage II CC patients.
Patients with RCC have more negative prognostic factors and worse long-term outcomes than those with LCC in stage II CC. Tumour sidedness is a high-risk factor in stage II CC patients.
Osteoarthritis (OA) is initiated by pathogenic factors produced by multiple stimuli, including mechanical stress, metabolic stress, and/or inflammaging. This work was performed to identify novel low-grade inflammation-associated pathogenic mediators of OA.

Candidate molecules were screened from microarray data of chondrocytes treated with OA-associated catabolic factors. Low-grade inflammation was induced by high-fat diet (HFD) or endotoxemia. Functions of candidate molecules in OA pathogenesis were examined using primary-culture mouse chondrocytes and mouse models of OA, such as destabilization of the medial meniscus (DMM) surgery or intra-articular injection of adenovirus expressing the candidate gene. Specific functions of candidate genes were evaluated using whole-body knockout mice.

Bioinformatic analysis identified multiple candidate pathogenic factors that are associated with low-grade inflammation, including components of the toll-like receptor (TLR) signaling pathways (e.g., TLR2, TLR4, LBP, CD14, etc.). Overexpression of the individual TLR signaling components in mouse joint tissues did not alter cartilage homeostasis. However, the low-grade inflammation caused by HFD or endotoxemia markedly enhanced post-traumatic OA cartilage destruction, and this exacerbation of cartilage destruction was significantly abrogated in Lbp
and Cd14
mice. Additionally, LBP and CD14 were found to be necessary for the expression of matrix-degrading enzymes in chondrocytes treated with pro-inflammatory cytokines.

LBP and CD14, which are accessory molecules of TLRs, are necessary for the exacerbation of post-traumatic OA cartilage destruction caused by low-grade inflammation, such as that triggered by HFD or endotoxemia.
LBP and CD14, which are accessory molecules of TLRs, are necessary for the exacerbation of post-traumatic OA cartilage destruction caused by low-grade inflammation, such as that triggered by HFD or endotoxemia.
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