8 research outputs found
Effectiveness of Swiss Ball Vs Floor Exercises on Core Muscles Strengthening in Elite Cricketers
BACKGROUND:
Cricket is one of the most popular game in India played by men and women of all ages. The increased physical demands on the players may be associated with an increased risk of injuries. Core muscle strength is important to prevent risk of injuries in elite cricketers. The beginners in the cricket must have enough strength of core muscles, as core is the bridge between upper and lower limbs. So, it should be strong enough to prevent low back and lower limb injuries in cricketers.
AIM OF THE STUDY:
The aim is to determine the effectiveness of swiss ball exercises versus floor exercises on core muscle strength in elite cricketers.
OBJECTIVES:
1. To determine the effect of swiss ball on core muscle strengthening in elit cricketers.
2. To determine the effect of floor exercise on core muscle strengthening in elite cricketers.
3. To determine the effect of swiss ball vs floor exercise on core muscle strengthening in elite cricketers.
METHODS:
The total number of students in this study were 30 elite cricketers between 16-25 years out of which 15 subjects were included each in floor exercise(n=15) and swiss ball group(n=15). Back strength was measured before and after the intervention of 6 weeks using double leg lowering test.
RESULT:
After the analysis, the results revealed significant improvement of back strength in both the groups (p< 0.00). The swiss ball group showed significant results when compared with floor exercise group.
CONCLUSION:
Although the study showed beneficial results in both the groups, the results reflected that swiss ball group had better improvement of core muscle strength than the floor exercise group
Reversal of neurological deficits by painless nerve growth factor in a mouse model of Rett syndrome
: Rett syndrome is a rare genetic neurodevelopmental disease, affecting 1 in over 10,000 females born worldwide, caused by de novo mutations in the X-chromosome-located methyl-CpG-binding protein 2 (MeCP2) gene. Despite the great effort put forth by the scientific community, a therapy for this devastating disease is still needed. Here, we tested the therapeutic effects of a painless mutein of the Nerve Growth Factor, called human NGF painless (hNGFp), via a non-invasive intranasal delivery in female MeCP2+/- mice. Of note, previous work had demonstrated a broad biodistribution of hNGFp in the mouse brain by the nasal delivery route. We report that (1) the long-term lifelong treatment of MeCP2+/- mice with hNGFp, starting at 2 months of age, increased the chance of survival while also greatly improving behavioral parameters. Furthermore, when we assessed the phenotypic changes brought forth by (2) a short-term 1-month-long hNGFp-treatment, starting at 3 months of age (right after the initial presentation of symptoms), we observed the rescue of a well-known neuronal target population of NGF, cholinergic neurons in the medial septum. Moreover, we reveal a deficit in microglial morphology in MeCP2+/- mice, completely reversed in treated animals. This effect on microglia is in line with reports showing microglia to be a TrkA-dependent non-neuronal target cell population of NGF in the brain. To understand the immunomodulatory activity of hNGFp, we analyzed the cytokine profile after hNGFp treatment in MeCP2+/- mice, to discover that the treatment recovered the altered expression of key neuroimmune-communication molecules, such as fractalkine. The overall conclusion is that hNGFp delivered intranasally can ameliorate symptoms in the MeCP2+/- model of Rett syndrome, by exerting strong neuroprotection with a dual mechanism of action: directly on target neurons and indirectly via microglia
Fast diffusing p75NTR monomers support apoptosis and growth cone collapse by neurotrophin ligands
The p75 neurotrophin (NT) receptor (p75NTR) plays a crucial role in balancing survival-versus-death decisions in the nervous system. Yet, despite 2 decades of structural and biochemical studies, a comprehensive, accepted model for p75NTR activation by NT ligands is still missing. Here, we present a single-molecule study of membrane p75NTR in living cells, demonstrating that the vast majority of receptors are monomers before and after NT activation. Interestingly, the stoichiometry and diffusion properties of the wild-type (wt) p75NTR are almost identical to those of a receptor mutant lacking residues previously believed to induce oligomerization. The wt p75NTR and mutated (mut) p75NTR differ in their partitioning in cholesterol-rich membrane regions upon nerve growth factor (NGF) stimulation: We argue that this is the origin of the ability of wt p75NTR , but not of mut p75NTR, to mediate immature NT (proNT)-induced apoptosis. Both p75NTR forms support proNT-induced growth cone retraction: We show that receptor surface accumulation is the driving force for cone collapse. Overall, our data unveil the multifaceted activity of the p75NTR monomer and let us provide a coherent interpretative frame of existing conflicting data in the literature
SynActive’ – a genetic toolbox to study the connectome and proteome of learning and memory-associated synapses
Learning and memory correlate with activity-dependent synaptic plasticity processes at appropriate synaptic circuits. The underlying mechanisms of information storage in the brain are currently investigated at a whole-neuron scale to identify cellular memory engrams i.e., ensembles of neurons whose recruitment and activation are necessary and sufficient for the retrieval of a specific memory. Traditional methods for structural and functional analysis of synapses are not sufficient for investigating which subset of synapses encodes and stores a specific memory in a given neuron. To address this fundamental question, we have developed ‘SynActive’, a genetic toolbox exploiting regulatory sequences from the Arc mRNA and synapse-targeting peptides, that allows the expression of any protein of interest specifically at potentiated synapses. Here I have extended the SynActive toolbox to express the protein of interest, including fluorescent reporters, an affinity purification tag, and an optogenetic actuator specifically at in vitro and in vivo potentiated spines.
In SynActive-eGRASP, which allows input-specific labeling of potentiated synapses, one split-GFP fragment was expressed constitutively by presynaptic neurons, while the postsynaptic half was synthesized in an activity-dependent fashion at potentiated spines. After extensive validation in cultured neurons, SynActive-eGRASP was employed to map CA3-CA1 synapses potentiated during an associative memory task – contextual fear conditioning. Semi-automated analysis using a custom-made algorithm revealed a spatially nonuniform and clustered distribution of SynActive-eGRASP-positive synapses. SynActive controlled expression of fluorescent reporters- mVenus, and DsRED-E5 labeled dendritic spines undergoing potentiation in primary neuronal cultures. These optimized vectors should facilitate large-scale, possibly brain-wide as well as time-dependent, mapping of potentiated spines. For the proteomic profiling of in vivo potentiated spines, SynActive AAVs expressing FLAG-tagged PSD95 was delivered to the mouse hippocampus and the PSD95-interactome was immunoprecipitated from potentiated synapses after contextual fear conditioning. In primary neuronal cultures, photoactivation of channelrhodopsin expressed at potentiated spines via SynActive method induced neuronal spiking. In vivo, this construct can be used to tag memory-specific synapses, and optically activating them might induce memory retrieval. These novel tools and the initial results they produced provide the first step towards a shift in the study of memory engrams from a cellular to a synaptic resolution. In addition, our quantitative maps of synaptic potentiation in whole brain areas or specific synaptic circuits can be used to refine computational models of neural plasticity. Ongoing experiments are aimed at performing a comparative analysis of synaptic maps obtained in different phases of memory encoding and recall, in both physiological conditions and models of neurodegenerative and neurodevelopmental diseases
Formin 2 regulates the stabilization of filopodial tip adhesions in growth cones and affects neuronal outgrowth and pathfinding in vivo
Growth cone filopodia are actin-based mechanosensory structures that are essential for chemoreception and the generation of contractile forces necessary for directional motility. However, little is known about the influence of filopodial actin structures on substrate adhesion and filopodial contractility. Formin 2 (Fmn2) localizes along filopodial actin bundles and its depletion does not affect filopodia initiation or elongation. However, Fmn2 activity is required for filopodial tip adhesion maturation and the ability of filopodia to generate traction forces. Dysregulation of filopodia in Fmn2-depleted neurons leads to compromised growth cone motility. Additionally, in mouse fibroblasts, Fmn2 regulates ventral stress fiber assembly and affects the stability of focal adhesions. In the developing chick spinal cord, Fmn2 activity is required cellautonomously for the outgrowth and pathfinding of spinal commissural neurons. Our results reveal an unanticipated function for Fmn2 in neural development. Fmn2 regulates structurally diverse bundled actin structures, parallel filopodial bundles in growth cones and anti-parallel stress fibers in fibroblasts, in turn modulating the stability of substrate adhesions. We propose Fmn2 as a mediator of actin bundle integrity, enabling efficient force transmission to the adhesion sites
Activity-dependent expression of Channelrhodopsin at neuronal synapses
Increasing evidence points to the importance of dendritic spines in the formation and allocation of memories, and alterations of spine number and physiology are associated to memory and cognitive disorders. Modifications of the activity of subsets of synapses are believed to be crucial for memory establishment. However, the development of a method to directly test this hypothesis, by selectively controlling the activity of potentiated spines, is currently lagging. Here we introduce a hybrid RNA/protein approach to regulate the expression of a light-sensitive membrane channel at activated synapses, enabling selective tagging of potentiated spines following the encoding of a novel context in the hippocampus. This approach can be used to map potentiated synapses in the brain and will make it possible to re-activate the neuron only at previously activated synapses, extending current neuron-tagging technologies in the investigation of memory processes
PEG-<i>ran</i>-PPG Modified Epoxy Thermosets: A Simple Approach To Develop Tough Shape Memory Polymers
In
this work, we prepared thermoresponsive shape memory epoxy thermosets
by blending epoxy resin with polyÂ(ethylene glycol-<i>ran</i>-propylene glycol) random copolymer (PEG-<i>ran</i>-PPG
or RCP). Incorporation of RCP precisely tuned the temperature showing
the shape memory effect of epoxy thermoset, which was established
by dynamic mechanical analysis (DMA) and fold-deploy test. FTIR spectroscopy
confirmed that the compatibility of the system is caused by intermolecular
hydrogen bonding and only at high RCP concentration some phase separation
starts. DMA and thermomechanical analysis provided evidence for the
interactions of RCP chains with epoxy thermoset. The impact strength
considerably increased especially for 30 and 40 wt % RCP modified
blends. Furthermore, the blends exhibited good thermal stability in
conjunction with excellent UV resistance