A System for the Measurement of the Subjective Visual Vertical using a Virtual Reality Device.

The Subjective Visual Vertical (SVV) is a common test for evaluating the perception of verticality. Altered verticality has been connected with disorders in the otolithic, visual or proprioceptive systems, caused by stroke, Parkinson's disease or multiple sclerosis, among others. Currently, this test is carried out using a variety of specific, mostly homemade apparatuses that include moving planes, buckets, hemispheric domes or a line projected in a screen. Our aim is to develop a flexible, inexpensive, user-friendly and easily extensible system based on virtual reality for the measurement of the SVV and several related visual diagnostic tests, and validate it through an experimental evaluation. Two different hardware configurations were tested with 50 healthy volunteers in a controlled environment; 28 of them were males and 22 females, with ages ranging from 18 to 49 years, being 23 the average age. The Intraclass Correlation Coefficient (ICC) was computed in each device. In addition, a usability survey was conducted. ICC = 0.85 in the first configuration (CI = 0.75-0.92), ICC = 0.76 in the second configuration (CI = 0.61-0.87), both with 95% of confidence, which means a substantial reliability. Moreover, 92.2% of subjects rated the usability of the system as "very good". Our evaluation showed that the proposed system is suitable for the measurement of SVV in healthy subjects. The next step is to perform a more elaborated experimentation on patients and compare the results with the measurements obtained from traditional methods.

Effect of the long-term treatment with trandolapril on endoglin expression in rats with experimental renal fibrosis induced by renal mass reduction.

BACKGROUND: Endoglin is a membrane glycoprotein that regulates TGF-beta1 signaling. Previous studies have revealed that endoglin is upregulated in several models of experimental fibrosis, and that endoglin expression can counteract the fibrogenic effects of TGF-beta1. As treatment with angiotensin converting enzyme (ACE) inhibitors reduces renal fibrosis by mechanisms that are, in part, not dependent on angiotensin II blockade, we have assessed the hypothesis that this effect could be mediated by endoglin upregulation. METHODS: We have used the 5/6-nephrectomy renal mass reduction (RMR) model of renal fibrosis in rats treated (RMR+T) or not treated with the ACE inhibitor trandolapril (0.7 mg/kg/day). One, 3 and 5 months after RMR, mean arterial pressure and renal function were measured. In addition, renal fibrosis was evaluated quantitatively and endoglin, TGF-beta1, collagen type I and collagen type IV expression was assessed by Northern blot and immunohistochemistry. RESULTS: RMR induced a progressive increase in mean arterial pressure, urinary protein excretion and glomerular and tubulointerstitial fibrosis, which is accompanied by an increased expression of TGF-beta1, endoglin and collagen types I and IV. Trandolapril treatment reduced systemic blood pressure and lessened proteinuria after RMR, as well as expression of TGF-beta1, endoglin and collagens. CONCLUSION: The present study demonstrates an increased TGF-beta1, endoglin, collagen type I and collagen type IV expression in rats with severe hypertension and renal damage. The effect of trandolapril to decrease renal fibrosis seems to be based in a reduced TGF-beta1 expression but not in an increased expression of endoglin.