Balance factors affecting the quality of life in patients with knee osteoarthritis.

Background: Knee osteoarthritis (OA) affects the quality of life (QOL) and balance control of elderly people; our study explored the balance factors that affected the QOL in patients with knee OA. Objectives: To determine the balance factors that affected the QOL of patients with knee OA who attended general clinics. Method: A total of 30 healthy controls and 60 patients with mild-to-moderate bilateral knee OA, all aged 55-75 years, were enrolled in our cross-sectional study. All participants were interviewed; the Medical Outcomes Study 36-Item Short-Form Health Survey was used to assess their QOL in eight dimensions, and the Balance Master System was used to evaluate their balance control according to six parameters. Descriptive statistics were used to reduce the data; an independent t-test determined differences between the two groups, and a multiple regression analysis was undertaken to establish associations between variables from the balance control test and SH36 physical and mental health components. The level of statistical significance was set at 5%. Results: In the OA group, significant negative correlations were observed between sway velocity and the physical health component (p = 0.003) and between sway velocity and the mental health component (p = 0.006). Thus, sway velocity had a major impact on the QOL of patients with knee OA. Conclusions: The sway velocity at the centre of gravity in balance control was a crucial factor for determining the QOL of patients with bilateral knee OA. Clinical implications: Sway velocity is a key factor affecting the QOL and may provide a basis to formulate preventive actions and design treatment goals for patients with knee OA.

Monthly Disposable Income Is a Crucial Factor Affecting the Quality of Life in Patients with Knee Osteoarthritis.

Knee osteoarthritis (OA) affects the quality of life (QOL) of elderly people; this study examines the demographic characteristics and QOL of patients with knee OA and identifies demographic characteristics that affect the QOL of these patients. In this cross-sectional study, 30 healthy controls and 60 patients with mild-to-moderate bilateral knee OA aged between 55 and 75 years were enrolled. All participants completed a questionnaire containing questions on 10 demographic characteristics and the Medical Outcome Study 36-Item Short-Form Health Survey (SF-36), and their QOL scores in the eight dimensions of the SF-36 were evaluated. In the OA group, significant correlations were observed between monthly disposable income and physical and mental health components. Monthly disposable income was found to considerably affect the QOL of patients with bilateral knee OA (i.e., it is a crucial factor affecting these patients). The findings of this study may provide a reference for formulating preventive strategies for healthy individuals and for future confirmatory research.

Urothelial Calcium-Sensing Receptor Modulates Micturition Function via Mediating Detrusor Activity and Ameliorates Bladder Hyperactivity in Rats.

The urothelium displays mechano- and chemosensory functions via numerous receptors and channels. The calcium-sensing receptor (CaSR) detects extracellular calcium and modulates several physiological functions. Nonetheless, information about the expression and the role of CaSR in lower urinary tract has been absent. We aimed to determine the existence of urothelial CaSR in urinary bladder and its effect on micturition function. We utilized Western blot to confirm the expression of CaSR in bladder and used immunofluorescence to verify the location of the CaSR in the bladder urothelium via colocalization with uroplakin III A. The activation of urothelial CaSR via the CaSR agonist, AC-265347 (AC), decreased urinary bladder smooth muscle (detrusor) activity, whereas its inhibition via the CaSR antagonist, NPS-2143 hydrochloride (NPS), increased detrusor activity in in vitro myography experiments. Cystometry, bladder nerve activities recording, and bladder surface microcirculation detection were conducted to evaluate the effects of the urothelial CaSR via intravesical administrations. Intravesical AC inhibited micturition reflex, bladder afferent and efferent nerve activities, and reversed cystitis-induced bladder hyperactivity. The urothelial CaSR demonstrated a chemosensory function, and modulated micturition reflex via regulating detrusor activity. This study provided further evidence of how the urothelial CaSR mediated micturition and implicated the urothelial CaSR as a potential pharmacotherapeutic target in the intervention of bladder disorders.

Aromatherapy: Activating olfactory calcium-sensing receptors impairs renal hemodynamics via sympathetic nerve-mediated vasoconstriction.

AIM: This study determines whether the activation of olfactory calcium-sensing receptor initiates a sympathetic activation-dependent neurovascular reflex subsequently contributing to renal hemodynamic depression. METHODS: Immunohistochemistry and nose-loading calcium-sensitive dye were used to explore the location and function of calcium-sensing receptor on the olfactory sensory neuron. The renal sympathetic nervous activity, renal hemodynamics and the microcirculation of kidney, liver and intestine were evaluated after liquid-phase intranasal administrations of saline, lidocaine, calcium-sensing receptor agonists and antagonist in sham and bilateral renal denervated rats. Real-time renal glomerular filtration rate was measured by a magnetic resonance renography. RESULTS: Calcium-sensing receptors were expressed on the cilia the olfactory sensory neuron and their activation depolarized olfactory sensory neuron and induced the calcium influx in the terminal side on olfactory glomeruli. Activating olfactory calcium-sensing receptors significantly increased arterial blood pressure and renal sympathetic nervous activities and subsequently decreased renal blood flow, renal, hepatic and enteral microcirculation. Cotreatments with calcium-sensing receptor antagonist or lidocaine inhibited these physiological alterations. The renal hemodynamic depressions by olfactory calcium-sensing receptor activation were significantly blocked by bilateral renal denervation. The intranasal manganese administration decreased the glomerular filtration rate. CONCLUSION: Calcium-sensing receptor acts as a functional chemosensory receptor on olfactory sensory neuron, and its activation causes the global sympathetic enhancement contributing to systematic vasoconstriction and subsequently depresses renal blood flow and glomerular filtration rate. These data implicate a possibly clinical aspect that several environmental stimuli may activate olfactory calcium-sensing receptors to evoke a sympathetic nervous system-mediated neurovascular reflex to depress renal hemodynamics.

Glucagon-like peptide-1 receptor agonist activation ameliorates venous thrombosis-induced arteriovenous fistula failure in chronic kidney disease.

High shear stress that develops in the arteriovenous fistula of chronic kidney diseases (CKD) may increase H2O2 and thromboxane A2 (TXA2) release, thereby exacerbating endothelial dysfunction, thrombosis, and neointimal hyperplasia. We investigated whether glucagon-like peptide-1 receptor agonist/exendin-4, a potentially cardiovascular protective agent, could improve TXA2-induced arteriovenous fistula injury in CKD. TXA2 administration to H2O2-exposed human umbilical vein endothelial cells increased apoptosis, senescence, and detachment; these phenotypes were associated with the downregulation of phosphorylated endothelial nitric oxide synthase/heme oxygenase-1 (eNOS/HO-1) signalling. Exendin-4 reduced H2O2/TXA2-induced endothelial injury via inhibition of apoptosis-related mechanisms and restoration of phosphorylated eNOS/HO-1 signalling. Male Wistar rats subjected to right common carotid artery-external jugular vein anastomosis were treated with exendin-4 via cervical implant osmotic pumps for 16-42 days. High shear stress induced by the arteriovenous fistula significantly increased venous haemodynamics, blood and tissue H2O2 and TXB2 levels, macrophage/monocyte infiltration, fibrosis, proliferation, and adhesion molecule-1 expression. Apoptosis was also increased due to NADPH oxidase gp91 activation and mitochondrial Bax translocation in the proximal end of the jugular vein of CKD rats. Exendin-4-treatment of rats with CKD led to the restoration of normal endothelial morphology and correction of arteriovenous fistula function. Exendin-4 treatment or thromboxane synthase gene deletion in CKD mice markedly reduced ADP-stimulated platelet adhesion to venous endothelium, and prevented venous occlusion in FeCl3-injured vessels by upregulation of HO-1. Together, these data reveal that the use of glucagon-like peptide-1 receptor agonists is an effective strategy for treatment of CKD-induced arteriovenous fistula failure.