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1.
Sex Med Rev ; 7(3): 508-515, 2019 07.
Article in English | MEDLINE | ID: mdl-30612978

ABSTRACT

INTRODUCTION: Peyronie's disease (PD) is a debilitating condition that affects a sizable number of men worldwide. Current treatment options consist of oral therapy, intralesional injections, and surgery. Penile stretching has been used as a treatment for PD, including penile traction therapy (PTT) and vacuum erection devices (VEDs), with numerous trials completed or underway. AIM: To present and summarize the current literature on penile stretching for the treatment of PD. METHODS: Using PubMed, we performed a literature review of studies from January 1990 through July 2018 that focused on penile stretching for PD management. PTT and VED were included in the search criteria. MAIN OUTCOME METHODS: Penile curvature correction was effective, and stretched penile length was improved. RESULTS: PD therapies that use penile stretching as a mechanical intervention to alter tissue characteristics were studied. PTT has been successful in primary penile lengthening and curvature correction in the acute phase of PD. PTT also improved length retention in men undergoing plication and incision/grafting procedures. Combination of PTT and intralesional injection therapy for PD treatment requires further investigation. There are fewer studies investigating VEDs and their role in PD management, but initial small trials suggest a role in curvature correction and penile lengthening. CONCLUSIONS: Penile stretching is an effective therapy for PD. Data from limited trials suggest a role for PTT and VEDs in the management of PD, although further research is needed. Cowper MG, Burkett CB, Le TV et al. Penile Stretching as a Treatment for Peyronie's Disease: A Review. Sex Med Rev 2019;7:508-515.


Subject(s)
Penile Erection/physiology , Penile Induration/therapy , Penis/physiopathology , Humans , Male , Penile Induration/physiopathology , Vacuum
2.
Genetics ; 204(1): 337-53, 2016 09.
Article in English | MEDLINE | ID: mdl-27412712

ABSTRACT

We identified loci responsible for natural variation in Arabidopsis thaliana (Arabidopsis) responses to a bacterial pathogen virulence factor, HopAM1. HopAM1 is a type III effector protein secreted by the virulent Pseudomonas syringae strain Pto DC3000. Delivery of HopAM1 from disarmed Pseudomonas strains leads to local cell death, meristem chlorosis, or both, with varying intensities in different Arabidopsis accessions. These phenotypes are not associated with differences in bacterial growth restriction. We treated the two phenotypes as quantitative traits to identify host loci controlling responses to HopAM1. Genome-wide association (GWA) of 64 Arabidopsis accessions identified independent variants highly correlated with response to each phenotype. Quantitative trait locus (QTL) mapping in a recombinant inbred population between Bur-0 and Col-0 accessions revealed genetic linkage to regions distinct from the top GWA hits. Two major QTL associated with HopAM1-induced cell death were also associated with HopAM1-induced chlorosis. HopAM1-induced changes in Arabidopsis gene expression showed that rapid HopAM1-dependent cell death in Bur-0 is correlated with effector-triggered immune responses. Studies of the effect of mutations in known plant immune system genes showed, surprisingly, that both cell death and chlorosis phenotypes are enhanced by loss of EDS1, a regulatory hub in the plant immune-signaling network. Our results reveal complex genetic architecture for response to this particular type III virulence effector, in contrast to the typical monogenic control of cell death and disease resistance triggered by most type III effectors.


Subject(s)
Arabidopsis/genetics , Arabidopsis/immunology , Quantitative Trait Loci/immunology , Arabidopsis/microbiology , Arabidopsis Proteins/genetics , Arabidopsis Proteins/immunology , Genes, Plant , Genome-Wide Association Study , Phenotype , Plant Diseases/genetics , Plant Diseases/immunology , Plant Diseases/microbiology , Pseudomonas syringae/genetics , Pseudomonas syringae/immunology , Virulence Factors/metabolism
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