Effects of upper limbs' neuromuscular electrical stimulation (NMES) superimposed to voluntary contraction added to a protocol of intradialytic leg cycle ergometer exercise, in muscle strength, functional capacity and quality of life of adult patients with CKD: a randomized clinical trial protocol.

Objective: To investigate the effects of unilateral upper limbs' (ULM) neuromuscular electrical stimulation (NMES) superimposed on a voluntary contraction added to a protocol of intradialytic leg cycle ergometer exercise on muscle strength, functional capacity and quality of life of adult patients with chronic kidney disease (CKD).

Methods: This randomized controlled clinical trial will be carried out at a Brazilian University Hospital. The patients will be evaluated and randomly allocated to an intervention group (i.

Transcranial direct current stimulation provides no clinically important benefits over walking training for improving walking in Parkinson's disease: a systematic review.

Questions: Does walking training combined with transcranial direct current stimulation (tDCS) improve walking (ie, speed, cadence and step length) and reduce falls and freezing, compared with no/sham intervention, in people with Parkinson's disease? Is walking training combined with tDCS superior to walking training alone? Are any benefits carried over to social participation and/or maintained beyond the intervention period?

Design: A systematic review with meta-analyses of randomised clinical trials.

Participants: Ambulatory adults with a clinical diagnosis of Parkinson's disease.

Intervention: tDCS combined with walking training.

One-pot synthesis of β-O-4 lignin models via the insertion of stable 2-diazo-1,3-dicarbonyls into O-H bonds.

Because lignin is a macromolecule that is a sustainable source of aromatic compounds, model substrates are commonly used to increase our understanding of its complex structure. However, few methods have been described for the synthesis of these models. Herein, we describe a new route towards the synthesis of β-O-4 lignin models by intermolecular O-H insertion reactions with simple and stable diazocarbonyls.

Energetic supplementation for maintenance or development of L. colonies.

Background: The nutritional requirements of honeybees () for their complete development need to be supplied through food sources available in the environment, since honeybees are insects that depend directly on blossoming food sources. However, at certain times a food-supply reduction can promote nutritional stress, thus necessitating food supplementation for maintenance or production stimulus of the colonies. Thus, the determination of optimal energy supplementation can assist in the maintenance and production of colonies.

Loss of STI1-mediated neuronal survival and differentiation in disease-associated mutations of prion protein.

Cellular prion protein (PrP ) is widely expressed and displays a variety of well-described functions in the central nervous system (CNS). Mutations of the PRNP gene are known to promote genetic human spongiform encephalopathies, but the components of gain- or loss-of-function mutations to PrP remain a matter for debate. Among the proteins described to interact with PrP is Stress-inducible protein 1 (STI1), a co-chaperonin that is secreted from astrocytes and triggers neuroprotection and neuritogenesis through its interaction with PrP .

Crystal structure of (2)-3-[4-(di-methyl-amino)-phen-yl]-1-(thio-phen-2-yl)prop-2-en-1-one.

The equimolar reaction between 4-(di-methyl-amino)-benzaldehyde and 2-acetyl-thio-phene in basic ethano-lic solution yields the title compound, CHNOS, whose mol-ecular structure matches the asymmetric unit. The mol-ecule is not planar, the dihedral angle between the aromatic and the thio-phene rings being 11.4 (2)°.

Prion protein binding to HOP modulates the migration and invasion of colorectal cancer cells.

Colorectal cancer (CRC) is one of the most frequently diagnosed malignancies. The generation of conventional treatments has improved, but approximately 50 % of patients with CRC who undergo potentially curative surgery ultimately relapse and die, usually as a consequence of metastatic disease. Our previous findings showed that engagement of the cellular prion protein (PrP(C)) to its ligand HSP70/90 heat shock organizing protein (HOP) induces proliferation of glioblastomas.

Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1(G93A) Amyotrophic Lateral Sclerosis mouse model.

Early molecular events related to cytoskeleton are poorly described in Amyotrophic Lateral Sclerosis (ALS), especially in the Schwann cell (SC), which offers strong trophic support to motor neurons. Database for Annotation, Visualization and Integrated Discovery (DAVID) tool identified cytoskeleton-related genes by employing the Cellular Component Ontology (CCO) in a large gene profiling of lumbar spinal cord and sciatic nerve of presymptomatic SOD1(G93A) mice. One and five CCO terms related to cytoskeleton were described from the spinal cord deregulated genes of 40 days (actin cytoskeleton) and 80 days (microtubule cytoskeleton, cytoskeleton part, actin cytoskeleton, neurofilament cytoskeleton, and cytoskeleton) old transgene mice, respectively.

5-HMF and carbohydrates content in stingless bee honey by CE before and after thermal treatment.

This study aimed to assess 5-hydroximethylfurfural and carbohydrates (fructose, glucose, and sucrose) in 13 stingless bee honey samples before and after thermal treatment using a capillary electrophoresis method. The methods were validated for the parameters of linearity, matrix effects, precision, and accuracy. A factorial design was implemented to determine optimal thermal treatment conditions and then verify the postprocedural 5-HMF formation, but once 5-HMF were View Article and Find Full Text PDF

Early gene expression changes in skeletal muscle from SOD1(G93A) amyotrophic lateral sclerosis animal model.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons. Familial ALS is strongly associated to dominant mutations in the gene for Cu/Zn superoxide dismutase (SOD1). Recent evidences point to skeletal muscle as a primary target in the ALS mouse model.

Early gene expression changes in spinal cord from SOD1(G93A) Amyotrophic Lateral Sclerosis animal model.

Amyotrophic Lateral Sclerosis (ALS) is an adult-onset and fast progression neurodegenerative disease that leads to the loss of motor neurons. Mechanisms of selective motor neuron loss in ALS are unknown. The early events occurring in the spinal cord that may contribute to motor neuron death are not described, neither astrocytes participation in the pre-symptomatic phases of the disease.

Early motor and electrophysiological changes in transgenic mouse model of amyotrophic lateral sclerosis and gender differences on clinical outcome.

Amyotrophic lateral sclerosis (ALS) is a progressive degenerative disorder affecting motoneurons and the SOD1(G93A) transgenic mice are widely employed to study disease physiopathology and therapeutic strategies. Despite the cellular and biochemical evidences of an early motor system dysfunction, the conventional behavioral tests do not detect early motor impairments in SOD1 mouse model. We evaluated early changes in motor behavior of ALS mice by doing the analyses of tail elevation, footprint, automatic recording of motor activities by means of an infrared motion sensor activity system and electrophysiological measurements in male and female wild-type (WT) and SOD1(G93A) mice from postnatal day (P) 20 up to endpoint.

The importance of molecular histology to study glial influence on neurodegenerative disorders. Focus on recent developed single cell laser microdissection.

Neuron-glia interaction is involved in physiological function of neurons, however recent evidences have suggested glial cells as participants in neurotoxic and neurotrophic mechanisms of neurodegenerative/neuroregenerative processes. Histological techniques employing immunolabeling, historadiography and in situ hybridization have been useful to localize at cell levels molecules in normal and pathological situations. The intercellular accomplishment leading to neuronal injury in central nervous system disorders implies the performance of quantitative assays to better interpret the role of related molecules or signal pathways, however one limitation employing the whole tissue is the loss of cellular resolution.

A method to immunolabel rodent spinal cord neurons and glia for molecular study in specific laser microdissected cells involved in neurodegenerative disorders.

Neuron-glia interaction is involved in physiological function of neurons, however, recent evidences have suggested glial cells as participants in neurotoxic and neurotrophic mechanisms of neurodegenerative/neuroregenerative processes. Laser microdissection offers a unique opportunity to study molecular regulation in specific immunolabeled cell types. However, an adequate protocol to allow morphological and molecular analysis of rodent spinal cord astrocyte, microglia and motoneurons remains a big challenge.

Differential regulation of FGF-2 in neurons and reactive astrocytes of axotomized rat hypoglossal nucleus. A possible therapeutic target for neuroprotection in peripheral nerve pathology.

Despite the favorable treatment of cranial nerve neuropathology in adulthood, some cases are resistant to therapy leading to permanent functional impairments. In many cases, suitable treatment is problematic as the therapeutic target remains unknown. Basic fibroblast growth factor (bFGF, FGF-2) is involved in neuronal maintenance and wound repair following nervous system lesions.