Stem Cell Treatment for Erectile Dysfunction

Stem Cell Treatment for Erectile Dysfunction

STEM CELL TREATMENT ERECTILE DYSFUNCTION

Stem Cell Treatment for Erectile Dysfunction

  • Erectile Dysfunction is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual performance.

  • Stem Cell Treatmentst aims to effect the Calcium-sensitive potassium channel and therefore help increase the flow of blood into the Corpus.

STEM CELL TREATMENT ERECTILE DYSFUNCTIONA penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis. Erectile dysfunction is indicated when an erection is difficult to produce. There are various circulatory causes, including alteration of the voltage-gated potassium channel, as in arsenic poisoning from drinking water.

The most important organic causes are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects.

Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this is somewhat less frequent but often can be helped. Notably in psychological impotence, there is a strong response to placebo treatment. Erectile dysfunction, tied closely as it is about ideas of physical well being, can have severe psychological consequences.

Stem Cell Treatment for Erectile Dysfunction

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Related Articles Rat cavernous nerve reconstruction with CD133+ cells derived from human bone marrow. J Sex Med. 2014 May;11(5):1148-58 Authors: Miyamoto K, Inoue S, Kobayashi K, Kajiwara M, Teishima J, Matsubara A Abstract INTRODUCTION: Erectile dysfunction remains a major complication after surgery of pelvic organs, especially after radical prostatectomy. AIM: The aim of this study was to assess the effect of endothelial progenitor cells on the regeneration of cavernous nerves in a rat injury model. METHODS: A 2 mm length of the right and left cavernous nerves of 8-week-old male nude rats were excised. Alginate gel sponge sheets supplemented with 1 × 10(4) CD133+ cells derived from human bone marrow were then placed over the gaps on both sides (CD group). The same experiments were performed on sham-operated rats (SH group), rats with only the nerve excision (EX group), and rats with alginate gel sheets placed on the injured nerves (AL group). MAIN OUTCOME MEASURES: Immunofluorescence staining and molecular evaluation were performed 4 days later. Functional and histological evaluations were performed 12 weeks later. RESULTS: The intracavernous pressure elicited by electrical stimulation and the neuronal nitric oxide synthase-positive area in surrounding tissues of the prostate was significantly greater in the CD group. Immunofluorescence microscopy showed that CD133+ cells were assimilated as vascular endothelial cells, and the real-time polymerase chain reaction showed upregulation of nerve growth factor and vascular endothelial growth factor in the alginate gel sponge sheets of the CD group. CONCLUSIONS: Transplantation of CD133+ cells accelerated the functional and histological recovery in this cavernous nerve injury model, and the recovery mechanism is thought to be angiogenesis and upregulation of growth factors. CD133+ cells could be an optional treatment for cavernous nerve injury after prostatectomy in clinical settings. PMID: 24576198 [PubMed - indexed for MEDLINE]
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Related Articles 2014 Update Of Erectile Dysfunction Management Following Radical Prostatectomy: From Basic Research To Clinical Management. Curr Pharm Des. 2014 Oct 29; Authors: Gur S, Sikka SC, Kadowitz PJ, Silberstein J, Hellstrom WJ Abstract Radical prostatectomy (RP) is the most commonly employed curative intervention for the treatment of prostate cancer. However, due to the proximity of the cavernous nerves (CN) to the prostate, RP results in transient and/often permanent erectile dysfunction (ED). While the prevention of traction injuries during the RP is critical for the preservation of erectile function, several preclinical studies have demonstrated the beneficial effects of neuroprotective (or neuroregenerative) agents in mitigating neuronal injuries sustained during RP. The maintenance or restoration of erectile function after injury may be enhanced in the postoperative period by the stimulation of neurogenesis to protect and restore injured nerves from further deterioration. The present review aims to evaluate and summarize research of these treatment strategies as published in the National Library of Medicine (Pubmed) from 2000 to 2014. The keywords used for the search were ED, RP, CN injury, immunophilin ligands, neurotrophins and phosphodiesterase (PDE)-5 inhibitors, and animal models. Current guidelines for treatment targeting CN recovery recommend the use of immunophilin ligands, neurotrophins, brain-derived neurotrophic factor, glial cell-line derived neurotrophic factor, sonic hedgehog (Shh), Rho-kinase, PDE-5 inhibitors, erythropoietin (EPO), hyperbaric oxygen therapy, super enzyme gene therapy, stem cells, and triiodothyronine (T3) therapy. Additionally, this review identifies remaining gaps in general knowledge and recent updates recognizing the need for further preclinical and clinical trials. PMID: 25354178 [PubMed - as supplied by publisher]
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