The First Steps of the Visual Cycle in Human Rod and Cone Photoreceptors.

Purpose: Light detection destroys the visual pigment. Its regeneration, necessary for the recovery of light sensitivity, is accomplished through the visual cycle. Release of all-trans retinal by the light-activated visual pigment and its reduction to all-trans retinol comprise the first steps of the visual cycle.

Predicting Reasons for Drinking in a Dually-Diagnosed Sample with PTSD and Substance Use Disorders.

Using the negative reinforcement and common factors frameworks, this work assessed whether and how anxiety sensitivity, distress tolerance, and impulsivity relate to reasons for drinking (RFD) in a residential treatment sample with co-occurring alcohol use disorder and posttraumatic stress disorder (AUD-PTSD). Demographic differences were also examined. Participants were 75 (52.

Pre- to Posttreatment Changes in Trauma-Cued Negative Emotion Mediate Improvement in Posttraumatic Stress Disorder, Depression, and Impulsivity.

Posttraumatic stress disorder (PTSD) is characterized by strong negative emotions, often in response to trauma cues or reminders. Subsequent emotion regulation strategies impact the maintenance of PTSD symptoms and other trauma-related outcomes (depression, substance use). This study aimed to examine a range of trauma-cued emotions to enhance our understanding of changes following treatment and their potential role in improving relevant outcomes.

Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus.

Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self-tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane-inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed.

Have a heart: failure to increase GLP-1 caused by heart failure increases the risk of diabetes.

Incretins represent a group of gut-derived peptide hormones that, at physiological concentrations, potentiate the release of insulin. Work leading to the discovery of incretins began as early as the late 1800s where scientists, including Claude Bernard who is widely considered the father of modern physiology (Rehfeld, J.F.

GORE-TEX SCLERAL-SUTURED ENVISTA INTRAOCULAR LENS DISLOCATION: THREE CASES AND AN ASSESSMENT OF EYELET TENSILE STRENGTH, FRACTURE CHARACTERISTICS, AND RISK FACTORS.

Purpose: Three cases of dislocation of a Gore-Tex scleral-sutured EnVista intraocular lens are reported. The tensile strength of the lens eyelets under two suturing methods is assessed. Pursuant surgical considerations are discussed.

Blood pressure and albuminuria in a female mouse model of systemic lupus erythematosus: impact of long-term high salt consumption.

Hypertension and kidney involvement are common in patients with autoimmune disease. Sodium intake is linked to hypertension in both human and animal studies. Evidence suggests that dietary salt may be an important environmental factor that promotes autoimmune activity.

Temporal hemodynamic changes in a female mouse model of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease characterized by circulating autoantibodies, prevalent hypertension, renal injury, and cardiovascular disease. Onset of the disease often occurs in young women of childbearing age. Although kidney involvement is common to patients with SLE, little is known about temporal changes in renal hemodynamic function and its relationship to the pathogenesis of hypertension during autoimmune diseases.

The glucagon-like peptide 1 receptor agonist liraglutide attenuates placental ischemia-induced hypertension.

Preeclampsia is a hypertensive disorder of pregnancy characterized by systemic perturbations of nitric oxide function, reflective of generalized endothelial dysfunction. Therapies that target the nitric oxide pathway have shown promise in both clinical and preclinical studies of preeclampsia. The glucagon-like peptide 1 agonists have been shown to increase nitric oxide and lower blood pressure in patients with diabetes, in part, through activation of nitric oxide synthase (NOS).

Freedom isn't always free: immunoglobulin free light chains promote renal fibrosis.

Multiple myeloma (MM) is a relatively common hematologic malignancy, and up to half of patients with MM present with renal dysfunction at the time of diagnosis. MM-associated renal injury has been linked to an excess level of monoclonal immunoglobulin free light chains (FLCs) in the circulation; however, it is not clear how these FLCs drive renal pathology. In this issue of the JCI, Ying et al.

Cyclophosphamide treatment for hypertension and renal injury in an experimental model of systemic lupus erythematosus.

Cardiovascular disease is the major cause of mortality among patients with the autoimmune disorder systemic lupus erythematosus (SLE). Our laboratory previously reported that immunosuppression with mycophenolate mofetil, a common therapy in patients with SLE, attenuates the development of hypertension in an experimental model of SLE. Cyclophosphamide (CYC) is another common therapy for patients with SLE that has contributed to improved disease management; however, its impact on the development of hypertension associated with SLE is not clear.

Pathophysiology of Cerebral Vascular Dysfunction in Pregnancy-Induced Hypertension.

Purpose Of Review: To review and summarize what is known about cerebrovascular derangements during preeclampsia.

Recent Findings: Preeclampsia is a devastating disorder of pregnancy with no known cure. Little is known about the pathophysiological mechanisms which lead to the symptoms of the disorder, particularly with regard to individual vascular beds such as the cerebral circulation.

Menopause and FOXP3 Treg cell depletion eliminate female protection against T cell-mediated angiotensin II hypertension.

Although it is known that the prevalence and severity of hypertension increases in women after menopause, the contribution of T cells to this process has not been explored. Although the immune system is both necessary and required for the development of angiotensin II (ANG II) hypertension in men, we have demonstrated that premenopausal women are protected from T cell-mediated hypertension. The goal of the current study was to test the hypotheses that ) female protection against T cell-mediated ANG II hypertension is eliminated following progression into menopause and ) T regulatory cells (Tregs) provide premenopausal protection against ANG II-induced hypertension.

Expansion of regulatory T cells using low-dose interleukin-2 attenuates hypertension in an experimental model of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disorder that is characterized by prevalent hypertension, renal injury, and cardiovascular disease. Numerous studies have reported a low prevalence and/or impaired function of regulatory T (T) cells in both patients with SLE and murine models of the disease. Evidence suggests that T cell dysfunction in SLE results from a deficiency in IL-2.

Glycoproteomic Profiling Provides Candidate Myocardial Infarction Predictors of Later Progression to Heart Failure.

We hypothesized that identifying plasma glycoproteins that predict the development of heart failure following myocardial infarction (MI) could help to stratify subjects at risk. Plasma collected at visit 2 (2005-2008) from an MI subset of Jackson Heart Study participants underwent glycoproteomics and was grouped by the outcome: (1) heart failure hospitalization after visit 2 ( = 15) and (2) without hospitalization by 2012 ( = 45). Proteins were mapped for biological processes and functional pathways using Ingenuity Pathway Analysis and linked to clinical characteristics.

Towards better definition, quantification and treatment of fibrosis in heart failure. A scientific roadmap by the Committee of Translational Research of the Heart Failure Association (HFA) of the European Society of Cardiology.

Fibrosis is a pivotal player in heart failure development and progression. Measurements of (markers of) fibrosis in tissue and blood may help to diagnose and risk stratify patients with heart failure, and its treatment may be effective in preventing heart failure and its progression. A lack of pathophysiological insights and uniform definitions has hampered the research in fibrosis and heart failure.

Mechanisms of hypertension in autoimmune rheumatic diseases.

Patients with autoimmune rheumatic diseases including rheumatoid arthritis and systemic lupus erythematosus have an increased prevalence of hypertension. There is now a large body of evidence showing that the immune system is a key mediator in both human primary hypertension and experimental models. Many of the proposed immunological mechanisms leading to primary hypertension are paralleled in autoimmune rheumatic disorders.

Autoimmune Disease-Associated Hypertension.

Purpose Of Review: To highlight important new findings on the topic of autoimmune disease-associated hypertension.

Recent Findings: Autoimmune diseases including systemic lupus erythematosus and rheumatoid arthritis are associated with an increased risk for hypertension and cardiovascular disease. A complex interaction among genetic, environmental, hormonal, and metabolic factors contribute to autoimmune disease susceptibility while promoting chronic inflammation that can lead to alterations in blood pressure.

Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.

Cardiac fibroblasts are the major producers of extracellular matrix (ECM) to form infarct scar. We hypothesized that fibroblasts undergo a spectrum of phenotype states over the course of myocardial infarction (MI) from early onset to scar formation. Fibroblasts were isolated from the infarct region of C57BL/6J male mice (3-6 months old, n = 60) at days 0 (no MI control) and 1, 3, or 7 after MI.

Matrix metalloproteinase-12 as an endogenous resolution promoting factor following myocardial infarction.

Following myocardial infarction (MI), timely resolution of inflammation promotes wound healing and scar formation while limiting excessive tissue damage. Resolution promoting factors (RPFs) are agents that blunt leukocyte trafficking and inflammation, promote necrotic and apoptotic cell clearance, and stimulate scar formation. Previously identified RPFs include mediators derived from lipids (resolvins, lipoxins, protectins, and maresins), proteins (glucocorticoids, annexin A1, galectin 1, and melanocortins), or gases (CO, HS, and NO).

Extracellular matrix in cardiovascular pathophysiology.

The extracellular matrix (ECM) actively participates in diverse aspects of cardiovascular development and physiology as well as during disease development and progression. ECM roles are determined by its physical and mechanical properties and by its capacity to both release bioactive signals and activate cell signaling pathways. The ECM serves as a storage depot for a wide variety of molecules released in response to injury or with aging.

Congenital Zika Virus Infection in Immunocompetent Mice Causes Postnatal Growth Impediment and Neurobehavioral Deficits.

A small percentage of babies born to Zika virus (ZIKV)-infected mothers manifest severe defects at birth, including microcephaly. Among those who appeared healthy at birth, there are increasing reports of postnatal growth or developmental defects. However, the impact of congenital ZIKV infection in postnatal development is poorly understood.

Sex differences in the vascular function and related mechanisms: role of 17β-estradiol.

The incidence of cardiovascular disease (CVD) is lower in premenopausal women but increases with age and menopause compared with similarly aged men. Based on the prevalence of CVD in postmenopausal women, sex hormone-dependent mechanisms have been postulated to be the primary factors responsible for the protection from CVD in premenopausal women. Recent Women's Health Initiative studies, Cochrane Review studies, the Early Versus Late Intervention Trial with Estradiol Study, and the Kronos Early Estrogen Prevention Study have suggested that beneficial effects of hormone replacement therapy (HRT) are seen in women of <60 yr of age and if initiated within <10 yr of menopause.