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991.
992.
Paola Paci Federico Martini Massimo Bernaschi Gianpiero D'Offizi Filippo Castiglione 《BMC infectious diseases》2011,11(1):56
Background
When to initiate antiretroviral therapy in HIV infected patients is a diffcult clinical decision. Actually, it is still a matter of discussion whether early highly active antiretroviral therapy (HAART) during primary HIV infection may influence the dynamics of the viral rebound, in case of therapy interruption, and overall the main disease course. 相似文献993.
Galli M Cimolin V Rigoldi C Castori M Celletti C Albertini G Camerota F 《Research in developmental disabilities》2011,32(5):1663-1668
The aim of this study was to quantify the gait patterns of adults with joint hypermobility syndrome/Ehlers-Danlos syndrome (JHS/EDS-HT) hypermobility type, using Gait Analysis. We quantified the gait strategy in 12 JHS/EDS-HT adults individuals (age: 43.08 + 6.78 years) compared to 20 healthy controls (age: 37.23 ± 8.91 years), in terms of kinematics and kinetics. JHS/EDS-HT individuals were characterized by a non-physiological gait pattern. In particular, spatio-temporal parameters evidenced lower anterior step length and higher stance phase duration in JHS/EDS-HT than controls. In term of kinematics, in JHS/EDS-HT patients the main gait limitations involved pelvis, distal joints and ankle joint. Conversely, hip and knee joint showed physiological values. Ankle moment and power revealed reduced peak values during terminal stance. Differences in stiffness at hip and ankle joints were found between JHS/EDS-HT and controls. JHS/EDS-HT patients showed significant decreased of Kh and Ka parameters very probably due to congenital hypotonia and ligament laxity. These findings help to elucidate the complex biomechanical changes in JHS/EDS-HT and may have a major role in the multidimensional evaluation and tailored management of these patients. 相似文献
994.
Optogenetics has revolutionized the toolbox arsenal that neuroscientists now possess to investigate neuronal circuit function in intact and living animals. With a combination of light emitting 'sensors' and light activated 'actuators', we can monitor and control neuronal activity with minimal perturbation and unprecedented spatiotemporal resolution. Zebrafish neuronal circuits represent an ideal system to apply an optogenetic based analysis owing to its transparency, relatively small size and amenability to genetic manipulation. In this review, we describe some of the most recent advances in the development and applications of optogenetic sensors (i.e., genetically encoded calcium indicators and voltage sensors) and actuators (i.e., light activated ion channels and ion pumps). We focus mostly on the tools that have already been successfully applied in zebrafish and on those that show the greatest potential for the future. We also describe crucial technical aspects to implement optogenetics in zebrafish including strategies to drive a high level of transgene expression in defined neuronal populations, and recent optical advances that allow the precise spatiotemporal control of sample illumination. 相似文献
995.
Barbi F Ariatti A Funakoshi K Meacci M Odaka M Galassi G 《Journal of neurology》2011,258(8):1551-1552
Journal of Neurology - 相似文献
996.
Stromillo ML Malandrini A Dotti MT Battaglini M Borgogni F Tessa A Storti E Denora PS Santorelli FM Gaudiano C Battisti C Federico A De Stefano N 《Journal of neurology》2011,258(12):2240-2247
The goal of this work was to assess brain structural and metabolic abnormalities of subjects with SPG11 and their relevance to clinical disability by using quantitative magnetic resonance (MR) metrics. Autosomal recessive hereditary spastic paraplegia (AR-HSP) with thin corpus callosum and cognitive decline is a complex neurological disorder caused by mutations in the SPG11 gene in most cases. Little is known about the process leading to corticospinal and white matter degeneration. We performed conventional MRI/MR spectroscopic imaging ((1)H-MRSI) examinations in 10 HSP patients carrying an SPG11 mutation and in 10 demographically matched healthy controls (HC). We measured in each subject cerebral white matter hyperintensities (WMHs), normalized global and cortical brain volumes, and (1)H-MRSI-derived central brain levels of N-acetylaspartate (NAA) and choline (Cho) normalized to creatine (Cr). Clinical disability was assessed according to patients' autonomy in walking. Conventional MRI showed WMHs in all patients. Global brain volumes were lower in patients than in HC (p < 0.001). Decreased values were diffusely found also in cortical regions (p < 0.01). On (1)H-MRSI, NAA/Cr values were lower in SPG11 patients than in HC (p = 0.002). Cho/Cr values did not differ between patients and HC. Cerebral volume decreases and NAA/Cr in the corona radiata correlated closely with increasing disability scores (p < 0.05). Quantitative MR measures propose that widespread structural and metabolic brain damage occur in SPG11 patients. The correlation of these MR metrics with measures of patients' disease severity suggests that they might represent adequate surrogate markers of disease outcome. 相似文献
997.
Judica E Martinelli Boneschi F Ungaro D Comola M Gatti R Comi G Rossi P 《Journal of neurology》2011,258(5):835-839
Fatigue is considered to be one of the most common and disabling symptoms among individuals with multiple sclerosis (MS).
The aim of this study is to investigate if an intensive, short-term inpatient rehabilitation program is able to improve fatigue
in MS, and if fatigue is able to negatively influence the clinical and functional outcome of rehabilitation in MS. One-hundred
eighty six consecutively recruited MS patients underwent an intensive, short-term inpatient rehabilitation program. Sixty-four
of them were selected for this study according to our inclusion criteria and compared to a control group of 22 MS patients
who did not follow a rehabilitation program. We measured fatigue symptoms with the Fatigue Severity Scale (FSS) before and
after rehabilitation, and classified patients into fatigued (FMS) in the case of an FSS score ≥36 and into non-fatigued MS
(NFMS) in the case of an FSS <36. Expanded Disability Status Scale (EDSS) and Functional Independence Measure (FIM) were used
as clinical outcome measures of the efficacy of the rehabilitation program. In our sample, an intensive, short-term rehabilitation
treatment is able to determine a significant reduction of fatigue symptoms compared to untreated MS patients (p < 0.0001); however, the presence of fatigue at the beginning of the rehab program seems not to have any impact on the clinical
and functional outcome of rehabilitation. An intensive inpatient rehabilitation trial decreases symptom of fatigue in MS patients;
furthermore fatigue seems not to modify the amelioration of disability and impairment determined by a rehabilitation program. 相似文献
998.
Caraci F Pistarà V Corsaro A Tomasello F Giuffrida ML Sortino MA Nicoletti F Copani A 《Journal of neuroscience research》2011,89(4):592-600
Anabolic-androgenic steroid (AAS) abuse is associated with multiple neurobehavioral disturbances. The sites of action and the neurobiological sequels of AAS abuse are unclear at present. We investigated whether two different AASs, nandrolone and methandrostenolone, could affect neuronal survival in culture. The endogenous androgenic steroid testosterone was used for comparison. Both testosterone and nandrolone were neurotoxic at micromolar concentrations, and their effects were prevented by blockade of androgen receptors (ARs) with flutamide. Neuronal toxicity developed only over a 48-hr exposure to the steroids. The cell-impermeable analogues testosterone-BSA and nandrolone-BSA, which preferentially target membrane-associated ARs, were also neurotoxic in a time-dependent and flutamide-sensitive manner. Testosterone-BSA and nandrolone-BSA were more potent than their parent compounds, suggesting that membrane-associated ARs were the relevant sites for the neurotoxic actions of the steroids. Unlike testosterone and nandrolone, toxicity by methandrostenolone and methandrostenolone-BSA was insensitive to flutamide, but it was prevented by the glucocorticoid receptor (GR) antagonist RU-486. Methandrostenolone-BSA was more potent than the parent compound, suggesting that its toxicity relied on the preferential activation of putative membrane-associated GRs. Consistently with the evidence that membrane-associated GRs can mediate rapid effects, a brief challenge with methandrostenolone-BSA was able to promote neuronal toxicity. Activation of putative membrane steroid receptors by nontoxic (nanomolar) concentrations of either nandrolone-BSA or methandrostenolone-BSA became sufficient to increase neuronal susceptibility to the apoptotic stimulus provided by β-amyloid (the main culprit of AD). We speculate that AAS abuse might facilitate the onset or progression of neurodegenerative diseases not usually linked to drug abuse. 相似文献
999.
1000.
Ferreira M Evangelista T Almeida LS Martins J Macario MC Martins E Moleirinho A Azevedo L Vilarinho L Santorelli FM 《Neuromuscular disorders : NMD》2011,21(7):483-488
Diseases affecting mtDNA stability, termed nuclear-mitochondrial intergenomic communication disorders, are caused by a primary nuclear gene defect resulting in multiple mtDNA deletions.The aim of this study was to estimate the frequency of known etiologies and the spectrum of mutations in a cohort of 21 patients harboring multiple mtDNA deletions in skeletal muscle.We showed that 10 cases (48%) display mutations in POLG, including eight previously reported variants and two novel mutations (namely, p.Trp585X and p.Arg1081Gln). The novel mutations affect evolutionary conserved residues and were absent in a large set of control chromosomes. These findings expand the array of mutations associated with multiple rearranged mtDNA attributed to mutations in POLG. The relatively high diagnostic yield (about one in two cases) supports the notion that it is recommended to test POLG routinely in diagnostic laboratories whenever multiple mtDNA deletions are present, regardless of the age of onset of patients and their clinical phenotype. 相似文献