Aim: To determine retrospectively the safety and efficacy of extracorporeal shock wave therapy (ESWT) in patients with Peyronie's disease.
Methods: Fifty-three patients with stable Peyronie's disease underwent ESWT (group 1). Fifteen patients matched with the baseline characteristic of the patients in group 1, who received no treatment, were used as the control (group 2). The patients' erectile function (International Index of Erectile Function [IIEF-5] score), pain severity (visual analog scale), plaque size and degree of penile angulation were assessed before and after the treatment in group 1 and during the follow-up in group 2.
Results: The mean follow-up time was 32 months (range: 6-64 months) in group 1 and 35 months (range: 9-48 months) in group 2. All the patients were available for the follow-up. Considering erectile function and plaque size, no significant changes (P > 0.05) were observed in group 1 before or after the ESWT. A total of 39 patients (74%) reported a significant effect in pain relief in group 1 after ESWT. However, regarding improvement in pain, IIEF-5 score and plaque size, no significant differences were observed between the two groups. In 21 patients (40%) of group 1, the deviation angle was decreased more than 10 degrees with a mean reduction in all patients of 11 degrees (range: 6-20 degrees). No serious complications were noted considering ESWT procedure.
Conclusion: ESWT is a minimally invasive and safe alternative procedure for the treatment of Peyronie's disease. However, the effect of ESWT on penile pain, sexual function and plaque size remains questionable.
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http://dx.doi.org/10.1111/j.1745-7262.2006.00138.x | DOI Listing |
Alzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
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December 2024
Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: Genome-wide association studies (GWAS) in Alzheimer's disease (AD) leveraging endophenotypes beyond case/control diagnosis, such as brain amyloid β pathology, have shown promise in identifying novel variants and understanding their potential functional impact. In this study, we leverage two brain amyloid β pathology measurement modalities, PET imaging and neuropathology, to address sample size limitations and to discover novel genetic drivers of disease.
Method: We conducted a meta-analysis on an amyloid PET imaging GWAS (N = 7,036, 35% amyloid positive, 53.
Alzheimers Dement
December 2024
School of Biomedical Sciences, Kent State University, Kent, OH, USA.
Background: Accumulation of β-amyloid (Aβ) plaque in the brain is a pathological hallmark of Alzheimer's Disease (AD). We recently reported that the application of mild magnetic hyperthermia is feasible to target and disrupt Aβ plaques by means of generating localized heat on the surface of magnetic nanoparticles (MNPs) targeted to Aβ aggregates in response to a remotely applied alternating magnetic field (AMF) (Nanomedicine:NBM, 2021). The objective of the current study is to demonstrate the feasibility of mild magnetic hyperthermia stimulation (MNP/AMF) in clearing Aβ deposits in vivo using 5xFAD mice, a well-established transgenic AD mouse model.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Utah, Salt Lake City, UT, USA.
Background: Neurodegenerative disorders such as Alzheimer's Disease (AD) are increasingly associated with irregular lipid accumulation. Dysfunction in the catabolism of sphingolipids leads to many neurodegenerative disorders but has only recently garnered interest in AD. Excess ceramide deposition has been observed in Aβ-plaques, plasma, and cerebrospinal fluid in AD patients and AD mouse models.
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December 2024
University of Western Ontario, London, ON, Canada.
Background: Apolipoprotein E (ApoE) exhibits isoform-specific interactions with Alzheimer's disease (AD)-related pathology. In comparison with the more common ApoE3 isoform, ApoE4 promotes amyloid-β (Aβ) deposition, enhances tau-mediated neurodegeneration and inflammation. However, the lack of appropriate preclinical models has limited the ability to evaluate the potential synergistic effect of Aβ, tau and ApoE on cognition and disease progression.
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