Modern role of sacrospinous ligament fixation for pelvic organ prolapse surgery--a systemic review.

Pelvic organ prolapse (POP) is a common condition in women. Women with POP often experience pelvic discomfort, urinary and fecal problems, sexual dysfunction, and an overall decrease in their quality of life. Surgical treatment is a feasible option if conservative management fails. Various surgical techniques have been proposed to correct POP with or without the use of graft material. Owing to recent U.S. Food and Drug Administration warnings about mesh-related complications, sacrospinous ligament fixation (SSF), as a traditional vaginal procedure, may play an important role again. To answer this question and evaluate quantitatively the efficacy of SSF in POP, we conducted a systemic review of the available data about SSF and POP. Interventions had to include SSF as a point of attachment. To eliminate confounding bias and effect modification, at least one arm must include SSF without mesh or graft. All follow-up periods were allowed. Information on the following parameters was extracted and entered into a database: study design, type of intervention, number of patients, follow-up in months, cure rate, recurrence rate, intra/postoperative complications, and/or uni/bilateral, preventive/therapeutic, or concomitant procedures. Published papers from the years 1995 to 2011 were selected for analysis.

Genome-based expression profiling study of Hunner's ulcer type interstitial cystitis: an array of 40-gene model.

INTRODUCTION AND HYPOTHESIS: The aim of this study was to explore potential molecular mechanisms contributing to the pathogenesis of Hunner's ulcer type interstitial cystitis (IC). METHODS: Dataset acquisitions from Gene Expression Omnibus under platform accession no GSE 11783. We compared global gene expression profiles in bladder epithelial cells from IC patients with Hunner's ulcer corresponding to normal controls. We re-sampling and exploit the correlation structure presented in the dataset through the transcriptional response. For each patient, two bladder biopsies were studied, one from an ulcer area and one from a non-ulcer area. RNA was extracted, and all labeled samples were hybridized to Human Genome U133 Plus 2.0 Array (Affymetrix, CA, USA). RESULTS: The Mahalanobis distance in hierarchical cluster analysis revealed a model of 40 genes expression which is increased in IC and ulcerated IC. Our results can be summarized as follows: First, the expressions of major histocompatibility complex (MHC) class IF and II molecules, leukocyte immunoglobulin-like receptors, hepatitis A virus cellular receptor 2, and interleukin 32 were increased in bladder epithelial from IC and ulcerative IC area. Next, there is an indication of antigen-mediated aggregation of the high-affinity Fc epsilon and gamma RI leading to allergic inflammation through the disease status. Third, the high-affinity Fc gamma RI subunit facilitated T-cell-mediated immune response through the disease status. Such changes, jointly termed "bladder remodeling," can constitute an important long-term consequence of Hunner's ulcer type IC. CONCLUSIONS: Our results indicate that genome-based expression profiling can be used for the diagnostic tests of Hunner's ulcer type IC in clinical practice.

Genome-based expression profiling study following spinal cord injury in the rat: An array of 48-gene model.

AIM: To explore the potential molecular mechanisms underlying experimental neurogenic bladder dysfunction. METHODS: With the aid of Affymetrix GeneChip Rat Genome U34A arrays, we examined microarray gene expression profiles in bladder wall tissue from female Sprague-Dawley rats within the first 3 weeks following spinal cord injury. Gene transcripts expressed in rat bladder wall tissue at 3 days, 7 days, and 3 weeks following spinal cord injury were compared to normal rat bladder wall tissue. RESULTS: The Mahalanobis distance in hierarchical cluster analysis revealed a 48-gene model, which contained high expressions in rat bladder wall tissue at 3 days, 7 days, and 3 weeks following spinal cord injury. According to gene ontology, plausible molecular alterations in rat bladder wall tissue following spinal cord injury include: (1) the release of nerve growth factor (NGF) and transforming growth factor beta 1 (Tgfb1) (2) the secretion of histamine from mast cells, (3) the occurrence of blood coagulation, (4) the occurrence of N-terminal protein myristoylation, and (5) Axon guidance mediated by Ena/Vasodilator-stimulated phosphoprotein (Ena/VASP) promotes reestablishment of the bladder reflex following spinal cord injury. Such changes, jointly termed "bladder remodeling," can constitute an important long-term consequence of neurogenic bladder dysfunction. CONCLUSION: The success of this innovation has supported the use of microarray-based expression profiling as a commonplace platform for the pathogenesis and therapeutic interventions of experimental neurogenic bladder dysfunction. dysfunction.

Genome-based expression profiles study for the pathogenesis of pelvic organ prolapse: an array of 33 genes model.

INTRODUCTION AND HYPOTHESIS: To explore the potential molecular mechanisms contributing to the pathogenesis of pelvic organ prolapse (POP) with the aid of high-density oligonucleotide microarrays. METHODS: We compared microarray gene expression profiles in pelvic connective tissue from women with POP and nonprolapse controls. The round ligament and uterosacral ligament tissues were removed from each subject at the time of laparoscopic hysterectomy. RNA was then extracted, and all labeled samples were hybridized to ABI Human Genome Survey Microarray version 2.0 (Applied Biosystems, CA, USA). RESULTS: The Mahalanobis distance in hierarchical cluster analysis revealed a model of 33 genes, which contained high expressions of round and uterosacral ligaments from women with POP. According to gene ontology, the expressions of mitochondrial genes encoding ribosomal protein were upregulated. Genes involved in potential interactions with mitochondrial electron transport, nucleosome assembly, cell cycle, and apoptosis were also upregulated. As a result, defective mitochondrial translation caused by ribosomal protein contributes to the potential molecular etiology of POP. Such changes, jointly termed "remodeling of pelvic connective tissue", can constitute an important long-term consequence of POP. CONCLUSIONS: Our results support the use of genome-based expression profiling as a commonplace platform for diagnostic tests of POP.

Genome-based expression profiles as a single standardized microarray platform for the diagnosis of bladder pain syndrome/interstitial cystitis: an array of 139 genes model.

INTRODUCTION AND HYPOTHESIS: The aim of the study was to investigate the molecular signatures underlying bladder pain syndrome/interstitial cystitis (BPS/IC) using cDNA microarray. METHODS: Microarray gene expression profiles were [corrected] studied in a matched case-control study [corrected] by using a system of conditional regression modeling. RESULTS: The main [corrected] findings are summarized as follows: Firstly, a "139-gene" model was discovered to contain high expressions of bladder epithelium, which feature in BPS/IC. Secondly, complex metabolic reactions, including carbohydrate, lipid, cofactors, vitamins, xenobiotics, nucleotide, and amino acid metabolisms, were [corrected] found to have a strong relationship with bladder smooth muscle contraction through IC status. Thirdly, we [corrected] found the transcriptional regulations of IC-induced bladder smooth muscle contraction status, including the level of contractile force, tissue homeostasis, energy homeostasis, and the development of the [corrected] nervous system. In addition, our study suggested the mast-cell activation mediated by the high-affinity receptor of Fc epsilon [corrected] RI triggering allergic inflammation through IC status. Such genetic changes, jointly termed "bladder remodeling," [corrected] can constitute an important long-term consequence of BPS/IC. [corrected]. CONCLUSIONS: The success of this innovation has supported the use of microarray-based expression profiling as a single standardized platform for diagnosis of PBS/IC and offers [corrected] drug discovery.

Genome-based expression profiles as a single standardized microarray platform for the diagnosis of experimental interstitial cystitis: an array of 75 genes model.

INTRODUCTION AND HYPOTHESIS: To investigate the molecular signature underlying experimental interstitial cystitis (IC) using cDNA microarray. METHODS: Microarray gene expression profiles are studied in bladder epithelium of C57BL/6 mice with ovalbumin or substance P-induced experimental IC versus Escherichia coli lipopolysaccharide-induced bacterial cystitis. RESULTS: Main findings are summarized as follows: firstly, a "75-gene" model was discovered to contain high expressions of bladder epithelium which feature in experimental IC. Secondly, glucose, lipid, nucleotide, xenobiotics, and amino acid metabolisms are involved in. Thirdly, T-cell-mediated immune and inflammatory responses are observed. Fourthly, Wnt, Tgf-beta, Mapk, and insulin growth factor receptor signaling pathways are also involved in. In addition, experimental IC leads to Ephrin- and Semaphorin-mediated axon guidance promoting parasympathetic inflammatory reflexes. CONCLUSIONS: Further characterization of human IC-induced gene expression profiles would enable the use of genome-based expression profiling for the therapeutic targets and diagnosis of IC.