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The complement alternative pathway (AP) is tightly regulated and changes in two important AP components, factor B (FB) and factor H (FH) are linked to severe dengue in humans. Here, a mouse model of dengue was investigated to define the changes in FB and FH and assess the utility of this model to study the role of the AP in severe dengue. Throughout the period of viremia in the AG129 IFN signalling-deficient mouse, an increase in FB and a decrease in FH was observed following dengue virus (DENV) infection, with the former only seen in a model of more severe disease associated with antibody-dependent enhancement (ADE). Terminal disease was associated with a decrease in FB and FH, with greater changes during ADE, and accompanied by increased C3 degradation consistent with complement activation. In silico analysis of NFκΒ, signal transducer and activator of transcription (STAT) and IFN-driven FB and FH promoter elements to reflect the likely impact of the lack of IFN-responses in AG129 mice, demonstrated that these elements differed markedly between human and mouse, notably with mouse FH lacking NFκΒ and key IFN-stimulated response elements (ISRE), and FB with many more NFκΒ and STAT-responsive elements than human FB. Thus, the AG129 mouse offers utility in demonstrating changes in FB and FH that, similar to humans, are associated with severe disease, but lack predicted important human-specific and IFN-dependent responses of FB and FH to DENV-infection that are likely to regulate the subtleties of the overall AP response during dengue disease in humans.

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Mycoplasma hominis can be isolated frequently from the genitourinary tract of some healthy individuals. On rare occasions, it acts as a pathogen in immunocompromised patients such as transplant recipients. Here, we describe the case of a 39-year-old man with end-stage kidney disease secondary to diabetic nephropathy who received a simultaneous pancreas-kidney transplant. He developed pancreatitis and arterial thrombosis 2 weeks post-transplant and required a pancreatectomy. His kidney allograft function remained normal. He developed severe left hip pain 2 weeks post-transplant with a trochanteric bursal effusion detected on magnetic resonance imaging. The effusion grew M. hominis. The patient was treated with 100 mg of doxycycline twice daily for 9 months with full resolution of the effusion at 4 months post-treatment. We also review all previously reported M. hominis infections in transplant recipients.

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Dengue disease is an inflammatory-driven pathology, and complement overactivation is linked to disease severity and vascular leakage. Additionally, dysregulation of complement alternative pathway (AP) components has been described, such as upregulation of complement factor D and downregulation of complement factor H (FH), which activate and inhibit the AP, respectively. Thus, the pathology of severe dengue could in part result from AP dysfunction, even though complement and AP activation usually provide protection against viral infections. In dengue virus-infected macrophages and endothelial cells (ECs), the site of replication and target for vascular pathology, respectively, the AP is activated. The AP activation, reduced FH and vascular leakage seen in dengue disease in part parallels other complement AP pathologies associated with FH deficiency, such as atypical haemolytic uraemic syndrome (aHUS). aHUS can be therapeutically targeted with inhibitors of complement terminal activity, raising the idea that strategies such as inhibition of complement or delivery of FH or other complement regulatory components to EC may be beneficial to combat the vascular leakage seen in severe dengue.

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Plant growth-promoting rhizobacteria (PGPR) are increasingly used in crops worldwide. While selected PGPR strains can reproducibly promote plant growth under controlled greenhouse conditions, their efficacy in the field is often more variable. Our overall aim was to determine if pectin or orange peel (OP) amendments to Bacillus velezensis (Bv) PGPR strains could increase soybean growth and nodulation by Bradyrhizobium japonicum in greenhouse and field experiments to reduce variability. The treatments included untreated soybean seeds planted in field soil that contained Bv PGPR strains and non-inoculated controls with and without 0.1% (w/v) pectin or (1 or 10 mg/200 µL) orange peel (OP) amendment. In greenhouse and field tests, 35 and 55 days after planting (DAP), the plants were removed from pots, washed, and analyzed for treatment effects. In greenhouse trials, the rhizobial inoculant was not added with Bv strains and pectin or OP amendment, but in the field trial, a commercial B. japonicum inoculant was used with Bv strains and pectin amendment. In the greenhouse tests, soybean seeds inoculated with Bv AP193 and pectin had significantly increased soybean shoot length, dry weight, and nodulation by indigenous Bradyrhizobium compared to AP193 without pectin. In the field trial, pectin with Bv AP193 significantly increased the shoot length, dry weight, and nodulation of a commercial Bradyrhizobium japonicum compared to Bv AP193 without pectin. In greenhouse tests, OP amendment with AP193 at 10 mg significantly increased the dry weight of shoots and roots compared to AP193 without OP amendment. The results demonstrate that pectin-rich amendments can enhance Bv-mediated soybean growth promotion and nodulation by indigenous and inoculated B. japonicum.

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The aging and elderly population are particularly susceptible to cardiovascular disease. Age is an independent risk factor for cardiovascular disease (CVD) in adults, but these risks are compounded by additional factors, including frailty, obesity, and diabetes. These factors are known to complicate and enhance cardiac risk factors that are associated with the onset of advanced age. Sex is another potential risk factor in aging adults, given that older females are reported to be at a greater risk for CVD than age-matched men. However, in both men and women, the risks associated with CVD increase with age, and these correspond to an overall decline in sex hormones, primarily of estrogen and testosterone. Despite this, hormone replacement therapies are largely shown to not improve outcomes in older patients and may also increase the risks of cardiac events in older adults. This review discusses current findings regarding the impacts of age and gender on heart disease.

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Target spot, caused by Corynespora cassiicola, has recently emerged as a problematic foliar disease of cotton. This pathogen causes premature defoliation during boll set and maturation that can subsequently impact yield, and on certain cotton cultivars loss can be substantial. This study sought to better understand target spot epidemics and disease-incited yield losses on cotton. In order to establish a range of disease, varying numbers of fungicide applications were made to each of two cotton cultivars in each of four site-years. Target spot intensity was rated over several dates beginning in late July or early August and continuing into September. Yield of seed plus lint (seed cotton) was recorded at harvest. When analyzed across cultivars, a second or third fungicide application increased yield compared with no treatment. Lack of significant yield response with a single fungicide application may have been due to timing of that application which preceded disease onset. The cultivar PhytoGen 499 WRF had consistently greater defoliation than any of the three Deltapine cultivars grown in each site-year. However, yields of both cultivars responded similarly to the fungicide regimes. Yield loss models based on late August defoliation were only predictive at site-years where conditions favored target spot development, i.e., abundant rain and moderate temperatures. Epidemic development fit the Gompertz growth model better than it did a logistic model. Knowledge of the underlying mathematical character of the epidemiology of target spot will prove useful for development of a predictive model for the disease.

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Cloning and sequencing of the cDNA indicates that dentin sialophosphoprotein (DSPP) is a precursor of both dentin sialoprotein (DSP) and dentin phosphoprotein (DPP). Dentin sialophosphoprotein must be proteolytically processed to form these two extracellular matrix (ECM) proteins. Numerous studies led us to conclude that DSP (and DSPP) are exclusively expressed by odontoblasts and preameloblasts. However, recent observations suggest a wider distribution. To test this hypothesis, we conducted systematic studies on rat first molar during root formation with immunohistochemical techniques using specific anti-DSP polyclonal and monoclonal antibodies. We also performed in situ hybridization, using high-stringency RNA probes to detect DSP transcripts. Immunohistochemical studies demonstrated that DSP is not only localized in odontoblasts, dentin ECM and preameloblasts, but also in alveolar bone, cellular cementum, osteocytes, cementocytes, and their matrices. The results of in situ hybridization were consistent with those from immunohistochemistry, showing the expression of DSP transcripts in osteoblasts of alveolar bone, fibroblasts in periodontal ligament and cementoblasts in cellular cementum. Together, these observations suggest that DSP is involved in formation of the periodontium as well as tooth structures.

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