A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice.

Endometriosis is a leading cause of pelvic pain and infertility. It is defined by the presence of endometrial tissue in extrauterine locations. The development of novel therapies and diagnostic tools for endometriosis has been limited due in part to challenges in studying the disease.

Techniques for successful vaginal anastomosis in the uterine transplantation patient.

Objective: To demonstrate techniques for successful donor-to-recipient vaginal anastomosis in uterine transplantation including illustration of a tension-free technique.

Design: This video uses live-action footage from surgery, detailed animations, and illustrations to review the step-by-step technique we use for vaginal anastomosis in uterine transplantation. Institutional Review Board approval was obtained for this experimental surgery.

The role of pharmacotherapy in the treatment of endometriosis across the lifespan.

Introduction: Endometriosis is estimated to affect 10% of reproductive-aged women. The gold standard for treatment is surgery; however, surgery carries a significant morbidity and cost burden. There is an ongoing need for safe, effective medical therapies for endometriosis patients, both in conjunction with and independent of surgical interventions.

Management of Endometriomas.

Importance: Endometriomas are a unique and complex representation of the classic phenotypes of endometriosis. Associated symptoms, high recurrence rate, and multimodal approach represent ongoing challenges in the management of this chronic disease.

Objective: To review current literature regarding medical and surgical management of endometriomas.

Uterine Factor Infertility: A Clinical Review.

Uterine factor infertility (UFI) may affect up to 1 in 500 reproductive age women. The uterus is an essential component of achieving pregnancy and carrying a pregnancy to term successfully. There are many etiologies of UFI which may be categorized into either congenital or acquired causes.

Nebivolol improves insulin sensitivity in the TGR(Ren2)27 rat.

Hypertension is often associated with increased oxidative stress and systemic insulin resistance. Use of β-adrenergic receptor blockers in hypertension is limited because of potential negative influence on insulin sensitivity and glucose homeostasis. We sought to determine the impact of nebivolol, a selective vasodilatory β₁-adrenergic blocker, on whole-body insulin sensitivity, skeletal muscle oxidative stress, insulin signaling, and glucose transport in the transgenic TG(mRen2)27 rat (Ren2).

Nebivolol reduces proteinuria and renal NADPH oxidase-generated reactive oxygen species in the transgenic Ren2 rat.

Background/aims: Renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system activation are crucial in the pathogenesis of hypertension, cardiovascular and renal disease. NADPH oxidase-mediated increases in reactive oxygen species (ROS) are an important mediator for RAAS-induced cardiovascular and renal injury. Increased levels of ROS can diminish the bioactivity of nitric oxide (NO), a critical modulator of RAAS effects on the kidney.

Direct renin inhibition improves systemic insulin resistance and skeletal muscle glucose transport in a transgenic rodent model of tissue renin overexpression.

Renin is the rate-limiting enzyme in renin-angiotensin system (RAS) activation. We sought to determine the impact of renin inhibition on whole-body insulin sensitivity and skeletal muscle RAS, oxidative stress, insulin signaling, and glucose transport in the transgenic TG(mRen2)27 rat (Ren2), which manifests increased tissue RAS activity, elevated serum aldosterone, hypertension, and insulin resistance. Young (aged 6-9 wk) Ren2 and age-matched Sprague Dawley control rats were treated with aliskiren [50 mg/kg .

Mineralocorticoid receptor antagonism attenuates vascular apoptosis and injury via rescuing protein kinase B activation.

Emerging evidence indicates that mineralocorticoid receptor (MR) blockade reduces the risk of cardiovascular events beyond those predicted by its blood pressure-lowering actions; however, the underlying mechanisms remain unclear. To investigate whether protection elicited by MR blockade is through attenuation of vascular apoptosis and injury, independently of blood pressure lowering, we administered a low dose of the MR antagonist spironolactone or vehicle for 21 days to hypertensive transgenic Ren2 rats with elevated plasma aldosterone levels. Although Ren2 rats developed higher systolic blood pressures compared with Sprague-Dawley littermates, low-dose spironolactone treatment did not reduce systolic blood pressure compared with untreated Ren2 rats.