urinary bladder neck obstruction/hypoxia

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Partial bladder outlet obstruction in mice may cause E-cadherin repression through hypoxia induced pathway.

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OBJECTIVE Posterior urethral valves are the most common cause of partial bladder outlet obstruction in the pediatric population. Posterior urethral valves is a devastating clinical problem that ultimately results in urinary incontinence, neurogenic bladder and renal impairment. Despite improvements

Effects of varying degrees of partial bladder outlet obstruction on urinary bladder function of rats: A novel link to inflammation, oxidative stress and hypoxia.

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OBJECTIVE The aim of the present study was to investigate the effects of different degrees of obstruction, and the roles of inflammation, oxidative stress, and hypoxia parameters on bladder function. METHODS Thirty male Sprague-Dawley rats were divided into 3 groups (n = 10 in each group): (i)

Ischemia, Hypoxia and Oxidative Stress in Bladder Outlet Obstruction and Bladder Overdistention Injury.

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Ischemia and the accompanied hypoxia significantly impair the function of the urinary bladder, which is further damaged by ischemia/reperfusion (I/R) injury following the re-establishment of the blood supply. Current evidences have confirmed that blood flow of the bladder is decreased by bladder

[Role of blood supply disturbance and tissue hypoxia in the development of bladder dysfunction in bladder outlet obstruction caused by the prostatic adenoma].

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Enhanced angiogenesis and relaxation of bladder as early response to bladder outlet obstruction.

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OBJECTIVE To provide insights into the pathogenesis of bladder insult secondary to bladder outlet obstruction. METHODS Six-week-old female Sprague-Dawley rats (n = 80) were divided into eight groups, 10 rats each, according to the duration of bladder outlet obstruction, including 0, 3, 6, 12, 24,

Hypoxia and an angiogenic response in the partially obstructed rat bladder.

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Previous molecular and blood flow studies performed on animal models of partial bladder outlet obstruction (PBOO) caused us to propose that bladder hypoxia/ischemia was a significant effector of the cellular and functional changes that occur in the bladder as a result of this condition. To confirm

The restorative effect of a selective cyclooxygenase-2 inhibitor on urothelial cell-cell interactions after partial bladder outlet obstruction in rats.

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OBJECTIVE To determine the changes in cyclooxygenase-2 (COX-2), E-cadherin and alpha-catenin expression after partial bladder outlet obstruction (PBOO), and whether a selective COX-2 inhibitor (celecoxib) might inhibit COX-2 expression and have beneficial effects on urothelial cell-to-cell

Bladder outlet obstruction accelerates bladder carcinogenesis.

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OBJECTIVE To examine the correlation between partial bladder outlet obstruction (PBOO) and bladder carcinogenesis. METHODS Female Wistar rats (6 weeks old) were divided into three groups of 10 each: group 1 was exposed to n-butyl-n-butanol nitrosamine (BBN, a carcinogen) in drinking water for 8

Hypoxia-increased expression of genes involved in inflammation, dedifferentiation, pro-fibrosis, and extracellular matrix remodeling of human bladder smooth muscle cells.

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Partial bladder outlet obstruction (pBOO) is characterized by exaggerated stretch, hydrodynamic pressure, and inflammation which cause significant damage and fibrosis to the bladder wall. Several studies have implicated hypoxia in its pathophysiology. However, the isolated progressive effects of

Modulation of the hypoxic response following partial bladder outlet obstruction.

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OBJECTIVE Tissue level hypoxia has been noted in animal models of partial bladder outlet obstruction. The key mechanisms linking hypoxia and obstruction induced bladder dysfunction remain unknown. 2-Methoxyestradiol is a natural derivative of 17β-estradiol and is currently used as an oncologic agent

Inhibition of HIF Reduces Bladder Hypertrophy and Improves Bladder Function in Murine Model of Partial Bladder Outlet Obstruction.

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OBJECTIVE Posterior urethral valves are the most common cause of partial bladder outlet obstruction in the pediatric population. However, to our knowledge the etiology and the detailed mechanisms underlying pathological changes in the bladder following partial bladder outlet obstruction remain to be

Mesenchymal stem cells inhibit hypoxia-induced inflammatory and fibrotic pathways in bladder smooth muscle cells.

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OBJECTIVE Partial bladder outlet obstruction is a multifactorial urological condition in which hypoxia plays a significant role. We recently investigated hypoxia's role as a single stressor and found that hypoxia induced an intense inflammatory and profibrotic switch in bladder smooth muscle cells

The effect of alpha-blocker treatment on bladder hypoxia inducible factor-1 alpha regulation during lower urinary tract obstruction.

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OBJECTIVE To determine whether alpha1-blocker treatment, in chronic bladder outlet obstruction (BOO), influences bladder tissue ischemia. METHODS This prospective study included 60 patients with BOO, of which 40 were under alpha1-blocker medication and 20 without treatment. Patients underwent

Acute intravesical infusion of a cobalt solution stimulates a hypoxia response, growth and angiogenesis in the rat bladder.

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OBJECTIVE Experimental partial bladder outlet obstruction of rats induces a bladder growth and remodeling process similar to that in humans with benign prostatic hyperplasia. Previously we have proposed that bladder hypoxia associated with partial bladder outlet obstruction is a stimulus of this

Mesenchymal stem cell therapy inhibited inflammatory and profibrotic pathways induced by partial bladder outlet obstruction and prevented high-pressure urine storage.

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Partial bladder outlet obstruction (pBOO) is characterized by an initial inflammatory response that progresses to smooth muscle hypertrophy and fibrosis. Current treatment modalities carry high risk of morbidity. Mesenchymal stem cells (MSCs) are undifferentiated adult cells with

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