HIV-associated sensory peripheral neuropathy (HIV-SN) afflicts approximately 50% of patients on antiretroviral therapy, and is associated with significant neuropathic pain. Simple accurate diagnostic instruments are required for clinical research and daily practice in both high- and low-resource setting. A 4-item clinical tool (CHANT: Clinical HIV-associated Neuropathy Tool) assessing symptoms (pain and numbness) and signs (ankle reflexes and vibration sense) was developed by selecting and combining the most accurate measurands from a deep phenotyping study of HIV positive people (Pain In Neuropathy Study-HIV-PINS).
View Article and Find Full Text PDFThe Babinski reflex is a clinical diagnostic tool; however, the interrater reliability of this tool is currently greatly contested. A comparison between rater groups with objective measurements of the Babinski reflex was therefore conducted. Fifteen recorded Babinski reflexes were assessed by 12 neurologists and 12 medical students as being either pathological or nonpathological.
View Article and Find Full Text PDFIntroduction: Measurement precision and accuracy of spinal reflexes plays an essential role in the clinical neurological examination. Reflexes are conventionally assessed either electromyographically or with rating scales. In this study we compared objective kinematic T-reflex and subjective assessments of patellar reflexes in 15 normal healthy subjects.
View Article and Find Full Text PDFBackground: Although aldosterone influences the effect of salt intake on blood pressure (BP), the extent to which this occurs at a population level is uncertain. We therefore aimed to determine, at a community level in a group of African descent, whether in the absence of primary aldosteronism, the relationship between salt intake and BP is modified by circulating aldosterone, and the extent to which this occurs.
Methods: In 575 participants of African ancestry (age >16 years), we assessed whether aldosterone-to-renin ratio (ARR) is associated with the relationship between urinary sodium (Na(+))-to-potassium (K(+)) ratio (urinary Na(+)/K(+)) (from 24-h urine samples), an index of salt intake, and BP.
Although in hypertension beta-adrenoreceptor activation promotes the transition from cardiac hypertrophy to pump dysfunction, the use of beta-blockers is controversial. As adrenergic activation may mediate adverse effects on the heart through the renin-angiotensin-aldosterone system, we evaluated the effects of the aldosterone receptor blocker, spironolactone (SPIRO), on isoproterenol (ISO)-induced changes in left ventricular cavity size and pump function and the determinants thereof in spontaneously hypertensive rats (SHR). ISO administered for 4.
View Article and Find Full Text PDFTo investigate possible mechanisms of the hyperalgesia induced by the nucleoside reverse transcriptase inhibitor (NRTI) stavudine in rats, we examined neuronal death and inflammatory cytokine secretion in the spinal cord, and cytokine and lactate secretion in the plasma. Stavudine (50 mg kg(-1)) or placebo was administered orally to Sprague-Dawley rats once daily for three or six weeks. In one group, rats' responses to a blunt noxious mechanical stimulus applied to their tails were recorded before and at the end of the period of stavudine or placebo administration.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2008
We explored whether the hypertensive heart is susceptible to myocardial dysfunction in viable noninfarcted tissue post-myocardial infarction (MI), the potential mechanisms thereof, and the impact of these changes on pump function. Six to seven months after the ligation of the left anterior descending coronary artery, left ventricular (LV) myocardial systolic function, as assessed from the percent shortening of the noninfarcted lateral wall segmental length determined over a range of filling pressures (ultrasonic transducers placed in the lateral wall in anaesthetized, open-chest, ventilated rats) and the percent thickening of the posterior wall (echocardiography), was reduced in infarcted spontaneous hypertensive rats (SHR-MI) (P < 0.05) but not in normotensive Wistar-Kyoto (WKY-MI) animals compared with corresponding controls [SHR-sham operations (Sham) and WKY-Sham].
View Article and Find Full Text PDFThe cellular signaling pathways responsible for the transition from compensated left ventricular hypertrophy (LVH) to LV dilatation (remodeling) and heart failure are unclear. As chronic administration of a beta-adrenoreceptor (beta-AR) agonist mediates the premature onset of cardiac remodeling without myocyte necrosis or myocardial dysfunction in LVH, we suggest that beta-AR activation is critical in promoting the transition from compensated LVH to cardiac dilatation. However, beta-AR mediated effects in the heart can occur via either the cyclic adenosine monophosphate (cAMP) system or via cAMP independent signaling pathways.
View Article and Find Full Text PDFThe transition from compensated to decompensated left ventricular hypertrophy (LVH) in hypertension involves excessive beta-adrenoreceptor (beta-AR) stimulation. To explore whether aldosterone receptor activation contributes toward beta-AR-induced left ventricular (LV) decompensation in hypertensive LVH, the effect of spironolactone (SPIRO; 80 mg x kg(-1) x day(-1)) on LV cavity dimensions, function, and chamber remodeling mechanisms was evaluated in spontaneously hypertensive rats (SHR) receiving a low dose of the beta-AR agonist isoproterenol (ISO) at 0.02 to 0.
View Article and Find Full Text PDFThe segmental method for estimating the centre of mass (COM) location of the human body has been widely used since 1889. How closely this method agrees with direct measurements of the location and movement of COM during activity however, remains unclear. To test this, a novel reaction-board utilizing life sized projections of human subjects is designed for measuring COM location.
View Article and Find Full Text PDFChronic beta-adrenoreceptor (beta-AR) activation increases left ventricular (LV) cavity size by promoting a rightward shift in LV diastolic pressure-volume (P-V) relations in association with increases in low-tensile strength myocardial (non-cross-linked) collagen concentrations. Because diastolic P-V relations are determined by chamber remodeling as well as by myocardial material properties (indexed by myocardial stiffness), both of which are associated with modifications in myocardial collagen cross-linking, we evaluated whether chamber remodeling or alterations in myocardial material properties govern beta-AR-mediated modifications in diastolic P-V relations. The effects of chronic administration of isoproterenol (Iso; 0.
View Article and Find Full Text PDFIt is uncertain whether chronic beta-adrenoreceptor (beta-AR)-activation in hypertension could initiate the progression from compensated left ventricular (LV) hypertrophy to pump dysfunction. It is also uncertain if this effect is through adverse LV remodeling (chamber dilatation with wall thinning and pump dysfunction) or intrinsic myocardial contractile dysfunction. We evaluated the effect of 5 months of isoprenaline (0.
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