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- de Boer, T A, et al.
(författare)
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Pelvic organ prolapse and overactive bladder.
- 2010
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Ingår i: Neurourology and urodynamics. - : Wiley. - 1520-6777 .- 0733-2467. ; 29:1, s. 30-9
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Forskningsöversikt (refereegranskat)abstract
- AIMS: In this review we try to shed light on the following questions: *How frequently are symptoms of overactive bladder (OAB) and is detrusor overactivity (DO) present in patients with pelvic organ prolapse (POP) and is there a difference from women without POP? *Does the presence of OAB symptoms depend on the prolapsed compartment and/or stage of the prolapse? *What is the possible pathophysiology of OAB in POP? *Do OAB symptoms and DO change after conservative or surgical treatment of POP? METHODS: We searched on Medline and Embase for relevant studies. We only included studies in which actual data about OAB symptoms were available. All data for prolapse surgery were without the results of concomitant stress urinary incontinence (SUI) surgery. RESULTS: Community- and hospital-based studies showed that the prevalence of OAB symptoms was greater in patients with POP than without POP. No evidence was found for a relationship between the compartment or stage of the prolapse and the presence of OAB symptoms. All treatments for POP (surgery, pessaries) resulted in an improvement in OAB symptoms. It is unclear what predicts whether OAB symptoms disappear or not. When there is concomitant DO and POP, following POP surgery DO disappear in a proportion of the patients. Bladder outlet obstruction is likely to be the most important mechanism by which POP induces OAB symptoms and DO signs. However, several other mechanisms might also play a role. CONCLUSIONS: There are strong indications that there is a causal relationship between OAB and POP.
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- Liu, Fei, et al.
(författare)
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Systems Proteomics View of the Endogenous Human Claudin Protein Family
- 2016
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Ingår i: Journal of Proteome Research. - : American Chemical Society (ACS). - 1535-3893 .- 1535-3907. ; 15:2, s. 339-359
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Forskningsöversikt (refereegranskat)abstract
- Claudius are the major transmembrane protein components of tight junctions in human endothelia and epithelia. Tissue-specific expression of claudin members suggests that this protein family is not only essential for sustaining the role of tight junctions in cell permeability control but also vital in organizing cell contact signaling by protein protein interactions. How this protein family is collectively processed and regulated is key to understanding the role of junctional proteins in preserving cell identity and tissue integrity. The focus of this review is to first provide a brief overview of the functional context, on the basis of the extensive body of claudin biology research that has been thoroughly reviewed, for endogenous human claudin members and then ascertain existing and future proteomics techniques that may be applicable to systematically characterizing the chemical forms and interacting protein partners of this protein family in human. The ability to elucidate claudin-based signaling networks may provide new insight into cell development and differentiation programs that are crucial to tissue stability and manipulation.
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