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Cells in the body are regularly subjected to mechanical forces that influence their biological fate in terms of morphology, gene expression, and differentiation. The current gold standard method to replicate these effects in vitro is to culture cells on devices with elastic substrates and to impart mechanical stretch using mechanical or pneumatic pull-push methods. Microfluidic device designs offer several advantages in this context for general uniform and controlled stretching. However, the experimental setups are bulky, not user-friendly, and often involve several components that reside outside of the tissue culture incubator. Given the wide utility of mechanical stimulation in in-vitro research, our aim was to create a turn-key research tool that bioengineers can deploy in their cell-stretch assays, without having to deal with the complexity and nuances of ad hoc experimental setups. Here, we present an open-source, battery-powered, dual-channel cyclic pneumatic pulse generator box that can reside within an incubator and is compatible with custom microfluidic cell stretch devices. Our method depends on generating pressure-vacuum pulses simply using a linear miniature pneumatic air cylinder actuated using a continuous servo motor. To the best our knowledge, this is a first example of a completely battery-powered, standalone system that doesn't have any peripherals residing out of the incubator. We provide a detailed list of different components as well as the step-by-step assembly process. We validate its performance in a cell stretch assay using a commercially available microfluidic chip. Our results show an acute stimulation of cyclic stretching over 8â¯h on human umbilical vein endothelial cells (HUVECs) resulted in preferential alignment of cells perpendicular to the axis of stretch.
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Muscle spindles are stretch-sensitive mechanoreceptors found in the skeletal muscles of most four-limbed vertebrates. They are unique amongst sensory receptors in the ability to regulate their sensitivity by contraction of the intrafusal muscle fibres on which the sensory endings lie. Muscle spindles have revealed a remarkable diversity of functions, including reflex action in posture and locomotion, contributing to bodily self awareness, and influencing wound healing. What were the circumstances which gave rise to the evolution of such complex end-organs? We argue that spindles first appeared in early amniotes and only later in frogs and toads. This was considered an example of convergent evolution. Spindles in amphibians and reptiles are characterised by their simple structure, pointing to key features essential for spindle function. Spindle sensitivity in amphibians and reptiles is controlled by intrafusal fibre contractions evoked by branches of motor axons supplying extrafusal muscle. Modern phylogenetic evidence has revised our views on the origin of birds, placing them closer to the dinosaurs than had previously been thought. Birds are the only group, other than mammals, which has a dedicated fusimotor innervation of spindles, another example of convergent evolution, given the widely different origins of the two groups. One factor that may have played a role here was that both groups are endotherms, allowing motor control to develop further in an optimal internal environment. This, as well as other changes within the spindle, has led to the astonishing sophistication of motor control observed especially in many modern mammals.
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Background: Striae distensae (SD) is a common cutaneous disorder which appears as linear lesions seen mainly in women. Since previously described in 1889, SD has presented a significant challenge regarding its evaluation and treatment. Carboxytherapy was recently reported as an effective treatment for SD. Objectives: We sought to objectively compare the clinical effectiveness of carbon dioxide therapy (CDT) as monotherapy versus a combination of CDT and fractional CO2 laser in the treatment of SD. Methods: This randomized prospective study included twenty cases with bilateral and symmetrical SD. Each patient was treated with CDT only on the right (Rt) side of the body, while the left (Lt) side received a combination of CDT and fractional C02 laser. Results: Clinical evaluation revealed a clearly significant clinical improvement in SD lesions after both techniques regarding length, width, texture, and pigment changes. Although the Lt side showed slightly better improvement, however no statistically significant difference could be observed between both sides. In the meantime, the objective improvement observed by the 3D camera and histometric analysis correlated with the clinical improvement. Special stains showed collagen deposition which became more compact, dense and better organized, accompanied by evident increase in elastic fibers in a normal linear microfibrillar pattern after treatment on both sides. Conclusion: CDT demonstrated efficacy and safety as a minimally invasive modality for management of SD, as it induces collagen remodeling and better organization of elastic fibers with minimal side effects and downtime.
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BACKGROUND AND OBJECTIVE: It is an indisputable physiological phenomenon that the arterial axial pre-stretch ratio (AAPSR) decreases with age, but little attention has been paid to the effect of this reduction on chronic diseases during aging. METHODS: Here we reported an experimental method to simulate arteries aging, developed a fluid-structure interaction model with the effect of AAPSR changes, and compared it with the anatomy data and structural parameters of the human thoracic aorta. RESULTS: We showed that with the process of aging, the decrease of AAPSR leads to a decline of arterial elasticity, a decrease of arterial elastic strain energy, which weakens the ability to promote blood circulation, the corresponding decrease in cardiac output (CO) and cerebral blood flow (CBF) causes distal organ and body tissue ischemia, which is one of the main causes of increased blood pressure and decreased cerebral perfusion in the elderly. CONCLUSIONS: Thus, reduced AAPSR is the one of main manifestation of arteries aging and has an important impact on hypertension and hypoperfusion of the brain in the process of human aging. The research contributes to a better understanding of the physiological and pathological mechanisms of aging-related diseases.
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We conducted atomistic Molecular Dynamics (MD) simulations of DNA-Hairpin molecules encapsulated within Single-Walled Carbon Nanotubes (SWCNTs) at a temperature of 300 K. Our investigation revealed that the structural integrity of the DNA-Hairpin can be maintained within SWCNTs, provided that the diameter of the SWCNT exceeds a critical threshold value. Conversely, when the SWCNT diameter falls below this critical threshold, the DNA-Hairpin undergoes denaturation, even at a temperature of 300 K. The DNA-Hairpin model we employed consisted of a 12-base pair stem and a 3-base loop, and we studied various SWCNTs with different diameters. Our analyses identified a critical SWCNT diameter of 3.39 nm at 300 K. Examination of key structural features, such as hydrogen bonds (H-bonds), van der Waals (vdW) interactions, and other inter-base interactions, demonstrated a significant reduction in the number of H-bonds, vdW energy, and electrostatic energies among the DNA hairpin's constituent bases when confined within narrower SWCNTs (with diameters of 2.84 nm and 3.25 nm). However, it was observed that the increased interaction energy between the DNA-Hairpin and the inner surface of narrower SWCNTs promoted the denaturation of the DNA-Hairpin. In-depth analysis of electrostatic mapping and hydration status further revealed that the DNA-Hairpin experienced inadequate hydration and non-uniform distribution of counter ions within SWCNTs having diameters below the critical value of 3.39 nm. Our inference is that the inappropriate hydration of counter ions, along with their non-uniform spatial distribution around the DNA hairpin, contributes to the denaturation of the molecule within SWCNTs of smaller diameters. For DNA-Hairpin molecules that remained undenatured within SWCNTs, we investigated their mechanical properties, particularly the elastic properties. Our findings demonstrated an increase in the persistence length of the DNA-Hairpin with increasing SWCNT diameter. Additionally, the stretch modulus and torsional stiffness of the DNA-Hairpin were observed to increase as a function of SWCNT diameter, indicating that confinement within SWCNTs enhances the mechanical flexibility of the DNA-Hairpin.
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Background: The seated wall angel (SWA) is an intervention to improve upper quarter mobility but has not been described as a clinical test with scoring. Hypothesis/ Purpose: To explore the clinical utility of the SWA as a test with scoring. The authors hypothesized that SWA test scores would be lower on the injured than uninjured side, improve over time, and show stronger association with patient-reported shoulder function than shoulder mobility tests. Study Design: Prospective cohort. Methods: Patients diagnosed with anterior shoulder instability and referred to physical therapy participated. Testing occurred after physical therapy examination (initial) and six weeks later (follow-up). Rehabilitation was not controlled. Testing included clinical tests (SWA, passive shoulder external rotation range of motion, total arc of motion) and patient-reported outcomes including the American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, (ASES) and the Western Ontario Shoulder Instability Index (WOSI). The SWA test was scored 0 to 3 points bilaterally based on number of body contacts with the wall (i.e., elbows and fingertips, posterior fingers, posterior forearm). Passive range of motion was measured with a standard goniometer. SWA scores were compared between sides at initial testing and compared between testing timepoints on the injured side. Associations among injured side clinical test values and patient-reported outcome scores were examined. Results: Mean (SD) SWA score on the injured side was significantly lower than the uninjured side at initial testing [1.6 (1.0) vs 2.2 (1.1), p = 0.045] and significantly increased at follow-up testing [2.4 (1.0), p = 0.041]. Only SWA test score was significantly correlated with ASES (r=0.597) and WOSI (r=-0.648) scores at initial testing, and SWA test score was significantly correlated with WOSI score at follow-up testing (r=-0.611). Conclusions: The clinical utility of the SWA test is supported by distinguishing the injured and uninjured sides and having stronger associations with patient-reported shoulder function than shoulder mobility tests.
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The aim of this study was to investigate the effect of maturation on vertical jumping performance, in adolescent boys and girls, concerning plantar flexor activity and Achilles tendon (AT) stiffness. Thirty-nine adolescents were tested in a counter-movement jump (CMJ) at three different time points: 18 and 9 months before peak height velocity (PHV) and at PHV. The EMG activity of the medialis gastrocnemius (MG) and tibialis anterior (TA) muscles was evaluated, in relation to jump height. Boys showed higher jumping ability and AT stiffness than girls. Additionally, boys revealed increased eccentric (ecc) and concentric (con) MG activity, along with decreased ecc and con TA activity, near PHV. On the other hand, girls showed increased ecc and con TA/MG co-contraction compared to boys, mainly near PHV. In conclusion, a different mechanism of vertical jumping performance is adopted between early adolescent boys and girls. Nevertheless, no notable alterations in jumping capability were detected over time, indicating that the maturation process does not influence stretch-shortening cycle (SSC) performance.
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OBJECTIVE: VECs play a crucial role in regulating the function of neutrophils, which is essential for immune responses and inflammation. As stretch-sensitive cells, VECs sense mechanical stretch through surface mechanoreceptors, converting external mechanical stimuli into biochemical signals. This study aimed to explore the molecular mechanisms underlying the regulation of neutrophil behavior by stretched VECs. MATERIALS AND METHODS: The key cytokine-inducing neutrophil N2 polarization in the conditioned medium from stretched vascular endothelial cells (CM-stretch) was validated through multifactorial matrix and flow cytometry. Additionally, the molecular mechanism underlying the response of vascular endothelial cells to stretch was systematically verified through layer-by-layer analysis using WB. RESULTS: IL13, not IL4, was ultimately identified as a key cytokine-inducing neutrophil N2 polarization in CM-stretch. Inhibition of the transient receptor potential channel (TRPC1) and siRNA-mediated knockdown of TRPC1 both significantly decreased IL13 production. Furthermore, neutralizing IL13 in the CM-stretch or inhibiting STAT3 phosphorylation inhibited neutrophil N2 polarization, as evidenced by reduced CD206 and VEGFA expression. CONCLUSIONS: These results demonstrate that stretched VECs initiate a signaling cascade that induces neutrophil N2 polarization through the TRPC1-IL13-STAT3 axis, suggesting that mechanical stretching of VECs could shift neutrophil function from a pro-inflammatory to a more regulatory and healing role.
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Intermittent claudication is a primary symptom of peripheral artery disease (PAD). a chronic progressive disease caused primarily by atherosclerosis. It is usually characterized by leg pain, aches, cramps, or fatigue when walking, which improves with rest. Physical therapy, including a supervised exercise program, is often recommended as the first treatment for sprains. This study aims to evaluate the short-term effects of incorporating heel raise and calf stretch exercises with standard medical therapy compared to medical therapy alone in managing intermittent claudication. From May 2022 to November 2023, 160 patients with Stage II Fontaine PAD were randomly assigned to two equal groups. Group A (80 patients) received heel raise and calf stretch exercises in addition to medical treatment, while Group B (80 patients) received only medical treatment. Both groups underwent treadmill walking tests before and after three months to measure absolute walking distance (ACD), peak walking time (PWT), and Walking Impairment Questionnaire (WIQ) scores, including distance, speed, and symptom severity. At baseline, there were no significant differences between the groups in terms of ACD, peak walking time, ankle-brachial index, distance, speed, and symptoms. At follow-up, Group A showed significantly greater improvements in ACD (312.00 ± 45.43â m), peak walking time (8.54 ± 1.55â min), distance (29.46 ± 4.63â km), speed (20.01 ± 3.13 kph), and WIQ symptoms (22.10 ± 1.02) compared to Group B, which had ACD (276.55 ± 29.07â m), peak walking time (6.72 ± 1.70â min), distance (23.68 ± 3.89â km), speed (15.71 ± 2.71 kph), and WIQ symptoms (20.80 ± 1.47) (P < .001). The ankle-brachial index remained similar between the groups (P > .05). We concluded that integrating standard physical therapy exercises, such as calf raises and leg stretches, with medical therapy significantly enhances walking function in patients with ischemic intermittent claudication.
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Vascularization is a major challenge in the field of tissue engineering and regenerative medicine. Mechanical factors have been demonstrated to play a fundamental role in vasculogenesis and angiogenesis and can affect the architecture of the generated vascular network. Through the regulation of mechanical factors in engineered tissues, various mechanical strategies can be used to optimize the preformed vascular network and promote its rapid integration with host vessels. Optimization of the mechanical properties of scaffolds, including controlling scaffold stiffness, increasing surface roughness and anisotropic structure, and designing interconnected, hierarchical pore structures, is beneficial for the in vitro formation of vascular networks and the ingrowth of host blood vessels. The incorporation of hollow channels into scaffolds promotes the formation of patterned vascular networks. Dynamic stretching and perfusion can facilitate the formation and maturation of preformed vascular networks in vitro. Several indirect mechanical strategies provide sustained mechanical stimulation to engineered tissues in vivo, which further promotes the vascularization of implants within the body. Additionally, stiffness gradients, anisotropic substrates and hollow channels in scaffolds, as well as external cyclic stretch, boundary constraints and dynamic flow culture, can effectively regulate the alignment of vascular networks, thereby promoting better integration of prevascularized engineered tissues with host blood vessels. This review summarizes the influence and contribution of both scaffold-based and external stimulus-based mechanical strategies for vascularization in tissue engineering and elucidates the underlying mechanisms involved.
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Our previous studies have demonstrated the important roles of androgen receptor (AR) in myoblast proliferation regulated by 15 % (mimic appropriate exercise) and 20 % (mimic excessive exercise) mechanical stretches. Except for myoblast proliferation, differentiation is also an important factor affecting muscle mass and strength. But the role of AR in stretch-regulated myoblast differentiation and AR's upstream and downstream signals remain unknown. In the present study, firstly the differences of myogenic differentiation between C2C12 (with AR expression) and L6 (without AR expression) myoblasts induced by 15 % and 20 % mechanical stretches were compared; secondly, AR antagonist flutamide and AR agonist GTx-007 were used in 15 % and 20 % stretched myoblasts respectively to confirm AR's roles in stretch-regulated myoblast differentiation; thirdly, RNA-seq, molecular dynamic simulation (MD) and co-immunoprecipitation were performed to screen the downstream and upstream molecules of AR during stretches. We found that (1) 15 % stretch increased while 20 % stretch decreased myotube number in differentiating C2C12 and L6 myoblasts, with more significant changes in C2C12 cells than L6 cells; (2) in stretched C2C12 myoblasts, AR antagonist flutamide inhibited 15 % stretch-promoted differentiation while AR agonist GTx-007 reversed 20 % stretch-inhibited differentiation (reflected by changes in myotube number, MHC contents of fast-twitch and slow-twitch fiber, and the levels of myogenic regulatory factors (MRFs) such as MyoD and myogenin); (3) KEGG analysis of RNA-seq showed that the differently expressed genes (DEGs) in C2C12 cells induced by 15 % stretch were enriched in FoxO and JAK-STAT signaling pathways, while DEGs by 20 % stretch were enriched in FoxO and MAPK signaling pathways; (4) MD and co-immunoprecipitation showed that ß1 integrin could interact with AR and influence AR's activity in C2C12 cells. In conclusion, AR plays important roles in myoblast differentiation promoted by 15 % stretch while inhibited by 20 % stretch, which was fulfilled through FoxO-MRFs. In addition, α7ß1 integrin may be a bridge linking mechanical stretch and AR. This study is beneficial to deeply understand the roles and mechanisms of AR in stretch-regulated muscle mass and strength; and reports firstly that myoblasts sense mechanical stimulus and transmit into intracellular AR via α7ß1 integrin.
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The Snell dwarf mouse (Pit1dw/dw), an animal model of congenital combined pituitary hormone deficiency, displays skeletal muscle weakness. While enhanced responsivity to repeated exposures of muscle contractions have been documented for Snell dwarf mice, the response following single exposure to distinct contraction protocols remained uncharacterized. The purpose of this study was to investigate the muscle recovery of Snell dwarf and control littermate mice following a single exposure to two separate protocols-an intermittent slow velocity (30°/s) contraction protocol or a continuous rapid velocity (500°/s) contraction protocol. Following both protocols for control mice, torque values were 30% and 80% of pre-protocol values at 5 min and 3 days, respectively. At 10 days, performance returned to baseline for the 30°/s protocol and were depressed for the 500°/s protocol. For Snell dwarf mice following both protocols, torques were depressed to 5% of pre-protocol values at 5 min and returned to baseline by 3 days. Recovery following the 30°/s protocol for control mice and both protocols for Snell dwarf mice coincided with increased transcriptional output, upregulation of cytokine-mediated signaling genes, and a distribution shift to smaller muscle fibers with reduced area per nucleus. These features represent efficacious remodeling ubiquitous across distinct contraction paradigms in the context of the Pit1 mutation.
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Contração Muscular , Músculo Esquelético , Animais , Feminino , Masculino , Camundongos , Modelos Animais de Doenças , Nanismo Hipofisário/genética , Nanismo Hipofisário/fisiopatologia , Nanismo Hipofisário/metabolismo , Camundongos Endogâmicos C57BL , Músculo Esquelético/fisiologia , Músculo Esquelético/metabolismo , Fator de Transcrição Pit-1/genética , Fator de Transcrição Pit-1/metabolismoRESUMO
Neurons have a unique polarized nature that must adapt to environmental changes throughout their lifespan. During embryonic development, axon elongation is led by the growth cone,1 culminating in the formation of a presynaptic terminal. After synapses are formed, axons elongate in a growth cone-independent manner to accompany body growth while maintaining their ultrastructure and function.2,3,4,5,6 To further understand mechanical strains on the axon shaft, we developed a computer-controlled stretchable microfluidic platform compatible with multi-omics and live imaging. Our data show that sensory embryonic dorsal root ganglia (DRGs) neurons have high plasticity, with axon shaft microtubules decreasing polymerization rates, aligning with the direction of tension, and undergoing stabilization. Moreover, in embryonic DRGs, stretch triggers yes-associated protein (YAP) nuclear translocation, supporting its participation in the regulatory network that enables tension-driven axon growth. Other than cytoskeleton remodeling, stretch prompted MARCKS-dependent formation of plasmalemmal precursor vesicles (PPVs), resulting in new membrane incorporation throughout the axon shaft. In contrast, adolescent DRGs showed a less robust adaptation, with axonal microtubules being less responsive to stretch. Also, while adolescent DRGs were still amenable to strain-induced PPV formation at higher stretch rates, new membrane incorporation in the axon shaft failed to occur. In summary, we developed a new resource to study the biology of axon stretch growth. By unraveling cytoskeleton adaptation and membrane remodeling in the axon shaft of stretched neurons, we are moving forward in understanding axon growth.
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Axônios , Microtúbulos , Microtúbulos/metabolismo , Animais , Axônios/metabolismo , Axônios/fisiologia , Camundongos , Gânglios Espinais/embriologia , Gânglios Espinais/metabolismo , Gânglios Espinais/citologia , Substrato Quinase C Rico em Alanina Miristoilada/metabolismo , Membrana Celular/metabolismoRESUMO
Scars and stretch marks are extremely common. For scars, evidence of alterations of the dermal and hypodermic layers is known, while for stretch marks, less data are available, and they are considered purely aesthetic conditions. The intra- and inter-subject variability of the skin makes the comparison between these two particularly complex. This study presents the case of a 54-year-old man who had both stretch marks and a surgical scar on his abdomen. We performed ultrasound and elastosonographic investigations for both to analyse the structural alteration of the skin and subcutaneous layers. Their structures were also compared to the structure of intact skin. The two skin conditions appeared substantially morphologically different and different from intact skin. The alterations detected, particularly of the connective structures, allow us to state that both scars and stretch marks are alterations of both the dermis and the hypodermis and stretch marks differ from scars.
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Cicatriz , Humanos , Masculino , Pessoa de Meia-Idade , Cicatriz/diagnóstico por imagem , Cicatriz/patologia , Pele/diagnóstico por imagem , Pele/patologia , Técnicas de Imagem por Elasticidade , Ultrassonografia/métodos , Derme/diagnóstico por imagem , Derme/patologiaRESUMO
The trabecular meshwork (TM) plays an essential role in the circulation of aqueous humor by sensing mechanical stretch. The balance between the outflow and inflow of aqueous humor is critical in regulating intraocular pressure (IOP). A dysfunctional TM leads to resistance to the outflow of aqueous humor, resulting in an elevated IOP, a major risk factor for glaucoma. It is widely accepted that mutant myocilin (MYOC) can cause damage to the TM. However, few studies have investigated how TM cells carrying mutant MYOC respond to cyclic mechanical stretch (CMS) and whether these cells are more sensitive to CMS under this genetic background. In this study, we applied mechanical stretch to TM cells using the Flexcell system to mimic physiological stress. In addition, we performed genome-wide transcriptome analysis and oxidized lipidomics to systematically compare the gene expression and oxylipin profiles of non-stretched control human primary TM cells, human primary TM cells under CMS (TM-CMS), and human primary TM cells overexpressing MYOCS341P under CMS (S341P-CMS). We found that TM cells that overexpressed MYOCS341P were more sensitive to mechanical stress. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that downregulated genes were most enriched in oxidative phosphorylation, indicating mitochondria dysfunction and the likelihood of oxidative stress. Oxidized lipidomics analysis revealed significant changes in oxylipin profiles between the S341P-CMS and TM-CMS groups. Through further genome-wide transcriptomic analysis, we identified several genes that may be involved in the sensitivity of TM cells that overexpressed MYOCS341P to mechanical stress, including SARM1, AHNAK2, NT5C, and SOX8. The importance of these genes was validated by quantitative real-time PCR. Collectively, our findings indicate that mitochondrial dysfunction may contribute to the damage that occurs to TM cells with a MYOCS341P background under mechanical stretch.
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OBJECTIVE: Multicomponent bandages (MCBs) are recommended by the French Authority for Health (Haute Autorité de Santé) as first-line treatment for venous leg ulcers (VLUs). A first analysis of the data collected from the French administrative healthcare database (Système National des Données de Santé (SNDS)) on 25,255 patients with a VLU supported superiority of MCBs versus short stretch bandages when considering the healing outcomes and costs associated with closure of these wounds. The aim of this study was to assess how beneficial the primary dressing (technology lipido-colloid nano-oligosaccharide factor (TLC NOSF) or control dressing group (CDG)) could be, when used in combination with MCBs in the treatment of VLUs. METHOD: Data from the SNDS were collected for patients meeting the following inclusion criteria: treatment for a VLU with MCBs and with the same dressing type (TLC-NOSF or CDG) during the whole treatment period. Healing outcomes were documented on the global cohorts and propensity score-matched cohorts. The mean healthcare cost and the ecological impact were calculated for those patients healed within the study period. RESULTS: In total, 12,507 patients met the criteria for treatment with both MCBs and TLC-NOSF dressings (n=1134) versus MCBs and CDG (n=11,373); with 1134 and 2268 patients per group following propensity score matching. Healing outcomes were favourable for the TLC-NOSF group in the global cohort and were enhanced in the propensity score-matched cohorts. At every point of the analysis, the adjusted healing rates were significantly higher in the TLC-NOSF group than in the CDG group (p<0.001). In the propensity score-matched cohorts (n=3402), the healing rate at three months was 52% in the TLC-NOSF group versus 37% in the CDG group (p<0.001). The median healing time was 87 days versus 125.5 days in the TLC-NOSF and CDG groups, respectively (p<0.0001). TLC-NOSF dressings significantly reduced the average treatment cost per healed ulcer (2099) by 23.7% compared with dressings without TLC-NOSF (2751) (p<0.001), as well as the resources used. CONCLUSION: This SNDS analysis confirms, in the largest real-life study performed in VLU management, the superiority of the TLC-NOSF dressings versus those not impregnated with the NOSF compound. Better clinical outcomes associated with cost savings and a positive ecological impact support the combination of MCBs and TLC-NOSF dressings and should be considered as an optimal standard of care for the global management of VLUs. These outcomes reinforce the current positions of the international guidelines on the use of NOSF impregnated dressings (UrgoStart range; Laboratoires Urgo, France) in this pathology.
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Bandagens , Úlcera Varicosa , Cicatrização , Humanos , Feminino , Masculino , França , Úlcera Varicosa/terapia , Úlcera Varicosa/economia , Idoso , Bandagens/economia , Pessoa de Meia-Idade , Estudos de Coortes , Bases de Dados Factuais , Idoso de 80 Anos ou mais , Seguro Saúde/estatística & dados numéricos , Resultado do Tratamento , Custos de Cuidados de Saúde/estatística & dados numéricosRESUMO
Anterior cruciate ligament (ACL) injuries are widespread, particularly in sports that involve rapid changes in direction, such as badminton, and it incapacitates an athlete severely and for a long time. ACL reconstruction followed by a structured rehabilitation program is essential for returning to peak performance. Plyometric training, known for enhancing explosive power and agility, is increasingly incorporated in post-ACL reconstruction rehabilitation for athletes. This case report presents the rehabilitation of a 19-year-old female badminton player operated for ACL reconstruction through the inculcation of plyometric training in the later phase to optimize better performance outcomes. The athlete demonstrated significant improvements in knee stability, strength, and functional performance. Plyometric exercises played a crucial role in restoring explosive power and agility, essential for competitive badminton, thereby facilitating a successful return to sport.
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Background: The electrophysiological mechanism connecting mitral valve prolapse (MVP), premature ventricular complexes and life-threatening ventricular arrhythmia is unknown. A common hypothesis is that stretch activated channels (SACs) play a significant role. SACs can trigger depolarizations or shorten repolarization times in response to myocardial stretch. Through these mechanisms, pathological traction of the papillary muscle (PM), as has been observed in patients with MVP, may induce irregular electrical activity and result in reentrant arrhythmia. Methods: Based on a patient with MVP and mitral annulus disjunction, we modeled the effect of excessive PM traction in a detailed medical image-derived ventricular model by activating SACs in the PM insertion region. By systematically varying the onset of SAC activation following sinus pacing, we identified vulnerability windows for reentry with 1 ms resolution. We explored how reentry was affected by the SAC reversal potential ( E SAC ) and the size of the region with simulated stretch (SAC region). Finally, the effect of global or focal fibrosis, modeled as reduction in tissue conductivity or mesh splitting (fibrotic microstructure), was investigated. Results: In models with healthy tissue or fibrosis modeled solely as CV slowing, we observed two vulnerable periods of reentry: For E SAC of -10 and -30 mV, SAC activated during the T-wave could cause depolarization of the SAC region which lead to reentry. For E SAC of -40 and -70 mV, SAC activated during the QRS complex could result in early repolarization of the SAC region and subsequent reentry. In models with fibrotic microstructure in the SAC region, we observed micro-reentries and a larger variability in which times of SAC activation triggered reentry. In these models, 86% of reentries were triggered during the QRS complex or T-wave. We only observed reentry for sufficiently large SAC regions ( > = 8 mm radius in models with healthy tissue). Conclusion: Stretch of the PM insertion region following sinus activation may initiate ventricular reentry in patients with MVP, with or without fibrosis. Depending on the SAC reversal potential and timing of stretch, reentry may be triggered by ectopy due to SAC-induced depolarizations or by early repolarization within the SAC region.
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INTRODUCTION: Increases in contralateral range of motion (ROM) have been shown following acute high-intensity and high-duration static stretching (SS) with no significant change in contralateral force, power, and muscle activation. There are currently no studies comparing the effects of a high-intensity, short-duration (HISD) or low-intensity, long-duration (LILD) SS on contralateral performance. PURPOSE: The aim of this study was to examine how HISD and LILD SS of the dominant leg hamstrings influence contralateral limb performance. METHODS: Sixteen trained participants (eight females, eight males) completed three SS interventions of the dominant leg hamstrings; (1) HISD (6 × 10 s at maximal point of discomfort), (2) LILD (6 × 30 s at initial point of discomfort), and (3) control. Dominant and non-dominant ROM, maximal voluntary isometric contraction (MVIC) forces, muscle activation (electromyography (EMG)), and unilateral CMJ and DJ heights were recorded pre-test and 1 min post-test. RESULTS: There were no significant contralateral ROM or performance changes. Following the HISD condition, the post-test ROM for the stretched leg (110.6 ± 12.6°) exceeded the pre-test (106.0 ± 9.0°) by a small magnitude effect of 4.2% (p = 0.008, d = 0.42). With LILD, the stretched leg post-test (112.2 ± 16.5°) exceeded (2.6%, p = 0.06, d = 0.18) the pre-test ROM (109.3 ± 16.2°) by a non-significant, trivial magnitude. There were large magnitude impairments, evidenced by main effects for testing time for force, instantaneous strength, and associated EMG. A significant ROM interaction (p = 0.02) showed that with LILD, the stretched leg significantly (p = 0.05) exceeded the contralateral leg by 13.4% post-test. CONCLUSIONS: The results showing no significant increase in contralateral ROM with either HISD or LILD SS, suggesting the interventions may not have been effective in promoting crossover effects.