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1.
Prog Urol ; 27(17): 1069-1075, 2017 Dec.
Article in French | MEDLINE | ID: mdl-29030080

ABSTRACT

PURPOSE: The pelvic floor is now well known and its role in the mechanism of erection is demonstrated. We wanted to know what is the evidence of the effectiveness of perineal rehabilitation in erectile dysfunction. MATERIALS: An English search was performed in Google scholar and databases PubMed, Medline, Pedro with the keywords "pelvic floor, erectile dysfunction, impotence, physiotherapy, exercises, rehabilitation, PFMT". We have selected randomized clinical trials published in indexed journals. RESULTS: Six randomized trials were selected. Five of them have shown statistically and clinically significant effectiveness in populations of men with erectile dysfunction and various underlying pathologies. In the fifth trial, the difference in effectiveness was not statistically significant. At 3 months, the best-conducted study showed an average improvement of 7 points at IIEF-5 compared to the control group (P-value: 0.004). Rehabilitation has not resulted in any adverse side effects. However, these studies were conducted in heterogeneous populations and the protocols for pelvic floor muscle strengthening rehabilitation differed from one study to another, making it impossible to formulate a specific recommendation for clinical practice. CONCLUSION: Based on the results of this literature review, perineal physiotherapy may have a role to play in the management of erectile dysfunction.


Subject(s)
Erectile Dysfunction/therapy , Pelvic Floor Disorders/rehabilitation , Erectile Dysfunction/etiology , Humans , Male , Pelvic Floor Disorders/complications , Randomized Controlled Trials as Topic , Treatment Outcome
2.
Cell Death Dis ; 6: e1617, 2015 Jan 22.
Article in English | MEDLINE | ID: mdl-25611391

ABSTRACT

Huntington's disease (HD) is a fatal neurodegenerative disorder caused by aberrant expansion of CAG repeat in the huntingtin gene. Mutant Huntingtin (mHtt) alters multiple cellular processes, leading to neuronal dysfunction and death. Among those alterations, impaired mitochondrial metabolism seems to have a major role in HD pathogenesis. In this study, we used the Drosophila model system to further investigate the role of mitochondrial damages in HD. We first analyzed the impact of mHtt on mitochondrial morphology, and surprisingly, we revealed the formation of abnormal ring-shaped mitochondria in photoreceptor neurons. Because such mitochondrial spheroids were previously detected in cells where mitophagy is blocked, we analyzed the effect of PTEN-induced putative kinase 1 (PINK1), which controls Parkin-mediated mitophagy. Consistently, we found that PINK1 overexpression alleviated mitochondrial spheroid formation in HD flies. More importantly, PINK1 ameliorated ATP levels, neuronal integrity and adult fly survival, demonstrating that PINK1 counteracts the neurotoxicity of mHtt. This neuroprotection was Parkin-dependent and required mitochondrial outer membrane proteins, mitofusin and the voltage-dependent anion channel. Consistent with our observations in flies, we demonstrated that the removal of defective mitochondria was impaired in HD striatal cells derived from HdhQ111 knock-in mice, and that overexpressing PINK1 in these cells partially restored mitophagy. The presence of mHtt did not affect Parkin-mediated mitochondrial ubiquitination but decreased the targeting of mitochondria to autophagosomes. Altogether, our findings suggest that mitophagy is altered in the presence of mHtt and that increasing PINK1/Parkin mitochondrial quality control pathway may improve mitochondrial integrity and neuroprotection in HD.


Subject(s)
Drosophila melanogaster/metabolism , Huntington Disease/metabolism , Huntington Disease/pathology , Mitophagy , Neuroprotective Agents/metabolism , Protein Kinases/metabolism , Animals , Drosophila Proteins/metabolism , Eye/pathology , Eye/ultrastructure , Mice , Mitochondria/metabolism , Mitochondria/ultrastructure , Mutant Proteins/metabolism , Neostriatum/metabolism , Neostriatum/pathology , Nerve Degeneration/pathology , Neurons/metabolism , Neurons/pathology , Neurons/ultrastructure , Phagosomes/metabolism , Phagosomes/ultrastructure , Serotonin Plasma Membrane Transport Proteins/metabolism , Spheroids, Cellular/metabolism , Survival Analysis , Ubiquitin-Protein Ligases/metabolism
3.
Ann Fr Anesth Reanim ; 28(4): 358-64, 2009 Apr.
Article in French | MEDLINE | ID: mdl-19328644

ABSTRACT

Mild therapeutic hypothermia can provide neuroprotection in some clinical situations (postanoxic cardiac arrest, neonatal anoxia). Techniques to induce hypothermia are based on thermal exchanges, in particular conduction and convection. There are several external cooling techniques: application of ice packs, cold moistened towel, ice-cold devices, ventilation of cooled air, water- or air-cooled circulating mattresses or devices. These techniques are frequently used because of their reduced cost. Internal cooling techniques are more limited and more expensive: ice-cold perfusion, endovascular catheters, extracorporeal circulation, but they offer more efficiency (high speed to reach and to maintain the temperature target). Drugs can also induce hypothermia, either by decreasing body temperature, e.g. paracetamol and aspirin, or by blocking shivering, e.g. neuromuscular blocking agents, opioids and alpha2-agonist.


Subject(s)
Brain Damage, Chronic/prevention & control , Craniocerebral Trauma/therapy , Hypothermia, Induced/methods , Hypoxia, Brain/therapy , Adrenergic alpha-Agonists/therapeutic use , Adult , Analgesics, Non-Narcotic/therapeutic use , Analgesics, Opioid/therapeutic use , Beds , Catheterization , Combined Modality Therapy , Craniocerebral Trauma/complications , Extracorporeal Circulation , Fetal Hypoxia/therapy , Humans , Hypothermia, Induced/instrumentation , Hypoxia, Brain/etiology , Ice , Infant, Newborn , Neuromuscular Blocking Agents/therapeutic use , Perfusion , Refrigeration/instrumentation , Refrigeration/methods , Water
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