Longitudinal quantitative electroencephalographic study in mono-hemispheric stroke patients

The identification of individual factors modulating clinical recovery after a stroke is fundamental to personalize the therapeutic intervention to enhance the final clinical outcome.In this framework,electrophysiological factors are promising since are more directly related to neuroplasticity,which supports recovery in stroke patients,than neurovascular factors.In this retrospective observational study,we investigated brain neuronal activity assessed via spectral features and Higuchi's fractal dimension(HFD) of electroencephalographic signals in acute phase(2–10 days from symptom onset,T0) and sub-acute phase(2.5 months,T1) in 24 patients affected by unilateral middle cerebral artery stroke.Longitudinal assessment of the clinical deficits was performed using the National Institutes of Health Stroke Scale(NIHSS),together with the effective recovery calculated as the ratio between difference of NIHSS at T0 and T1 over the NIHSS value at T0.We observed that delta and alpha band electroencephalographic signal power changed between the two phases in both the hemispheres ipsilateral(ILH) and contralateral(CHL) to the lesion.Moreover,at T0,bilateral higher delta band power correlated with worse clinical conditions(Spearman's rs = 0.460,P = 0.027 for ILH and rs = 0.508,P = 0.013 for CLH),whereas at T1 this occurred only for delta power in ILH(rs = 0.411,P = 0.046) and not for CHL.Inter-hemispheric difference(ILH vs.CLH) of alpha power in patients was lower at T0 than at T1(P = 0.020).HFD at T0 was lower than at T1(P = 0.005),and at both phases,ILH HFD was lower than CLH HFD(P = 0.020).These data suggest that inter-hemispheric low band asymmetry and fractal dimension changes from the acute to the sub-acute phase are sensitive to neuroplasticity processes which subtend clinical recovery.The study protocol was approved by the Bioethical Committee of Ospedale San Giovanni Calibita Fatebenefretelli(No.40/2011) on July 14,2011.

INFLUENCE OF NALOXONE ON ANALGESIC EFFECT OF HYPOTHALAMIC ARCUATE NUCLEUS STIMULATION

It has been shown in our previous experiments that arcuate nucleus (ARC) stimulation had a marked analgesic effect. After selective lesion of ARC neurons by neonatally intrapcritoneal injection of monosodium glutamate (MSG), the analgesic effects of morphine, acupuncture and stress decreased significantly.

THE ROLE OF LOCUS COERULEUS-NORADRENERGIC AND DORSAL RAPHE NUCLEUS-SEROTONERGIC SYSTEMS IN ANALGESIC EFFECT OF HYPOTHA-LAMIC ARCUATE NUCLEUS STIMULATION

Previous studies ia our laboratory have shown that hypothalamic arcuate nucleus (ARC),locus coeruleus (LG) and dorsal raphe nucleus (DR) play an important role in pain modulation and acupuncture analgesia, There is sufficient evidence that LG and DR are main sites concentrated with noradrenergic (NE) and serotonergic (5-HT) neuronal peri-

Changes in microRNAs expression are involved in age-related atrial structural remodeling and atrial fibrillation

Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation （AF） was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. Methods Three groups of dogs were studied： adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AE

Short-term intensive atorvastatin therapy improves endothelial function partly via attenuating perivascular adipose tissue inflammation through 5-lipoxygenase pathway in hyperlipidemic rabbits

Background Atherosclerosis is a kind of disease with multiple risk factors,of which hyperlipidemia is a major classical risk factor resulting in its pathogenesis and development.The aim of this study was to determine the effects of short-term intensive atorvastatin （IA） therapy on vascular endothelial function and explore the possible mechanisms that may help to explain the clinical benefits from short-term intensive statin therapy.Methods After exposure to high-fat diet （HFD） for 8 weeks,the animals were,respectively,treated with IA or low-dose atorvastatin （LA） for 5 days.Blood lipids,C-reactive protein （CRP）,tumor necrosis factor-α （TNF-α）,interleukin-6 （IL-6）,nitric oxide （NO）,endothelin-1 （ET-1）,and endothelium-dependent vasorelaxation function were,respectively,measured.mRNA and protein expression of CRP,TNF-α,IL-6,macrophage chemoattractant protein-1 （MCP-1）,and 5-lipoxygenase （5-LO） were also evaluated in pericarotid adipose tissue （PCAT） and cultured adipocytes.Results HFD increased serum inflammatory factor levels; induced significant hyperlipidemia and endothelial dysfunction,including imbalance between NO and ET-1; enhanced inflammatory factors and 5-LO expression; and promoted macrophage infiltration into adipose tissue.Five-day IA therapy could significantly decrease serum inflammatory factor levels and their expression in PCAT; restore the balance between NO and ET-1; and improve endothelial function and macrophage infiltration without significant changes in blood lipids.However,all of the above were not observed in LA therapy.In vitro experiment found that lipopolysaccharide （LPS） enhanced the expression of inflammatory factors and 5-LO in cultured adipocytes,which could be attenuated by short-time （6 hours） treatment of high-dose （5 pmol/L） but not low-dose （0.5 μmol/L） atorvastatin.In addition,inhibiting 5-LO by Cinnamyl-3,4-dihydroxy-α-cyanocinnamate （CDC,a potent and direct 5-LO inhibitor） could significantly downregulate the above-mentioned gene expression in LPS-treated adipocytes.Conclusion Short-term IA therapy could significantly ameliorate endothelial dysfunction induced by HFD,which may be partly due to attenuating inflammation of PCAT through inhibiting 5-LO pathway.