Prepulse intervals ranged from 10 to 120 ms. Further
tests evaluated the effects of PAP on spontaneous locomotion, AMPH (1 mg/kg)-induced hyperlocomotion, and core body temperature (TA degrees).
HAL reversed APO-induced PPI deficits but PAP failed to reverse APO- and AMPH-induced PPI deficits at all doses, strains, pretreatment times, and prepulse intervals. PAP (30 mg/kg) significantly reduced AMPH hyperlocomotion in SD rats, and a similar pattern was detected in WI rats. This PAP dose also strongly reduced spontaneous locomotion and TA degrees in SD rats.
Our study does not support an antipsychotic-like profile of PAP in dopaminergic PPI models.”
“Background/Aims: Cardiac valve calcification (CVC) and left ventricular (LV) abnormalities are common indicators of a poor prognosis in dialysis patients. We determined the prevalence learn more of hypertension, CVC, LV hypertrophy (LVH) and LV geometry in peritoneal dialysis (PD) patients. Methods: Eighty-seven patients (50 female; mean Pritelivir order age 42 +/- 13 years; mean dialysis duration 46 +/- 24 months) on strict salt and volume restriction, none of whom were receiving antihypertensives, were included in the study.
Blood pressure (BP), biochemical parameters, CVC, LVH and LV geometry were determined. Results: Most patients were normotensive. CVC of the mitral and aortic valves and of both valves were noted in 22, 23 and 15% of patients, respectively. Patients with CVC had significantly higher diastolic BP (p = 0.023), cardiothoracic index (CTI; p = 0.037) and LV mass index (LVMI; p = 0.002). LVH, noted overall in 44% of cases, was present (-)-p-Bromotetramisole Oxalate in 62 and 36% of the patients with and without CVC, respectively (p = 0.028). Of the whole group, only 50.6% had normal LV geometry. LVH was associated with lower serum albumin (p = 0.002), higher CTI (p = 0.027) and more frequent CVC (p = 0.028). LVMI was greater in patients with CVC (p = 0.002). Conclusion: Strict salt restriction and the achievement of ideal dry weight result in normotension
in PD patients. CVC is associated with LVH, both of which are lower in normotensive patients. Copyright (C) 2012 S. Karger AG, Basel”
“It has become evident that many human disorders are characterised by mitochondrial dysfunction either at a primary level, due to mutations in genes whose encoded products are involved in oxidative phosphorylation, or at a secondary level, due to the accumulation of mitochondrial DNA (mtDNA) mutations. This has prompted keen interest in the development of cell and animal models and in exploring innovative therapeutic strategies to modulate the mitochondrial deficiencies observed in these diseases. Key advances in these areas are outlined in this review, with a focus on Leber hereditary optic neuropathy (LHON). This exciting field is set to grow exponentially and yield many candidate therapies to treat this class of disease.