Introduction Urethral trauma is often associated with erectile dysfunction (ED). Reconstructive surgery is complex and may impact negatively on sexual function. Aim The aim of this article is to investigate ED in patients with pelvic fracture urethral distraction defects (PFUDD) who underwent urethroplasty, and efficacy of treatment with sildenafil citrate. Main Outcome Measures A total of 41 patients with urethral stricture who suffered from PFUDD were assessed to exclude systemic diseases that may cause ED, such as hypertension, diabetes mellitus, heart disease, and chronic liver disease. The International Index of Erectile Function-5 was used as an evaluation tool. Assessments were made at three time points: the time of admission, two weeks after urethroplasty, and 3 months post-treatment with sildenafil. Methods Pharmacopenile duplex ultrasonography was used to examine blood flow of the cavernosum in order to distinguish arterial ED, venous ED, and nonvascular ED. All patients were treated with oral sildenafil, 100 mg once daily, three times a week, for 3 months. Results The incidence of ED following injury was 95.12%. There were no significant changes in scores following surgery. However, sildenafil had a success rate of approximately 81%, which appeared to be independent of age. Drug treatment seemed most effective for those with less severe ED at the outset. There was no significant difference in scores post-treatment between those who had vascular and nonvascular ED. Overall, the incidence of side effects due to sildenafil was 19.5%. Conclusions Urethral trauma is frequently associated with ED. Sildenafil citrate is useful in the drug treatment of ED in these patients and appears to be well-tolerated.
Gaucher disease (GD) is an autosomal recessive lysosomal storage disorder caused by mutations in the GBA gene. Enzyme replacement treatment is the most effective therapy available for type 1 GD patients, but it is very expensive and does not improve neurologic outcomes in type 2 and 3 GD patients. This study evaluated the effectiveness of an adeno-associated virus 9 (AAV9) vector expressing the Gba gene delivered systemically in GD mouse models. To detect the therapeutic effects of the AAV9-mediated Gba transfer on the systemic symptoms of GD, an inducible whole-body Gba knockout mouse was developed in which tamoxifen effectively induced whole-body Gba gene deletion, and the mice displayed systemic symptoms of GD. The AAV9-CMV-Gba vector, with the expression of Gba driven by the universal CMV promoter, restored GCase activity in multiple organs and prolonged the lifespan in tamoxifen-induced GD mice after intravenous injection. Mice with brain-specific Gba deletion were also included in this study as a model of neuropathic GD (nGD) and injected intraperitoneally on postnatal day 5 with the AAV9-SYN-Gba vector; this improved the GCase activity, ameliorated the neuropathological changes and extended the mean lifespan two-fold. This study demonstrates that AAV9-mediated gene transfer is a potentially effective treatment for GD.
Developing markers linked to key traits has been a focus of peanut (Arachis hypogaea L.) genomics in the postgenome era. Multiple disease resistance traits have been found to be qualitative and controlled by major quantitative trait loci (QTL) or even single genes while others are more complex. Southern stem rot (stem rot in short) is a devastating disease of peanut caused by the fungus Sclerotium rolfsii. It has been one of the most damaging diseases of peanut with regard to both cost of control and yield loss in the southeastern United States for the last decade. The disease is initiated annually from sclerotia in the soil. The nonuniform distribution of these propagules leads to the nonuniform development of disease, which makes phenotyping and genetic mapping of resistance difficult. Here we report the mapping of two QTL regions controlling stem rot resistance in peanut. Using careful field evaluation, resistant and susceptible bulks were identified from a recombinant inbred line (RIL) population and subjected to QTL sequencing (QTL‐seq). Developed SNP markers linked to the QTL were validated in a blind selection test by selecting only with markers in a part of the population not used for initial analysis. The lines selected for bulk sequencing also were shown to have strong separation for resistance in an independent field experiment. This work not only delivers markers for marker‐assisted selection (MAS) for an important disease in peanut but shows that QTL‐seq can work effectively even when considering highly complex, and quantitative traits.
Background and Objective: Type 2 diabetes (T2D)-associated periodontitis is severe and refractory in many cases. Considered an inflammatory disease, T2D predisposes to periodontitis by increasing whole-body inflammation. One mechanism of increased inflammation is thatT2D is mediated by loss of production or function of the antiinflammatory hormone adiponectin. In our previous report, AdipoRon, an adiponectin receptor agonist, and AdipoAI, a newly discovered, more specific agonist, attenuated T2D-associated inflammation by inhibiting osteoclastogenesis and LPS-induced endotoxemia. Autophagy plays an important role during osteoclast differentiation and function. The impact of AdipoAI on osteoclast function and autophagy involved in osteoclastogenesis is not known. Here, we compare AdipoRon and AdipoAI potency, side effects and mechanism of action in T2D-associated periodontitis. Methods:The RAW 264.7 cell line was used for in vitro studies. We analyzed the potential cytotoxicity of AdipoAI using the CCK-8 assay. The anti-osteoclastogenic potential of AdipoAI was studied by real-time qPCR and tartrate-resistant acid phosphatase staining. The actions of AdipoAI involved in autophagy were tested by real-time qPCR, western blot and immunofluorescence staining. In the diet-induced obesity model of T2D, we investigated the impact of AdipoAI on fasting blood glucose, alveolar bone loss, and gingival inflammation in mice with experimental periodontitis.Results: AdipoRon inhibited osteoclastogenesis and AdipoAI inhibited osteoclastogenesis at lower doses than AdipoRon without any cytotoxicity.
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