Pinch grip strength as an alternative assessment to hand grip strength for assessing muscle strength in patients with chronic kidney disease treated by haemodialysis: a prospective audit.

BACKGROUND: Muscle weakness and wasting are prevalent in haemodialysis (HD) patients, and substantially increase mortality. Convenient, readily applicable screening tests for routine clinical practice are required. Hand grip strength (HGS) has been validated in HD patients but cannot be readily measured during a HD session. On the other hand, pinch strength (PS) can be measured during a HD session, and we aimed to compare the two methods of assessing muscle strength. METHODS: We measured pinch strength (PS) and hand grip strength (HGS) in 209 adult HD patients. The mean of three measurements was taken. RESULTS: The mean (SD) HGS was 15.3 (7.1) kg, compared to a PS of 2.9 (1.5) kg (P < 0.0001). HGS was weaker in the arteriovenous fistula (AVF) arm than the non-AVF arm [14.01 (6.9) versus 16.4 (7.1) kg (P < 0.001)], as was PS [AVF arm 2.63 (1.30) versus 3.08 (1.65) kg (P < 0.001)]. We found a strong correlation between HGS and PS (r = 0.82, P < 0.001. Comparing HGS and PS, we found a mean difference of 12.08 kg (Bland-Altman analysis), although the absolute difference was smaller with lower HGS. CONCLUSIONS: We found PS to be highly correlated with HGS, and was more convenient for patients because PS could be readily performed during the HD session. PS may provide an easier screening tool for muscle strength than HGS for dialysis patients, although further validation studies are required.

Acute nicotine treatment prevents REM sleep deprivation-induced learning and memory impairment in rat.

Rapid eye movement (REM) sleep deprivation (SD) is implicated in impairment of spatial learning and memory and hippocampal long-term potentiation (LTP). An increase in nicotine consumption among habitual smokers and initiation of tobacco use by nonsmokers was observed during SD. Although nicotine treatment was reported to attenuate the impairment of learning and memory and LTP associated with several mental disorders, the effect of nicotine on SD-induced learning and memory impairment has not been studied. Modified multiple platform paradigm was used to induce SD for 24 or 48 h during which rats were injected with saline or nicotine (1 mg kg(-1) s.c.) twice a day. In the radial arm water maze (RAWM) task, 24- or 48-h SD significantly impaired learning and short-term memory. In addition, extracellular recordings from CA1 and dentate gyrus (DG) regions of the hippocampus in urethane anesthetized rats showed a significant impairment of LTP after 24- and 48-h SD. Treatment of normal rats with nicotine for 24 or 48 h did not enhance spatial learning and memory or affect magnitude of LTP in the CA1 and DG regions. However, concurrent, acute treatment of rats with nicotine significantly attenuated SD-induced impairment of learning and STM and prevented SD-induced impairment of LTP in the CA1 and DG regions. These results show that acute nicotine treatment prevented the deleterious effect of sleep loss on cognitive abilities and synaptic plasticity.

Chronic caffeine treatment prevents stress-induced LTP impairment: the critical role of phosphorylated CaMKII and BDNF.

Caffeine has been reported to enhance cognition in animal and humans. Additionally, caffeine alleviates cognitive impairment associated with a number of disorders including Alzheimer's disease. The lipophilic nature of caffeine allows for rapid absorption into the bloodstream where it freely crosses the blood-brain barrier. Caffeine promotes dendritic spine growth in cultured hippocampal neurons, which suggests a neuroprotective effect. We examined the effect of chronic caffeine treatment on stress-induced suppression of long-term potentiation (LTP) and impairment of molecules of its signaling cascade. Rats were subjected to daily stress using the psychosocial stress paradigm (intruder model), in vivo recordings from area CA1 of the hippocampus of adult rat, and immunoblot analysis of essential signaling molecules. Caffeine prevented stress-induced LTP impairment. Western blot analysis showed reduction of the basal levels of the phosphorylated calcium calmodulin kinase II (P-CAMKII), total CaMKII, and brain-derived neurotrophic factor (BDNF) in area CA1 of stressed rats. These reductions were prevented by chronic caffeine treatment (0.33 mg/L in drinking water). In addition, caffeine prevented the upregulation of calcineurin levels in stressed rats. High-frequency stimulation (HFS) normally increased P-CaMKII, total CaMKII, and calcineurin levels in control as well as in caffeine-treated stressed rats. However, in stressed rats, the same HFS induced increases in the levels of total CaMKII and calcineurin, but not those of P-CaMKII. The levels of signaling molecules may not reflect activities of these molecules. It appears that the neuroprotective effect of caffeine involves preservation of the levels of essential kinases and phosphatases in stressed rats. This may include preservation of basal levels of BDNF by chronic caffeine treatment in stressed animals. These findings highlight the critical role of P-CaMKII and BDNF in caffeine-induced prevention of stress-induced LTP impairment.