acute injury
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Abstract Knee joint is an important part of human body. People with poor knee condition generally have limited physical movement, rendering to mental stress and agony. Knee pain can be categorized into three groups, known as acute injury, chronic injury and medical condition. Current technology to support the knee diagnosis and treatment procedures are limited to the use of manual goniometer, x-ray and magnetic resonance imaging (MRI). Alternative devices with continuous measurement capability for knee monitoring are minimum at this time, mainly due to the difficulties to cover the wide angle of the knee flexion. X-ray and MRI technologies are useful to have some insight on the knee problem, but they are not applicable for continuous monitoring. Aside from being expensive for general use of MRI, x-ray on the other hand can cause short-term side effects due to radiation exposure. The aim of this paper is to demonstrate the use of optical sensor integrated with mechanical gear system as a knee monitoring device. A plastic compartment, made by using 3D printer is used to place the sensor and the gear system. The design of the overall device allows direct attachment on a knee brace for easy placement on the knee. Based on current study, the proposed sensor has a range of motion between 0 deg. to 160 deg., 0.08 deg. resolution as well as support continuous monitoring of the knee. The sensor performance has been demonstrated for gait motion, ascending and descending stairs, sit-to-stand movement and maximum knee flexion applications.

ObjectiveTo contrast the presentation and recovery of acute concussion and post-concussion syndrome (PCS) in order to identify factors for PCS prevention.BackgroundConcussions are classified as acute (<90 days to resolution) or post-concussion syndrome (PCS, = 90 days to resolution). PCS poses a great burden to the individual and to public health. Further investigation is warranted for understanding the progression of acute concussion to PCS and potential mitigating strategies.Design/MethodsRetrospective chart review of concussion patients seen by Sports Medicine and Exercise Physicians over a five-year period. Outcome measures included demographics, wait-times, injury mechanisms, Sport Concussion Assessment Tool (SCAT) scores, management plans, and recovery timelines.ResultsFour hundred ninety-six patients (289 male/207 female, 19.7 ± 9.4 years) presented with 561 concussions in 1,471 visits. Acute concussions accounted for 88% of injuries and 12% were PCS. Females (RR = 1.4) and adults = 25 years (RR = 3.6) were more likely to be diagnosed with PCS. In both, injuries occurred most commonly in hockey, football, and soccer. Family physicians were the most frequent referral provider (58% acute, 76% PCS). Median injury-appointment time was 11.0 days (acute) compared to 182.0 days (PCS). Initial total SCAT symptom score was significantly greater (p < 0.001) in PCS (56.0 ± 33.0) compared to acute concussion (39.8 ± 31.9). Therapies (i.e., referral, medication, intervention) were prescribed in 44% of acute injury visits compared to 73% of PCS visits. Recovery timelines for return to work, school, and sport were significantly longer in PCS patients than in those with acute concussions (p < 0.05).ConclusionsOur findings of the incidence/presentation of PCS agree with previous literature. Athletes who are female and/or = 25 years may be at greater risk for PCS progression, requiring close monitoring and further injury prevention efforts. Considering the number of referrals from family physicians, further concussion education may better optimize initial management and shorten delays in seeking necessary sports medicine consultation.

Netrins belong to the family of laminin-like secreted proteins, which guide axonal migration and neuronal growth in the developing central nervous system. Over the last 20 years, it has been established that netrin-1 acts as a chemoattractive or chemorepulsive cue in diverse biological processes far beyond neuronal development. Netrin-1 has been shown to play a central role in cell adhesion, cell migration, proliferation, and cell survival in neuronal and non-neuronal tissue. In this context, netrin-1 was found to orchestrate organogenesis, angiogenesis, tumorigenesis, and inflammation. In inflammation, as in neuronal development, netrin-1 plays a dichotomous role directing the migration of leukocytes, especially monocytes in the inflamed tissue. Monocyte-derived macrophages have long been known for a similar dual role in inflammation. In response to pathogen-induced acute injury, monocytes are rapidly recruited to damaged tissue as the first line of immune defense to phagocyte pathogens, present antigens to initiate the adaptive immune response, and promote wound healing in the resolution phase. On the other hand, dysregulated macrophages with impaired phagocytosis and egress capacity accumulate in chronic inflammation sites and foster the maintenance—and even the progression—of chronic inflammation. In this review article, we will highlight the dichotomous roles of netrin-1 and its impact on acute and chronic inflammation.

The thymus, the primary site of T cell development, is extremely sensitive to insult but also harbors tremendous capacity for repair. Using single cell sequencing of thymic structural cells, as well as functional and structural analyses, we revealed distinct regenerative programs by endothelial and mesenchymal subsets after injury that stimulated epithelial repair; the compartment primarily supporting T cell development. Thymic function not only declined over lifespan, contributing to immune aging, but the capacity of the thymus to regenerate after damage also declined in old mice. This could be attributed to an inability of the old microenvironment to induce reparative programs; leading to reduced ability to restore tissue structure and function. These findings provide a detailed framework for the response of structural cells to aging and acute damage, which could have considerable implications for our understanding of aging immunity and recovery from treatments such as chemotherapy and bone marrow transplant.

Rotator cuff pathology is usual, and the ailment's natural history suggests that tears enlarge with age. Rotator cuff tears are a familiar origin of pain and ailment in the shoulder. The research on treatment of rotator cuff tears is mixed. The aim of this review is to evaluate the evidence regarding the effectiveness of physiotherapy in lowering pain and enhance shoulder function in patients with symptomatic rotator cuff tears. Rotator cuff injuries are typically followed by a gradual onset of pain, but they can also be the result of an acute injury. Chronicity, underlying anatomic and physical factors, age, and the presence and severity of tendon tears all influence how rotator cuff conditions are managed. Conservative care, such as physical therapy, is typically used as the first line of defence, but surgical repair may be required later on. Rotator cuff (RC) tears can range from partial to full thickness tears of a single tendon to massive cuff tears. Rotator cuff tearing can be caused by glenohumeral trauma as well as pathological process. As a result, Treatment necessitates a diligent diagnosis as well as a distinguished approach that considers morphological and patient-specific effects. The therapeutic approach is determined by the patient's pathogenicity, tear morphology, clinical symptoms, and functional demands. The current case is about an 51 year old male who was admitted to the hospital with tear injury to right shoulder due to fall from truckmuscle strength and range of motion were main focus of physiotherapy intervention. The prime goal of this case study was to assess the patient’s response to physiotherapy for reinforcement and functional task.

Background: Acute kidney injury (AKI) occurs frequently in critically ill patients and is associated with adverse outcomes. Cellular mechanisms underlying AKI and kidney cell responses to injury remain incompletely understood. Methods: We performed single-nuclei transcriptomics, bulk transcriptomics, molecular imaging studies, and conventional histology on kidney tissues from 8 individuals with severe AKI (stage 2 or 3 according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria). Specimens were obtained within 1-2 hours after individuals had succumbed to critical illness associated with respiratory infections, with 4 of 8 individuals diagnosed with COVID-19. Control kidney tissues were obtained post-mortem or after nephrectomy from individuals without AKI. Results: High-depth single cell-resolved gene expression data of human kidneys affected by AKI revealed enrichment of novel injury-associated cell states within the major cell types of the tubular epithelium, in particular in proximal tubules, thick ascending limbs and distal convoluted tubules. Four distinct, hierarchically interconnected injured cell states were distinguishable and characterized by transcriptome patterns associated with oxidative stress, hypoxia, interferon response, and epithelial-to-mesenchymal transition, respectively. Transcriptome differences between individuals with AKI were driven primarily by the cell type-specific abundance of these four injury subtypes rather than by private molecular responses. AKI-associated changes in gene expression between individuals with and without COVID-19 were similar. Conclusion: The study provides an extensive resource of the cell type-specific transcriptomic responses associated with critical illness-associated AKI in humans, highlighting recurrent disease-associated signatures and inter-individual heterogeneity. Personalized molecular disease assessment in human AKI may foster the development of tailored therapies.

ObjectivesTo define incidence and injury patterns of International Ski Federation (FIS) World Cup (WC) women ski jumpers over three seasons.MethodsSki jump athletes competing in the Women’s FIS WC were recruited for prospective injury surveillance from 2017–2018 to 2019–2020. Team representatives recruited the athletes annually and prospectively recorded all injuries requiring medical attention. Retrospective end-of-season interviews corroborated injury surveillance. Medical doctors collected and processed the data. The 4-month competitive season was used to calculate the annual incidence of injuries per 100 athletes per season. Injury type, location, severity and aetiology were reported.ResultsAthletes from 19 nations were enrolled equalling 205 athlete-seasons. Mean age was 21.2 years (SD=3.8). Thirty-nine injury events resulted in 54 total injuries (26.3 injuries/100 athletes/season). Injuries were mostly acute (83%) and occurred on the ski jump hill (78%). The most common injury location was the knee (n=18, 33%). Crash landings were the most common cause of injury events (70%). Nearly half of the acute ski jump injury events occurred in snowy, windy or cloudy conditions (44%) and/or during telemark landings (46%), and most jumps (96%) were shorter than hill size. One third of the injuries were severe, and 78% of severe injuries involved the knee.ConclusionAcute injury events occur relatively frequently in elite women ski jumpers, most resulting in time-loss from sport and a significant proportion involving serious knee injuries. Crash landing was the leading cause of injury. This baseline information can be used to guide and evaluate future efforts at injury prevention.

Sepsis is a systemic inflammatory response syndrome caused by infection, following with acute injury to multiple organs. Sepsis-induced acute kidney injury (AKI) is currently recognized as one of the most severe complications related to sepsis. The pathophysiology of sepsis-AKI involves multiple cell types, including macrophages, vascular endothelial cells (ECs) and renal tubular epithelial cells (TECs), etc. More significantly, programmed cell death including apoptosis, necroptosis and pyroptosis could be triggered by sepsis in these types of cells, which enhances AKI progress. Moreover, the cross-talk and connections between these cells and cell death are critical for better understanding the pathophysiological basis of sepsis-AKI. Mitochondria dysfunction and oxidative stress are traditionally considered as the leading triggers of programmed cell death. Recent findings also highlight that autophagy, mitochondria quality control and epigenetic modification, which interact with programmed cell death, participate in the damage process in sepsis-AKI. The insightful understanding of the programmed cell death in sepsis-AKI could facilitate the development of effective treatment, as well as preventive methods.