Peyronie's Disease: Still a Surgical Disease.
Ontology highlight
ABSTRACT:
SUBMITTER: Martinez D
PROVIDER: S-EPMC3432524 | biostudies-other | 2012
REPOSITORIES: biostudies-other
Publications
Peyronie's Disease: Still a Surgical Disease.
Martinez Daniel D Ercole Cesar E CE Hakky Tariq S TS Kramer Andrew A Carrion Rafael R
Advances in urology 20120826
Peyronie's Disease (PD) remains a challenging and clinically significant morbid condition. Since its first description by François Gigot de la Peyronie, much of the treatment for PD remains nonstandardized. PD is characterized by the formation of fibrous plaques at the level of the tunica albuginea. Clinical manifestations include morphologic changes, such as curvatures and hourglass deformities. Here, we review the common surgical techniques for the management of patients with PD. ...[more]
Similar Datasets
Project description:BACKGROUND: To evaluate surgical outcome and survival benefit after quaternary cytoreduction (QC) in epithelial ovarian cancer (EOC) relapse. METHODS: We systematically evaluated all consecutive patients undergoing QC in our institution over a 12-year period (October 2000-January 2012). All relevant surgical and clinical outcome parameters were systematically assessed. RESULTS: Forty-nine EOC patients (median age: 57; range: 28-76) underwent QC; in a median of 16 months (range:2-142) after previous chemotherapy. The majority of the patients had an initial FIGO stage III (67.3%), peritoneal carcinomatosis (77.6%) and no ascites (67.3%). At QC, patients presented following tumour pattern: lower abdomen 85.7%; middle abdomen 79.6% and upper abdomen 42.9%. Median duration of surgery was 292 min (range: a total macroscopic tumour clearance could be achieved. Rates of major operative morbidity and 30-day mortality were 28.6% and 2%, respectively.Mean follow-up from QC was 18.41 months (95% confidence interval (CI):12.64-24.18) and mean overall survival (OS) 23.05 months (95% CI: 15.5-30.6). Mean OS for patients without vs any tumour residuals was 43 months (95% CI: 26.4-59.5) vs 13.4 months (95% CI: 7.42-19.4); P=0.001. Mean OS for patients who received postoperative chemotherapy (n=18; 36.7%) vs those who did not was 40.5 months (95% CI: 27.4-53.6) vs 12.03 months (95% CI: 5.9-18.18); P<0.001.Multivariate analysis indentified multifocal tumour dissemination to be of predictive significance for incomplete tumour resection, higher operative morbidity and lower survival, while systemic chemotherapy subsequent to QC had a protective significant impact on OS. No prognostic impact had ascites, platinum resistance, high grading and advanced age. CONCLUSION: Even in this highly advanced setting of the third EOC relapse, maximal therapeutic effort combining optimal surgery and chemotherapy appear to significantly prolong survival in a selected patients 'group'.
| S-EPMC3553531 | biostudies-other
Project description:Objective: Adult Still’s disease (ASD) is a systemic disorder of unknown etiology characterized by high spiking fever, rash and arthritis. The purpose of this study was to determine the pathogenic roles of specific genes in ASD. Methods: Differentially expressed genes (DEGs) were examined by DNA microarray and validated by quantitative PCR using monocytes isolated from patients with active-ASD, inactive-ASD and healthy controls. The correlation between validated DEGs and ASD activity was analyzed. After inflammasome activation with LPS and Nigericin, the production of IL-1β, IL-18, inflammasome and autophagy related proteins in DEGs-overexpressing THP-1 cells was carried out by ELISA or western blotting. DEGs-overexpressing THP-1 cells were treated with an inhibitor of autophagy followed by assessment of IL-1β and IL-18 production by ELISA and western blotting method.Conclusions: The overexpression of PLAC8 in monocytes might play a regulatory role in the production of IL-1β and IL-18 by the enhancement of autophagy, resulting in the suppression of ASD. Results:A total of 68 genes were highly expressed in monocytes isolated from active-ASD patients, relative to their expression in inactive-ASD patients and healthy controls. After validation of expression of 13 genes (CLU, FCGR1B, PLAC8, TLR1, S100A12, CD55, PIM1, BCL2A1, SOD2, PLSCR1, CYP1B1, STEAP4, IL1RN), the expression of PLAC8 was significantly higher in active-ASD patients than the other groups. In ASD, PLAC8 expression level correlated with serum levels of CRP, ferritin and IL-18. Stimulation of monocytes with lipopolysaccharide resulted in PLAC8 upregulation. LPS or Nigericin stimulation of PLAC8-overexpressing THP-1, but not THP-1 cells< was associated with significant decrease in IL-1β and IL-18 production. PLAC8 overexpressing in THP-1 cells was associated with enhanced autophagy and suppression of IL-1β and IL-18 production. Conclusions: PLAC8 upregulation in monocytes seemed to play a regulatory role in the production of IL-1β and IL-18 through enhanced autophagy, resulting in suppression of ASD. The results highlight the role of PLAC8 in the pathogenesis of ASD and suggest its potential suitability as a therapeutic target in ASD.
2018-11-10 | GSE113645 | GEO
Project description: Not available
| S-EPMC10643394 | biostudies-literature
Project description:The purpose of this article is to review the basic and clinical science relating plasma triglycerides and cardiovascular disease. Although many aspects of the basic physiology of triglyceride production, its plasma transport, and its tissue uptake have been known for several decades, the relationship of plasma triglyceride levels to vascular disease is uncertain. Are triglyceride-rich lipoproteins, their influence on high-density lipoprotein and low-density lipoprotein, or the underlying diseases that lead to defects in triglyceride metabolism the culprit? Animal models have failed to confirm that anything other than early fatty lesions can be produced by triglyceride-rich lipoproteins. Metabolic products of triglyceride metabolism can be toxic to arterial cells; however, these studies are primarily in vitro. Correlative studies of fasting and postprandial triglycerides and genetic diseases implicate very-low-density lipoprotein and their remnants and chylomicron remnants in atherosclerosis development, but the concomitant alterations in other lipoproteins and other risk factors obscure any conclusions about direct relationships between disease and triglycerides. Genes that regulate triglyceride levels also correlate with vascular disease. Human intervention trials, however, have lacked an appropriately defined population and have produced outcomes without definitive conclusions. The time is more than ripe for new and creative approaches to understanding the relationship of triglycerides and heart disease.
| S-EPMC3141088 | biostudies-literature
Project description: Not available
| S-EPMC4836804 | biostudies-literature
Project description:The receptor for advanced glycation end products (RAGE) is a multiligand receptor involved in inflammatory disorders, tumor outgrowth, diabetic complications and Alzheimer's disease (AD). RAGE transports circulating amyloid-β toxins across the blood-brain barrier (BBB) into the brain. RAGE-amyloid-β toxin interaction at the BBB leads to oxidative stress, inflammatory responses and reduced cerebral blood flow. Thus, regulating RAGE activity at the BBB and/or within brain could be beneficial to AD patients. Herein, the structure-function relation for RAGE-ligand interaction and the role of RAGE as a potential target in the development of treatments for AD and other RAGE-associated disorders are discussed. Despite recent setbacks in the development of RAGE-based therapies for AD, a new generation of compounds that regulate RAGE activity could be efficacious. Careful studies are needed in rodent and nonrodent animal models of AD with new the generation of RAGE antagonists to ensure safety and efficacy in chronic treatment before clinical trials.
| S-EPMC4973574 | biostudies-literature
Project description: Not available
| S-EPMC6934198 | biostudies-literature
Project description:Sickle cell disease (SCD) is an inherited blood disorder, due to a single point mutation in the β-globin gene (HBB) leading to multisystemic manifestations and it affects millions of people worldwide. The monogenic nature of the disease and the availability of autologous hematopoietic stem cells (HSCs) make this disorder an ideal candidate for gene modification strategies. Notably, significant advances in the field of gene therapy and genome editing that took place in the last decade enabled the possibility to develop several strategies for the treatment of SCD. These curative approaches were firstly based on the correction of disease-causing mutations holding the promise for a specific, effective and safe option for patients. Specifically, gene-editing approaches exploiting the homology directed repair pathway were investigated, but soon their limited efficacy in quiescent HSC has curbed their wider development. On the other hand, a number of studies on globin gene regulation, led to the development of several genome editing strategies based on the reactivation of the fetal γ-globin gene (HBG) by nuclease-mediated targeting of HBG-repressor elements. Although the efficiency of these strategies seems to be confirmed in preclinical and clinical studies, very little is known about the long-term consequences of these modifications. Moreover, the potential genotoxicity of these nuclease-based strategies must be taken into account, especially when associated with high targeting rates. The recent introduction of nuclease-free genome editing technologies brought along the potential for safer strategies for SCD gene correction, which may also harbor significant advantages over HBG-reactivating ones. In this Review, we discuss the recent advances in genome editing strategies for the correction of SCD-causing mutations trying to recapitulate the promising strategies currently available and their relative strengths and weaknesses.
| S-EPMC10652763 | biostudies-literature
Project description:Atherosclerotic renovascular disease (ARVD) is an unresolved therapeutic dilemma despite extensive pre-clinical and clinical studies. The pathophysiology of the disease has been widely studied, and many factors that may be involved in progressive renal injury and cardiovascular risk associated with ARVD have been identified. However, therapies and clinical trials have focused largely on attempts to resolve renal artery stenosis without considering the potential need to treat the renal parenchyma beyond the obstruction. The results of these trials show a staggering consistence: although nearly 100% of the patients undergoing renal angioplasty show a resolution of the vascular obstruction, they do not achieve significant improvements in renal function or blood pressure control compared with those patients receiving medical treatment alone. It seems that we may need to take a step back and reconsider the pathophysiology of the disease in order to develop more effective therapeutic strategies. This mini-review discusses potential therapeutic alternatives that focus on the renal parenchyma distal to the vascular obstruction and may provide additional tools to enhance current treatment of ARVD.
| S-EPMC6281014 | biostudies-literature
Project description:Akinesia is a major manifestation of Parkinson's disease (PD) related to difficulties or failures of willed movement to occur. Akinesia is still poorly understood and is not fully alleviated by standard therapeutic strategies. One reason is that the area of the clinical concept has blurred boundaries referring to confounded motor symptoms. Here, we review neuroimaging studies which, by providing access to finer-grained mechanisms, have the potential to reveal the dysfunctional brain processes that account for akinesia. It comes out that no clear common denominator could be identified across studies that are too heterogeneous with respect to the clinical/theoretical concepts and methods used. Results reveal, however, that various abnormalities within but also outside the motor and dopaminergic pathways might be associated with akinesia in PD patients. Notably, numerous yet poorly reproducible neural correlates were found in different brain regions supporting executive control by means of resting-state or task-based studies. This includes for instance the dorsolateral prefrontal cortex, the inferior frontal cortex, the supplementary motor area, the medial prefrontal cortex, the anterior cingulate cortex or the precuneus. This observation raises the issue of the multidimensional nature of akinesia. Yet, other open issues should be considered conjointly to drive future investigations. Above all, a unified terminology is needed to allow appropriate association of behavioral symptoms with brain mechanisms across studies. We adhere to a use of the term akinesia restricted to dysfunctions of movement initiation, ranging from delayed response to freezing or even total abolition of movement. We also call for targeting more specific neural mechanisms of movement preparation and action triggering with more sophisticated behavioral designs/event-related neurofunctional analyses. More work is needed to provide reliable evidence, but answering these still open issues might open up new prospects, beyond dopaminergic therapy, for managing this disabling symptom.
| S-EPMC6412010 | biostudies-literature