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ABSTRACT:
PROVIDER: PRJNA1044566 | ENA |
REPOSITORIES: ENA
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Project description:Obstruction in any part between the outlet of the bladder and the external urethra is called partial Bladder outlet obstruction (pBOO), which is a common disease in urology, which may cause bladder dysfunction. We have comfirmed that human urine-derived stem cells (hUSCs) could improve the bladder function of pBOO rats in our previous study. We thus explored the role of miRNAs in pBOO rats before and after treatment of hUSCs, and revealed that they could serve as effective prevention and treatment therapeutic targets. Rat bladder tissues were used for miRNA sequencing. We identified 8 differentially expressed miRNAs in the pBOO rats before and after treatment of hUSCs.
2021-04-02 | GSE171293 | GEO
Project description:This study is intended to investigate whether roux-en-y bypass surgery is superior to conventional loop gastrojejunostomy for Malignant gastric outlet obstruction in terms of tolerance to solid food intake. We hypothesize that roux-en-y bypass will be associated with improved solid food intake in the first 30 days after surgery.
| 70610 | ecrin-mdr-crc
Project description:Obstruction in any part between the outlet of the bladder and the external urethra is called partial Bladder outlet obstruction (pBOO), which is a common disease in urology, which may cause bladder dysfunction. We have comfirmed that human urine-derived stem cells (hUSCs) could improve the bladder function of pBOO rats in our previous study. We thus explored the role of miRNAs in pBOO rats before and after treatment of hUSCs, and revealed that they could serve as effective prevention and treatment therapeutic targets. Rat bladder tissues were used for circRNA, lncRNA and mRNA sequencing.
2021-04-02 | GSE171366 | GEO
Project description:Leucine-rich-repeats and immunoglobulin-like-domains (LRIG2) variants can occur in urofacial syndrome (UFS), an inherited disease characterised by functional bladder outlet obstruction. We aimed to define the pathobiology underlying UFS which we hypothesised would illuminate how the bladder becomes innervated. Lrig2 was detected in pelvic ganglia supplying autonomic neurons to the bladder, and in neurites and glia emanating from explanted ganglia. One week old Lrig2 mutant mice displayed abnormally patterned bladder nerves, as did mice with mutations of Hpse2, also mutated in some UFS patients. From two weeks postnatally, Lrig2 mutants had urination defects resembling UFS. Molecules implicated in neural biology, including Nos1 which relaxes the bladder outlet, were dysregulated in newborn Lrig2 mutant bladders. These molecular aberrations preceded manifest urination defects. We discovered novel homozygous missense LRIG2 variants in non-syndromic bladder outlet obstruction. Molecules mutated in UFS are required for bladder innervation and LRIG2 variants can occur in non-syndromic bladder disease as well as in UFS.
2020-04-27 | E-MTAB-6089 | biostudies-arrayexpress
Project description:Bladder outlet obstruction (BOO) causes lower urinary tract symptoms and objectifiable urodynamic changes in bladder function. We carried out an integrated transcriptome and proteome analysis of bladder samples from male patients with BOO before and 3 months after de-obstruction surgery (transurethral resection of the prostate, TURP). mRNA and protein profiles were correlated with urodynamic findings, specifically voiding detrusor pressure (PdetQmax) before TURP. Patients with high PdetQmax showed less advanced remodeling and inflammatory changes than those with lower values. We oberved significant dysregulation of gene expression, which was reversed by de-obstruction in both patients’ groups. We propose a series of biomarker genes, indicative of BOO, and possibly contributing to the bladder changes. Our data sheds light on the stages of progressive obstruction-induced bladder decompensation, and might add selecting the operation point to avoid the loss of contractility.
2024-05-21 | PXD044777 | Pride
Project description:SCI-induced and partial bladder outlet obstruction mouse models
| PRJEB58912 | ENA
Project description:Benign prostatic hyperplasia and related lower urinary tract symptoms remain common, costly, and impactful issues for aging males. Etiology and pathogenesis are multifactorial and include steroid hormone changes and inflammation. Noninvasive markers could one day inform personalized medicine, but interindividual variation and lack of healthy age-matched controls hamper research. Experimental models are appealing for insight into disease mechanisms. Here, we present a spatiotemporal proteomics study in a mouse model of hormone-induced urinary dysfunction. Urine samples were collected noninvasively across time: before, during, and after disease onset. Microcomputed tomography analysis implicated the prostate as a spatially relevant contributor to bladder outlet obstruction. Prostates were collected after disease onset and compared with control mice. Notable changes in urine include proteins representing oxidative stress defense and acute phase inflammatory response processes. In the prostate, hormone treatment led to perturbations related to oxidative stress response and H2O2 metabolism. Several protein changes coincided in both urine and prostate tissue, including Ctsb, Qsox1, and Gpx3. This study supports the concept of noninvasive urinary biomarkers for prostate disease diagnostics. Oxidative stress and acute phase inflammatory processes were identified as key consequences of hormone-induced bladder outlet obstruction. Future research into antioxidants and anti-inflammatories in prostate disease appears promising.
2021-09-08 | PXD014416 | Pride
Project description:Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antiinflammatory and antioxidant phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. However, because Eviprostat is a mixture of compounds from multiple natural sources, its mechanism of action has been difficult to investigate. In this study, we used oligonucleotide microarrays to identify changes in gene expression that occur in the prostate of rats with surgically induced partial bladder outlet obstruction and the effect of Eviprostat on those changes.
2009-07-21 | GSE16063 | GEO
Project description:Objective: Bladder outlet obstruction (BOO) is a common urologic disease associated with poorly understood molecular mechanisms. This study aimed to investigate the possible involvements of circRNAs (circular RNAs) and circRNA-encoded proteins in BOO development. Methods: The rat BOO model was established by the partial bladder outlet obstruction surgery. Differential expression of circRNA and protein profiles were characterized by deep RNA sequencing and iTRAQ quantitative proteomics respectively. Novel proteins encoded by circRNAs were predicted through ORF (open reading frame) selection using the GETORF software and verified by the mass spectrometry in proteomics, combined with the validation of their expressional alterations by quantitative RT-PCR. Results: Totally 3051 circRNAs were differentially expressed in bladder tissues of rat BOO model with widespread genomic distributions, including 1414 up-regulated and 1637 down-regulated circRNAs. Our following quantitative proteomics revealed significant changes of 85 proteins in rat BOO model, which were enriched in multiple biological processes and signaling pathways such as the PPAR and Wnt pathways. Among them, 21 differentially expressed proteins were predicted to be encoded by circRNAs and showed consistent circRNA and protein levels in rat BOO model. The expression of five protein-encoding circRNA were further validated by quantitative RT-PCR and mass spectrometry. Conclusion: The circRNA and protein profiles were substantially altered in rat BOO model, with great expressional changes of circRNA-encoded novel proteins.
2022-02-22 | PXD029337 | Pride