Stress Injury Research Articles

Cueing Dancers to "Externally Rotate From the Hips" Improves Potentially Injurious Ankle Joint Angles and Contact Forces During a Demipointe Ballet Position.

Introduction: The demipointe dance position puts the ankle at high risk of overuse injury and posteromedial ankle pain due to increased ankle valgus forces. Previous work has shown that creating lower limb external rotation intrinsic to demipointe with hip external rotation reduces foot pronation that causes ankle valgus stress. Therefore, the purpose of this work was to examine long axis rotation kinematics of the hip, knee, and ankle as well as the ankle joint contact forces in demipointe to better understand the biomechanical impact(s) of the specific cue to increase hip external rotation in this position. Methods: Three-dimensional motion capture and force plate data were collected from 23 contemporary or ballet pre-professional dancers (age: 19.94 ± 1.34 years) who each performed 3 dancer-selected (DS) demipointe positions and 3 demipointes with the cue to "externally rotate from the hips." Results: The cue to increase hip external rotation resulted in significantly increased hip external rotation angle [DS: 37.5; 9.42° (median; interquartile range), Cued: 39.9; 10.8°, P < .0001)] and significantly reduced ankle eversion angle (DS: 8.13; 11.4°, Cued: 7.77; 10.3°, P = .023). However, total turnout angle was also significantly decreased (DS: 75.8; 7.91°, Cued: 75.4; 7.73°, P < .0001), which is undesirable for proper esthetic performance of demipointe. Total ankle joint force remained unchanged, but ankle eversion force was significantly reduced (DS: 15.3; 4.18 %bodyweight (BW), Cued: 14.7; 4.99 %BW, P < .0001) with use of the cue. Discussion/Conclusion: Utilization of a cue to increase hip external rotation was successful in increasing hip contribution to turnout angle and reducing injurious ankle eversion force. Further coaching using this cue may allow dancers to produce these advantageous mechanics while maintaining turnout angle.

Comparative in vitro toxicological effects of water-soluble and insoluble components of atmospheric PM2.5 on human lung cells

Fine particulates in city air significantly impact human health, but the hazardous compositional mechanisms are still unclear. Besides the toxicity of environmental PM2.5 to in vitro human lung epithelial cells (A549), the independent cytotoxicity of PM2.5-bound water-soluble (WS-PM2.5) and water-insoluble (WIS-PM2.5) fractions were also compared by cell viability, oxidative stress (reactive oxygen species, ROS), and inflammatory injury (IL-6 and TNF-α). The cytotoxicity of PM2.5 varied significantly by sampling season and place, with degrees greater in winter and spring than in summer and autumn, related to corresponding trend of air PM2.5 level, and also higher in industrial than urban site, although their PM2.5 pollution levels were comparable. The PM2.5 bound metals (Ni, Cr, Fe, and Mn) may contribute to cellular injury. Both WS-PM2.5 and WIS-PM2.5 posed significant cytotoxicity, that WS-PM2.5 was more harmful than WIS-PM2.5 in terms of decreasing cell viability and increasing inflammatory cytokines production. In particular, industrial samples were usually more toxic than urban samples, and those from summer were generally less toxic than other seasons. Hence, in order to mitigate the health risks of PM2.5 pollution, the crucial targets might be components of heavy metals and soluble fractions, and sources in industrial areas, especially during the cold seasons.

Nogo-B Promotes Endoplasmic Reticulum Stress-Mediated Autophagy in Endothelial Cells of Diabetic Nephropathy.

Aims: Endothelial cells are the critical targets of injury in diabetic nephropathy (DN), and endothelial cell lesions contribute to the disease progression. Neurite outgrowth inhibitor B (Nogo-B), an endoplasmic reticulum (ER)-resident protein, plays a pivotal role in vascular remodeling after injury, and maintains the structure and function of the ER. Yet, the role of Nogo-B in the regulation of ER stress and endothelial cell injury remains largely unknown. Herein, we tested the hypothesis that Nogo-B activates ER stress-mediated autophagy and protects endothelial cells in DN. Results: The level of Nogo-B was decreased in glomerular endothelial cells in biopsy specimens from DN patients. In vivo and in vitro studies have shown that silencing Nogo-B activated ER stress signaling, and affected the expression of autophagy-related marker early growth response 1 and microtubule-associated protein light chain 3 (LC3) in endothelial cells in hyperglycemic condition. Conclusion and Innovation: These results denote that Nogo-B contributes to ER stress-mediated autophagy and protects endothelial cells in DN, providing new evidence for understanding the role of ER stress-mediated autophagy in endothelial cells of DN.

Flexor tendon pulley injuries in climbing: causes, diagnosis and treatment

Finger flexor pulley injuries are the most common overuse injuries sustained by climbers. These injuries are caused by forceful gripping techniques specific to climbing, making them uncommon in non-climbing activities. With the growing popularity of climbing, there is a rising need for accurate diagnosis and improved treatment methods. This paper explores current diagnostic techniques, including physical examination, ultrasound, and magnetic resonance imaging. It also discusses treatment options, which range from conservative rehabilitation to surgery, depending on the severity of the injury. Finally, it emphasizes the importance of injury prevention through proper warm-up and avoiding excessive strain. 

Radiographic and Advanced Imaging Evaluation of Posterior Shoulder Instability.

Posterior shoulder instability is an uncommon but important cause of shoulder dysfunction and pain which may occur as the result of seizure, high energy trauma, or repetitive stress related to occupational or sport-specific activities. This current review details the imaging approach to the patient with posterior shoulder instability and describes commonly associated soft tissue and bony pathologies identified by radiographs, CT, and MR imaging. Advances in MR imaging technology and techniques allow for more accurate evaluation of bone and soft tissue pathology associated with posterior shoulder instability while sparing patients exposure to radiation. Imaging can contribute significantly to the clinical management of patients with posterior shoulder instability by demonstrating the extent of associated injuries and identifying predisposing anatomic conditions. Radiologic evaluation should be guided by clinical history and physical examination, beginning with radiographs followed by CT and/or MRI for assessment of osseous and soft tissue pathology. Synthesis of a patient's clinical history, physical exam findings, and radiologic examinations should guide clinical management.

Elucidating ascorbate and aldarate metabolism pathway characteristics via integration of untargeted metabolomics and transcriptomics of the kidney of high-fat diet-fed obese mice.

Obesity is a major independent risk factor for chronic kidney disease and can activate renal oxidative stress injury. Ascorbate and aldarate metabolism is an important carbohydrate metabolic pathway that protects cells from oxidative damage. However the effect of oxidative stress on this pathway is still unclear. Therefore, the primary objective of this study was to investigate the ascorbate and aldarate metabolism pathway in the kidneys of high-fat diet-fed obese mice and determine the effects of oxidative stress. Male C57BL/6J mice were fed on a high-fat diet for 12 weeks to induce obesity. Subsequently, non-targeted metabolomics profiling was used to identify metabolites in the kidney tissues of the obese mice, followed by RNA sequencing using transcriptomic methods. The integrated analysis of metabolomics and transcriptomics revealed the alterations in the ascorbate and aldarate metabolic pathway in the kidneys of these high-fat diet-fed obese mice. The high-fat diet-induced obesity resulted in notable changes, including thinning of the glomerular basement membrane, alterations in podocyte morphology, and an increase in oxidative stress. Metabolomics analysis revealed 649 metabolites in the positive-ion mode, and 470 metabolites in the negative-ion mode. Additionally, 659 differentially expressed genes (DEGs) were identified in the obese mice, of which 34 were upregulated and 625 downregulated. Integrated metabolomics and transcriptomics analyses revealed two DEGs and 13 differential metabolites in the ascorbate and aldarate metabolic pathway. The expression levels of ugt1a9 and ugt2b1 were downregulated, and the ascorbate level in kidney tissue of obese mice was reduced. Thus, renal oxidative stress injury induced by high-fat diet affects metabolic regulation of ascorbate and aldarate metabolism in obese mice. Ascorbate emerged as a potential marker for predicting kidney damage due to high-fat diet-induced obesity.

Differences in nature killer cell response and interference with mitochondrial DNA induced apoptosis in moxifloxacin environment

ObjectivesAs antibiotics become more prevalent, accuracy and safety are critical. Moxifloxacin (MXF) have been reported to have immunomodulatory effects on a variety of immune cells and even anti-proliferative and pro-apoptotic effects, but the mechanism of action is not fully clear. MethodsPeripheral blood mononuclear cells (PBMC) from experimental groups of healthy adults (n = 3) were treated with MXF (10ug/ml) in vitro for 24 h. Single-cell sequencing was performed to investigate differences in the response of each immune cell to MXF. Flow cytometry determined differential gene expression in subsets of most damaged NK cells. Pseudo-time analysis identified drivers that influence MXF-stimulated cell differentiation. Detection of mitochondrial DNA and its involvement in the mitochondrial respiratory chain pathway clarifies the origin of MXF-induced stress injury. ResultsMoxifloxacin-environmental NK cells are markedly reduced: a new subset of NK cells emerges, and immediate-early-response genes in this subset indicate the presence of an early activation response. The inhibitory receptor-dominant subset shows enhanced activation, leading to increased expression of cytokines and chemokines. The near-mature subset showed greater cytotoxicity and the most pronounced cellular damage. CD56bright cells responded by antagonizing the regulation of activation and inhibitory signals, demonstrating a strong cleavage capacity. The severe depletion of mitochondrial genes was focused on apoptosis induced by the mitochondrial respiratory chain complex. ConclusionNK cells exhibit heightened sensitivity to the MXF environment. Different NK subsets upregulate the expression of cytokines and chemokines through different activation pathways. Concurrently, MXF induces impairment of the mitochondrial oxidative phosphorylation system, culminating in apoptosis.

A mouse model of chronic primary pain that integrates clinically relevant genetic vulnerability, stress, and minor injury.

Chronic primary pain conditions (CPPCs) affect over 100 million Americans, predominantly women. They remain ineffectively treated, in large part because of a lack of valid animal models with translational relevance. Here, we characterized a CPPC mouse model that integrated clinically relevant genetic (catechol-O-methyltransferase; COMT knockdown) and environmental (stress and injury) factors. Compared with wild-type mice, Comt+/- mice undergoing repeated swim stress and molar extraction surgery intervention exhibited pronounced multisite body pain and depressive-like behavior lasting >3 months. Comt+/- mice undergoing the intervention also exhibited enhanced activity of primary afferent nociceptors innervating hindpaw and low back sites and increased plasma concentrations of norepinephrine and pro-inflammatory cytokines interleukin-6 (IL-6) and IL-17A. The pain and depressive-like behavior were of greater magnitude and longer duration (≥12 months) in females versus males. Furthermore, increases in anxiety-like behavior and IL-6 were female-specific. The effect of COMT genotype × stress interactions on pain, IL-6, and IL-17A was validated in a cohort of 549 patients with CPPCs, demonstrating clinical relevance. Last, we assessed the predictive validity of the model for analgesic screening and found that it successfully predicted the lack of efficacy of minocycline and the CB2 agonist GW842166X, which were effective in spared nerve injury and complete Freund's adjuvant models, respectively, but failed in clinical trials. Yet, pain in the CPPC model was alleviated by the beta-3 adrenergic antagonist SR59230A. Thus, the CPPC mouse model reliably recapitulates clinically and biologically relevant features of CPPCs and may be implemented to test underlying mechanisms and find new therapeutics.

The antioxidant effect of tetrahedral framework nucleic acid-based delivery of small activating RNA targeting DJ-1 on retinal oxidative stress injury.

Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are the world's leading causes of blindness. The retinal pigment epithelium (RPE) and vascular endothelial cell exposed to oxidative stress is the major cause of AMD and DR. DJ-1, an important endogenous antioxidant, its overexpression is considered as a promising antioxidant treatment for AMD and DR. Here, we modified the tetrahedral frame nucleic acids (tFNAs) with DJ-1 saRNAs as a delivery system, and synthesized a novel nanocomplex (tFNAs-DJ-1 saRNAs). In vitro studies show that tFNAs-DJ-1 saRNAs can efficiently transfer DJ-1 saRNAs to human umbilical vein endothelial cells (HUVECs) and ARPE-19s, and significantly increased their cellular DJ-1 level. Reactive oxygen species expression in H2O2-treated HUVECs and ARPE-19s were decreased, cell viability was enhanced and cell apoptosis were inhibited when tFNAs-DJ-1 saRNAs were delivered. Moreover, tFNAs-DJ-1 saRNAs preserved mitochondrial structure and function under oxidative stress conditions. In the aspect of molecular mechanism, tFNAs-DJ-1 saRNAs activated Erk and Nrf2 pathway, which might contribute to its protective effects against oxidative stress damage. To conclude, this study shows the successfully establishment of a simple but effective delivery system of DJ-1 saRNAs associated with antioxidant effects in AMD and DR, which may be a promising agent for future treatment in oxidative stress-related retinal disorders.

Hesperidin ameliorates H2O2-induced bovine mammary epithelial cell oxidative stress via the Nrf2 signaling pathway

BackgroundHesperidin is a citrus flavonoid with anti-inflammatory and antioxidant potential. However, its protective effects on bovine mammary epithelial cells (bMECs) exposed to oxidative stress have not been elucidated.ResultsIn this study, we investigated the effects of hesperidin on H2O2-induced oxidative stress in bMECs and the underlying molecular mechanism. We found that hesperidin attenuated H2O2-induced cell damage by reducing reactive oxygen species (ROS) and malondialdehyde (MDA) levels, increasing catalase (CAT) activity, and improving cell proliferation and mitochondrial membrane potential. Moreover, hesperidin activated the Keap1/Nrf2/ARE signaling pathway by inducing the nuclear translocation of Nrf2 and the expression of its downstream genes NQO1 and HO-1, which are antioxidant enzymes involved in ROS scavenging and cellular redox balance. The protective effects of hesperidin were blocked by the Nrf2 inhibitor ML385, indicating that they were Nrf2 dependent.ConclusionsOur results suggest that hesperidin could protect bMECs from oxidative stress injury by activating the Nrf2 signaling pathway, suggesting that hesperidin as a natural antioxidant has positive potential as a feed additive or plant drug to promote the health benefits of bovine mammary.Graphical

Returning to Sport: A Level-Based Guide for Women’s Artistic Developmental Program Gymnasts

  Female artistic gymnasts, defined as gymnasts who compete in the vault, uneven parallel bars, balance beam, and floor events, may be affected by a wide variety of acute and overuse injuries throughout their athletic careers. Returning these athletes to their sport safely after an injury requires detailed knowledge of the various events in which they compete as well as a familiarity with what is expected of these gymnasts at the various levels of training and competition. Despite the complexity described above, there are few published resources to help providers guide the female artistic gymnast back to sport after injury. Therefore, we developed two purposes for this paper: (1) to review important concepts regarding return to play (RTP) in women’s artistic gymnastics and (2) to add to the existing literature on RTP in women’s gymnastics by providing RTP protocols that consider a gymnast’s training level as well as injured body area.

Screening for Relative Energy Deficiency in Sport and Female Athlete Triad: A Survey of Pediatric Sports Medicine Professionals

BACKGROUND: Relative Energy Deficiency in Sport, or RED-S, is a multi-scale physiological response to a mismatch between energy intake and exercise energy expenditure that affects up to 50% of adolescent athletes. RED-S symptomology was first described as the Female Athlete Triad (the Triad) and includes specifically low energy availability with or without disordered eating, menstrual dysfunction, and low bone mineral density. Despite the wide impact of RED-S/the Triad, there is a lack of standardization of screening in adolescent athletes. Therefore, the purpose of this study was to assess if there are differences in practitioner demographics when screening for RED-S/the Triad in adolescent athletes. In addition, we sought to assess if providers’ screening habits differ based on specific patient characteristics.  METHODS: We conducted a cross-sectional online questionnaire of members of the Pediatric Research in Sports Medicine (PRiSM) Society. PRiSM is an interdisciplinary group of professionals who are dedicated to advancing the research and medical care of young athletes. The questionnaire assessed screening tools that members used to assess for RED-S/the Triad, practices implemented when providers were concerned for RED-S/the Triad, demographic data, and type of training. RESULTS: Of 389 PRiSM members, 60 completed the survey and were included in subsequent analyses (15% response rate). Most participants were primary care sports medicine physicians (37%), orthopaedic surgeons (27%), or physical therapists (23%), and about half of respondents identified as a cis gender woman (55%). There was a trend toward more women screening for RED-S routinely than men (55% vs. 33%: p=0.10), and orthopaedic surgeons were less likely to screen than other specialties (25% vs. 52%, p = 0.06). Eating disorders (88%), menstrual dysfunction (76%), and bone stress injury (74%) were reported as specific red flags that make providers screen for RED-S/the Triad. Participants reported that lack of time (57%) and lack of resources (37%) were barriers to screen for RED-S/the Triad. The most commonly utilized tools to screen for RED-S/the Triad were the Female Athlete Screening Tool (FAST), Female Athlete Triad Risk Scale, Female Athlete Triad Consensus Panel Screening questions, and RED-S Specific Screening Tool (RST). CONCLUSION: Orthopaedic surgeons were less likely than other health care professionals to screen for RED-S/the Triad. Barriers that prevent healthcare providers from screening for RED-S/the Triad included limited time and resources. By describing current practices, we have identified gaps and areas of need to enhance screening for RED-S/the Triad across multiple sports medicine disciplines.

Hydrogen-rich solution alleviates acute radiation pneumonitis by regulating oxidative stress and macrophages polarization.

This study was aimed to investigate the effect of hydrogen-rich solution (HRS) on acute radiation pneumonitis (ARP) in rats. The ARP model was induced by X-ray irradiation. Histopathological changes were assessed using HE and Masson stains. Inflammatory cytokines were detected by ELISA. Immunohistochemistry and flow cytometry were performed to quantify macrophage (CD68) levels and the M2/M1 ratio. Western blot analysis, RT-qPCR, ELISA and flow cytometry were used to evaluate mitochondrial oxidative stress injury indicators. Immunofluorescence double staining was performed to colocalize CD68/LC3B and p-AMPK-α/CD68. The relative expression of proteins associated with autophagy activation and the adenosine 5'-monophosphate-activated protein kinase/mammalian target of rapamycin/Unc-51-like kinase 1 (AMPK/mTOR/ULK1) signaling pathway were detected by western blotting. ARP decreased body weight, increased the lung coefficient, collagen deposition and macrophage infiltration and promoted M1 polarization in rats. After HRS treatment, pathological damage was alleviated, and M1 polarization was inhibited. Furthermore, HRS treatment reversed the ARP-induced high levels of mitochondrial oxidative stress injury and autophagy inhibition. Importantly, the phosphorylation of AMPK-α was inhibited, the phosphorylation of mTOR and ULK1 was activated in ARP rats and this effect was reversed by HRS treatment. HRS inhibited M1 polarization and alleviated oxidative stress to activate autophagy in ARP rats by regulating the AMPK/mTOR/ULK1 signaling pathway.

P2X7 receptor: A receptor closely linked with sepsis-associated encephalopathy.

Sepsis is defined as a dysregulated host response to infection resulting in life-threatening organ dysfunction. Sepsis-associated encephalopathy (SAE) is the main manifestation of sepsis. Inflammation, peroxidation stress injury, and apoptosis are the main factors involved in the pathogenesis of SAE. A growing body of evidence has proved that P2X7 receptor (P2X7R), a cationic channel receptor that is widely distributed in the body, plays a major role in the occurrence and development of inflammatory injury. Therefore, this review mainly describes the activation of P2X7R in sepsis, which leads to the recruitment of inflammatory cells to the cerebral vasculature, the destruction of the blood-brain barrier, the activation of microglial cells in the brain, the apoptosis of brain cells, and other damage processes. This review also illustrates the potential therapeutic value of P2X7R inhibition in SAE.

AP39, a novel mitochondria-targeted hydrogen sulfide donor ameliorates doxorubicin-induced cardiotoxicity by regulating the AMPK/UCP2 pathway.

Doxorubicin (DOX) is a broad-spectrum, highly effective antitumor agent; however, its cardiotoxicity has greatly limited its use. Hydrogen sulfide (H2S) is an endogenous gaseous transmitter that exerts cardioprotective effects via the regulation of oxidative stress and apoptosis and maintenance of mitochondrial function, among other mechanisms. AP39 is a novel mitochondria-targeted H2S donor that, at appropriate concentrations, attenuates intracellular oxidative stress damage, maintains mitochondrial function, and ameliorates cardiomyocyte injury. In this study, DOX-induced cardiotoxicity models were established using H9c2 cells and Sprague-Dawley rats to evaluate the protective effect of AP39 and its mechanisms of action. Both in vivo and in vitro experiments showed that DOX induces oxidative stress injury, apoptosis, and mitochondrial damage in cardiomyocytes and decreases the expression of p-AMPK/AMPK and UCP2. All DOX-induced changes were attenuated by AP39 treatment. Furthermore, the protective effect of AP39 was significantly attenuated by the inhibition of AMPK and UCP2. The results suggest that AP39 ameliorates DOX-induced cardiotoxicity by regulating the expression of AMPK/UCP2.

Low-field magnetic resonance imaging of sagittal groove disease of the proximal phalanx in non-racing sport horses.

Injuries of the sagittal groove of the proximal phalanx (P1) in equine athletes are considered to predominantly occur due to chronic bone stress overload. To describe the range of abnormalities that is present in the sagittal groove in a large group of horses diagnosed with sagittal groove disease (SGD) on low-field MRI. Retrospective, cross-sectional. Medical records were searched to identify initial MRI images of horses diagnosed with SGD and these were blindly evaluated using a semi-quantitative grading scheme and novel SGD MRI classification system reflecting potential pathways of pathological progression and severity of stress injury. A total of 132 limbs from 111 horses were included in the study; predominantly warmbloods competing in showjumping (n = 83) and dressage (n = 18). SGD MRI classifications were: 0 (normal, n = 0), 1 (small subchondral defect, n = 2), 2 (osseous densification, n = 28), 3 (subchondral microfissure with osseous densification, n = 7), 4 (bone oedema-like signal within the subchondral ± trabecular bone and ± subchondral microfissure or demineralisation, n = 72), 5 (incomplete macrofissure/fracture, n = 23) and 6 (complete fracture, n = 0). Classification 4c (bone oedema-like signal with demineralisation) and 5 had higher proportions in the plantar third of hindlimbs (3% and 10%, respectively) compared with forelimbs (0% and 0%, respectively). SGD classification and extent of bone oedema-like signal were not significantly different between lame (n = 116) and non-lame limbs (n = 16) (both p > 0.05). Periosteal new bone and oedema-like signal were identified (either confidently or suspected) at the dorsoproximal aspect of P1 in 25% and 39% of limbs, respectively. Inclusion via diagnoses in original MRI reports, variable clinical history, small size of some classification groups. The presence or absence of lameness is not a dependable measure of the severity of SGD. The periosteal oedema-like signal of P1 has not previously been described in MRI of SGD and further supports the concept of bone stress injury.

Development and evaluation of the ARM algorithm: A novel approach to quantify musculoskeletal disorder risk factors in manual wheelchair users in the real world.

This study aimed to develop and evaluate the ARM (arm repetitive movement) algorithm using inertial measurement unit (IMU) data to assess repetitive arm motion in manual wheelchair (MWC) users in real-world settings. The algorithm was tested on community data from four MWC users with spinal cord injury and compared with video-based analysis. Additionally, the algorithm was applied to in-home and free-living environment data from two and sixteen MWC users, respectively, to assess its utility in quantifying differences across activities of daily living and between dominant and non-dominant arms. The ARM algorithm accurately estimated active and resting times (>98%) in the community and confirmed asymmetries between dominant and non-dominant arm usage in in-home and free-living environment data. Analysis of free-living environment data revealed that the total resting bout time was significantly longer (P = 0.049) and total active bout time was significantly shorter (P = 0.011) for the non-dominant arm. Analysis of active bouts longer than 10 seconds showed higher total time (P = 0.015), average duration (P = 0.026), and number of movement cycles per bout (P = 0.020) for the dominant side. These findings support the feasibility of using the IMU-based ARM algorithm to assess repetitive arm motion and monitor shoulder disorder risk factors in MWC users during daily activities.

Modulation efficiency of clove oil nano-emulsion against genotoxic, oxidative stress, and histological injuries induced via titanium dioxide nanoparticles in mice

Titanium dioxide nanoparticles (TiO2-NPs) have found wide applications in medical and industrial fields. However, the toxic effect of various tissues is still under study. In this study, we evaluated the toxic effect of TiO2-NP on stomach, liver, and kidney tissues and the amelioration effect of clove oil nanoemulsion (CLV-NE) against DNA damage, oxidative stress, pathological changes, and the apoptotic effect of TiO2-NPs. Four groups of male mice were subjected to oral treatment for five consecutive days including, the control group, the group treated with TiO2-NPs (50 mg/kg), the group treated with (CLV-NE) (5% of the MTD), and the group treated with TiO2-NPs plus CLV-NE. The results revealed that the treatment with TiO2-NPs significantly caused DNA damage in the liver, stomach, and kidney tissues due to increased ROS as indicated by the reduction of the antioxidant activity of SOD and Gpx and increased MDA level. Further, abnormal histological signs and apoptotic effect confirmed by the significant elevation of p53 expression were reported after TiO2-NPs administration. The present data reported a significant improvement in the previous parameters after treatment with CLV-NE. These results showed the collaborative effect of the oils and the extra role of nanoemulsion in enhancing antioxidant effectiveness that enhances its disperse-ability and further promotes its controlled release. One could conclude that CLV-NE is safe and can be used as a powerful antioxidative agent to assess the toxic effects of the acute use of TiO2-NPs.

A cross-sectional study to estimate the prevalence of text neck syndrome among medical students in a tertiary care teaching hospital in Andhra Pradesh

Abstract Background: The overuse of handheld mobile technology is leading to detrimental effects on the human body, one of which is text neck syndrome (TNS). This refers to neck pain and disability due to repetitive stress injury. Text neck can cause symptoms such as neck pain, shoulder pain, upper back pain, and increased curvature of spine. Objectives: The objective of this study was to estimate the prevalence, awareness, frequency, severity, and radiation of pain experienced by medical students and to determine the association between the duration of gadget usage and the severity of pain. Methodology: In this cross-sectional study, 1000 medical students were surveyed regarding the awareness and prevalence of TNS. The questionnaire consisted of 16 questions which included, demographic details and education details, and questions related to frequency, duration, purpose and time of usage, and position during use. Results: Out of 1000 students, 500 of the respondents did not know of TNS, 10 knew the term in detail, 160 were familiar with the term, and 330 had only heard of the term. The usage of electronic gadgets increased with age and was found statistically significant with P &lt; 0.05. A significant positive association (P &lt; 0.05) was found between the duration of usage of gadgets and the severity of pain. Conclusion: TNS is a real problem, and the students are not aware of the problem. The study showed that the longer the duration of gadget usage, the more adverse the symptoms.

Stress Fractures and Overuse Injuries in Children and Adolescents

There is an intricate connection between physical activity, bone health, and the susceptibility to stress fractures and overuse injuries. Physical activity has a positive impact on bone strength while a sedentary lifestyle can lead to a heightened risk for injury. The rise of early sports specialization has led to a substantial increase in overuse injuries, particularly in individual sports.Bone Stress Injuries (BSI) represent a category of overuse injuries closely linked to single sport specialization. BSI involves a spectrum of altered bone mechanics, ranging from edema of periosteum, endosteum, and bone; potentially leading to partial or full cortical breaks. This condition is prevalent in high-level athletes and encompasses stress reactions and fractures, resulting from an imbalance between injury creation and repair. Up to 20% of adolescents are affected, with the tibia being the most common location, predominantly occurring in athletes aged 15-25. A holistic approach integrating both physical and nutritional aspects is warranted to ensure sustained musculoskeletal health across diverse pediatric and adolescent groups and athletic endeavors. Key Concepts1.Early and single sports specialization has a substantial impact on overuse injuries.2.Bone stress injuries are common in high level athletes resulting from an imbalance between creation and repair of injury.3.Relative energy deficiency in sports (REDS) is related to a higher risk for recurrent Bone Stress Injuries.4.Athletes that are lacking Vitamin D are found to have an increased risk for stress fractures.