Centre de formation et physiothérapie de Lutry

Centre de formation et physiothérapie de Lutry Centre de formation et physiothérapie

12/02/2026
11/02/2026

𝗦𝗲𝗹𝗲𝗰𝘁𝗶𝘃𝗲 𝗺𝘂𝘀𝗰𝗹𝗲 𝘄𝗲𝗮𝗸𝗻𝗲𝘀𝘀 𝗶𝗻 𝗔𝗰𝗵𝗶𝗹𝗹𝗲𝘀 𝘁𝗲𝗻𝗱𝗶𝗻𝗼𝗽𝗮𝘁𝗵𝘆: 𝗶𝘀 𝗶𝘁 𝘁𝗶𝗺𝗲 𝘁𝗼 𝗹𝗼𝗼𝗸 𝗯𝗲𝘆𝗼𝗻𝗱 𝘁𝗵𝗲 𝘀𝗼𝗹𝗲𝘂𝘀?

📘 A brand-new review article by Fernandes and colleagues (https://pubmed.ncbi.nlm.nih.gov/41664282/) revisits the neuromuscular mechanisms underlying Achilles tendinopathy and questions the traditional soleus-centric explanation of plantarflexor deficits. While earlier models attributed reduced plantarflexion capacity primarily to soleus weakness, recent neurophysiological and biomechanical evidence suggests a more selective impairment within the triceps surae.

⬇️In particular, individuals with Achilles tendinopathy consistently demonstrate reduced neural drive, lower activation, and diminished force contribution of the gastrocnemius lateralis, especially during submaximal contractions (https://pubmed.ncbi.nlm.nih.gov/36418751/, https://pubmed.ncbi.nlm.nih.gov/40349309/). In contrast, soleus motor unit behaviour and force contribution appear largely preserved and may even increase as a compensatory response.

🦶 This altered coordination has important mechanical implications (graphic). Because the Achilles tendon is composed of distinct subtendons arising from each triceps surae muscle, changes in muscle-specific force sharing can modify how strain is distributed within the tendon. A reduced contribution from the gastrocnemius lateralis is therefore likely to create non-uniform strain patterns and elevated interfascicular shear stress, conditions associated with localised overload, microdamage, and maladaptive tendon remodelling. Structural findings such as selective gastrocnemius lateralis atrophy, altered muscle architecture, and reduced subtendon stiffness further support this mechanistic link. Nevertheless, whether these neuromuscular alterations precede tendon pathology or develop as protective adaptations to pain remains unresolved.

💡From a practical perspective, the review calls for a reassessment of current clinical practice. Rehabilitation approaches that focus predominantly on soleus strengthening—such as seated calf raises—may fail to address relevant muscle-specific deficits. Strategies that preferentially target the gastrocnemius lateralis, 𝗶𝗻𝗰𝗹𝘂𝗱𝗶𝗻𝗴 𝘀𝘁𝗿𝗮𝗶𝗴𝗵𝘁-𝗸𝗻𝗲𝗲 𝗹𝗼𝗮𝗱𝗶𝗻𝗴, 𝗶𝗻𝘄𝗮𝗿𝗱 𝗳𝗼𝗼𝘁 𝗽𝗼𝘀𝗶𝘁𝗶𝗼𝗻𝗶𝗻𝗴 𝗱𝘂𝗿𝗶𝗻𝗴 𝗽𝗹𝗮𝗻𝘁𝗮𝗿𝗳𝗹𝗲𝘅𝗶𝗼𝗻 (https://pubmed.ncbi.nlm.nih.gov/39985716/, https://pubmed.ncbi.nlm.nih.gov/32735428/), or biofeedback-guided activation training, may help restore more balanced force sharing within the triceps surae. However, these interventions remain hypothesis-driven, and their effectiveness for improving symptoms and function has yet to be established.

07/02/2026

Just published in “Clinical Journal of Pain” 🔥

𝗣𝗮𝘁𝗵𝗼𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝘆 𝗼𝗳 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗣𝗮𝗶𝗻

📘 Lyndon (2026, https://pubmed.ncbi.nlm.nih.gov/41614224/)

🤕 Chronic pain, defined as pain persisting beyond normal tissue healing, affects around 20% of the population and represents a major global health burden. Unlike acute pain, it no longer serves a protective function but reflects a maladaptive transformation of nociceptive processing shaped by biological, psychological, and social factors

1️⃣ Pathophysiologically, the chronification cascade emerges through interacting stages (s. illustration). It often begins with 𝗽𝗲𝗿𝗶𝗽𝗵𝗲𝗿𝗮𝗹 𝘀𝗲𝗻𝘀𝗶𝘁𝗶𝘀𝗮𝘁𝗶𝗼𝗻, where inflammatory mediators and ion-channel changes lower nociceptor thresholds, amplifying incoming nociceptive signals.

2️⃣ Sustained input then drives 𝗰𝗲𝗻𝘁𝗿𝗮𝗹 𝘀𝗲𝗻𝘀𝗶𝘁𝗶𝘀𝗮𝘁𝗶𝗼𝗻, characterised by spinal and supraspinal hyperexcitability, glial activation, reduced inhibitory control, and synaptic potentiation (“wind-up”). These processes allow pain to persist even in the absence of ongoing tissue injury.

3️⃣ With time, chronic pain induces 𝗺𝗮𝗹𝗮𝗱𝗮𝗽𝘁𝗶𝘃𝗲 𝗻𝗲𝘂𝗿𝗼𝗽𝗹𝗮𝘀𝘁𝗶𝗰 𝗰𝗵𝗮𝗻𝗴𝗲𝘀 in the CNS, altering the structure and function of nociceptive processing. Neuroimaging studies show cortical reorganisation, altered network connectivity, and impaired descending pain modulation, linking nociceptive processing with emotional and cognitive circuits.

⚖️Immune mechanisms play a central role. Neuro-immune crosstalk, driven by cytokines, glial activation, and peripheral immune-cell recruitment, sustains inflammation and neuronal hypersensitivity. Emerging work also implicates the gut microbiome, where dysbiosis may influence pain via immune and metabolic signalling.

🧠 Chronic pain is further shaped by psychosocial context. Stress, mood disorders, trauma exposure, and social adversity modulate neuroendocrine and neurotransmitter systems, altering pain perception and vulnerability. Genetic polymorphisms and epigenetic modifications add another layer, embedding environmental influences into long-term changes in gene expression.

💡Overall, the review frames chronic pain as a systems-level disorder arising from the dynamic interplay of sensitisation, neuroplasticity, immune dysregulation, and lived experience. This integrative perspective helps explain why persistent pain often outlasts its original injury and varies so profoundly between individuals.

03/02/2026

🎙️ FREE Webinar LAST CALL!

Discover what actually makes pain education effective, the challenges we face, and why getting it right matters more than ever.

📅 4 February 2026
⏰ 09:00 London | 19:30 Adelaide
🎟️ Free – https://shorturl.at/qVnlH

Whether you caught the first webinar or you're just joining us, this one's packed with insights that could shift how you approach pain education in practice.

Can't make it live? Register anyway and we'll send you the recording.

See you there! 👋

02/02/2026

Just published 🔥

𝗣𝗮𝗶𝗻 𝗮𝗻𝗱 𝘁𝗵𝗲 𝗶𝗺𝗺𝘂𝗻𝗲 𝘀𝘆𝘀𝘁𝗲𝗺

⚖️ Pain is increasingly understood as a multidimensional phenomenon arising from dynamic interactions between the nervous and immune systems. Early conceptual frameworks framed pain largely as a neurocentric process; however, seminal work in neuroimmunology demonstrated that immune signaling plays a critical role in both the initiation and persistence of pain (https://pubmed.ncbi.nlm.nih.gov/36775098/, https://pubmed.ncbi.nlm.nih.gov/12270950/). Building on this paradigm, recent research has highlighted the importance of neuroinflammation across nociceptive, neuropathic, and nociplastic pain states (https://pubmed.ncbi.nlm.nih.gov/36775098).

📘 A brand-new narrative review by Hodges et al. (2026, https://www.sciencedirect.com/science/article/pii/S2468781225002322) synthesizes current evidence on neuro-immune mechanisms underlying chronic pain and discusses implications for mechanism-based treatment approaches. The authors present a comprehensive narrative review examining how interactions between immune cells and the nervous system contribute to the development and maintenance of chronic pain. Pain should not be viewed solely as a neuronal output but rather as the product of continuous bidirectional signaling between neurons and immune cells across the peripheral and central nervous systems.

📊 Immune mediators—such as cytokines, chemokines, prostaglandins, reactive oxygen species, and autoantibodies—modulate nociceptor excitability at multiple anatomical levels, including peripheral tissues, peripheral nerves, dorsal root ganglia, the spinal cord, and supraspinal brain regions. These neuro-immune interactions differ across pain phenotypes. In neuropathic pain, nerve injury triggers local immune activation that expands along the neuraxis, creating self-sustaining feed-forward loops between immune cells, glia, and hyperexcitable neurons. In nociceptive inflammatory conditions such as rheumatoid arthritis and osteoarthritis, tissue-driven inflammation initially dominates but may progressively transition toward central neuroinflammatory and nociplastic mechanisms.

❎ A key contribution on pain chronicity seems to be a failure of inflammatory resolution rather than mere persistence of inflammation. Immune and glial cells are shown to play dual roles: while early pro-inflammatory responses are essential for tissue repair, insufficient engagement of anti-inflammatory and pro-resolving pathways promotes maladaptive plasticity and long-term pain. Specialized pro-resolving mediators, regulatory immune cells, and anti-inflammatory cytokines (e.g., IL-10) are critical modulators of pain resolution. Pain chronification may be viewed as a failure of anti-inflammatory processes to bring proinflammation to resolution.

🐁The review further discusses translational challenges, noting that much mechanistic knowledge derives from animal models that incompletely capture the complexity of human chronic pain. Nonetheless, emerging human evidence—from tissue studies, transcriptomics, and neuroimaging using PET markers of glial activation —supports a meaningful role of neuroinflammation in clinical pain conditions, particularly nociplastic pain.

💊 Finally, precision pain management strategies that align treatments with dominant neuro-immune mechanisms are needed. Both pharmacological and non-pharmacological interventions (including exercise, diet, and behavioral therapies) are proposed to exert their effects partly through modulation of immune activity. An improved mechanistic classification of pain is essential to matching the right treatment to the right patient and advancing personalized pain care.

📷 Figure: Overview of key neuroimmune processes at the level of the tissues, and the peripheral and central nervous systems.

21/01/2026

Hot off the Press🔥

𝗤𝘂𝗮𝗹𝗶𝘁𝗮𝘁𝗶𝘃𝗲 𝗮𝗻𝗱 𝗾𝘂𝗮𝗻𝘁𝗶𝘁𝗮𝘁𝗶𝘃𝗲 𝘀𝗶𝘁𝘂𝗮𝘁𝗶𝗼𝗻𝗮𝗹 𝗰𝗵𝗮𝗿𝗮𝗰𝘁𝗲𝗿𝗶𝘀𝘁𝗶𝗰𝘀 𝗼𝗳 𝗺𝘂𝘀𝗰𝗹𝗲 𝘀𝘁𝗿𝗮𝗶𝗻𝘀 𝗶𝗻 𝘀𝗽𝗼𝗿𝘁𝘀: 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺𝗮𝘁𝗶𝗰 𝗿𝗲𝘃𝗶𝗲𝘄 𝗮𝗻𝗱 𝗺𝗲𝘁𝗮-𝗮𝗻𝗮𝗹𝘆𝘀𝗶𝘀

📘 A brand-new systematic review and meta-analysis by Finnern and colleagues (2026, https://bjsm.bmj.com/content/early/2026/01/20/bjsports-2025-110327) examined the situational and biomechanical characteristics of indirect and non-contact muscle injuries across a range of sports, with the aim of identifying consistent injury patterns that could inform prevention and clinical practice. Drawing on video-based analyses from 21 studies encompassing 728 injuries, the authors synthesized both qualitative descriptors (such as contact mechanisms and injury-inciting activities) and quantitative measures (including joint positions and movement directions at the assumed moment of injury).

The findings indicate that non-contact mechanisms predominate, accounting for approximately three-quarters of all cases. Injuries most frequently occurred during running or sport-specific actions involving rapid lengthening of the muscle–tendon unit under high levels of active contraction. Despite these shared features, distinct kinematic patterns emerged for different muscle groups. Hamstring injuries were commonly associated with a nearly extended knee and a flexed hip, particularly during late swing or high-speed running. Adductor injuries typically involved rapid hip extension, abduction, and external rotation, often during kicking or reaching movements. Re**us femoris injuries were characterized by concurrent hip flexion and knee extension, while calf injuries most often occurred with the ankle in marked dorsiflexion and the knee close to full extension.

Across team sports, running and kicking were the most prevalent injury-inciting activities, and injuries were distributed relatively evenly between the first and second halves of match play. Methodological quality varied among included studies, though most demonstrated moderate to good rigor in video analysis procedures.

Overall, the review highlights that while general principles of muscle strain causation—such as high muscle activation at long muscle lengths—apply broadly, injury patterns show meaningful variation by muscle group and sport context. The authors conclude that integrating these situational and biomechanical insights into training design, clinical assessment, and prevention strategies may improve the effectiveness of interventions aimed at reducing muscle injury incidence.

📸 Illustrations of situational patterns for indirect and non- contact muscle injuries (muscle strains). Please note that only a selection of the most common injury patterns based on included studies is illustrated (acknowledging the predominance of studies investigating male football players).

▶️ (A-I) Hamstring (running/sprinting): hamstring injuries are frequently seen during high- speed running or acceleration phases. Modelling studies and case reports identified the open-chain late swing phase as being most vulnerable to injury. During this phase of the gait cycle, the muscle-tendon unit of the biceps femoris lengthens. However, confirmation of this finding appraising systematic real- world video data is yet to be done, and the specific running phase in which athletes are most vulnerable to hamstring injury remains a matter of debate.

▶️ (A- II) Hamstring (closed kinetic chain lunging injury pattern): the athlete performs a decelerating closed kinetic chain manoeuvre. At the assumed time of injury, the knee joint is close to full extension, the hip joint is in a flexed position (ie, lunging position).

▶️ (A- III) Hamstring (open-chain kicking or reaching injury pattern): open-chain injury patterns are typically observed during kicking or reaching manoeuvres. Injury kinematics comprise a flexed hip joint combined with an extending knee joint movement.

▶️ (B- I) Adductor (closed-chain change of direction injury pattern): changes of directions are common situational patterns for adductor muscle injuries. The athlete performs a change of direction to catch a ball opposite to the moving direction. At the assumed time of injury, the injured leg is abducted and externally rotated while the adductor muscles are simultaneously activated to perform the deceleration and change of direction manoeuvre.

▶️ (B- II) Adductor (closed-chain or open-chain reaching injury pattern): the athlete performs a reaching manoeuvre with the non-injured leg towards the ball. At the assumed time of injury, the adductor muscle- tendon unit of the injury leg is lengthening due to hip extension, hip abduction and hip external rotation.

▶️ (B- III) Adductor (open-chain kicking injury pattern): this injury pattern shows similar injury kinematics (including hip abduction and external rotation) but is an open- chain injury pattern due to the player’s intention of kicking a ball with the injury-sided leg.

▶️ (C–) Quadriceps (open- chain kicking injury pattern): a commonly observed injury kinematic of quadriceps injuries comprises a flexing hip joint and extending knee joint movement (ie, kicking manoeuvre).

▶️ (D- I) Calf (closed-chain stepping back injury pattern): in the illustrated example, the athlete is setting off to take a run (e.g, by performing a back- step manoeuvre). These manoeuvres are seen in running or football and are common in I racquet sports (leading gastrocnemius muscle injury to be named ‘tennis leg’) or basketball. The underlying joint movements are ankle dorsiflexion and knee extension, thereby lengthening the calf muscle tendon unit. At the assumed time of injury, the knee is close to full extension, the ankle in >10° dorsiflexion and the foot in external rotation.

20/01/2026

People with acute have concerns that may not be addressed by guideline-recommended advice 😔

This is drawn from the study published in the September 2024 issue of JOSPT

Infographic ➡️ https://ow.ly/6yVL50XYtc1
Full article ➡️ https://ow.ly/7huY50XYtbY

18/01/2026

Hot off the Press 🔥

𝗢𝘀𝘁𝗲𝗼𝗮𝗿𝘁𝗵𝗿𝗶𝘁𝗶𝘀 𝗮𝘀 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺𝗶𝗰 𝗱𝗶𝘀𝗲𝗮𝘀𝗲

Historically, osteoarthritis (OA) has been narrowly understood as an unavoidable, cartilage-centric, wear-and-tear disease that is inevitable with ageing (https://pubmed.ncbi.nlm.nih.gov/22392533/). Growing evidence from both preclinical and clinical research, however, challenges this narrow perspective. Instead, OA is increasingly understood as a systemic condition that affects the whole person, shaped by ongoing interactions between joint tissues and biological processes throughout the body (https://pubmed.ncbi.nlm.nih.gov/41339496/).

⚖️Rather than being limited to mechanical damage, OA involves a combination of disrupted cellular metabolism, breakdown of the extracellular matrix, impaired repair mechanisms, and activation of innate immune pathways. These processes are not confined to the joint itself. They are strongly influenced by broader systemic factors, including ageing, obesity, sex-specific biology, metabolic disturbances, chronic inflammation, and inter-organ communication (https://pubmed.ncbi.nlm.nih.gov/30209413/, https://pubmed.ncbi.nlm.nih.gov/31621562/, figure 1 top). This broader view also helps explain a common clinical observation: structural joint damage seen on imaging often correlates poorly with pain severity. Pain in OA appears to be shaped not only by local tissue pathology but also by central and systemic mechanisms such as pain sensitization and psychosocial influences (https://pubmed.ncbi.nlm.nih.gov/31621573/, https://pubmed.ncbi.nlm.nih.gov/30307131/).

📘 A brand-new review by Collins and colleagues (https://pubmed.ncbi.nlm.nih.gov/41339496/) emphasizes the role of adipose tissue and metabolic dysfunction as active drivers of OA, rather than passive consequences of increased joint loading. Experimental studies show that adipokines, including leptin (a satiety hormone), as well as components of the complement system, can directly promote both joint damage and pain (https://pubmed.ncbi.nlm.nih.gov/32078923/, https://pmc.ncbi.nlm.nih.gov/articles/PMC5341385/). Notably, obesity-related OA can develop even in the absence of excessive mechanical stress on the joints (https://pubmed.ncbi.nlm.nih.gov/33443201/).

💪Loss of muscle mass and conditions such as sarcopenic obesity further increase the risk of OA and contribute to functional decline, highlighting the importance of body composition rather than body weight alone (https://pubmed.ncbi.nlm.nih.gov/23312414/, https://pubmed.ncbi.nlm.nih.gov/40746030/).

💊 The authors also stress the need to move beyond a one-size-fits-all view of OA by applying phenotyping and endotyping approaches. Identifying distinct biological subtypes of OA may help explain why disease-modifying osteoarthritis drugs (DMOADs) have repeatedly failed in clinical trials (https://pubmed.ncbi.nlm.nih.gov/41339496/). Factors such as heterogeneous patient populations, treatment initiation at advanced disease stages, and an overemphasis on single tissues or pathways have likely limited therapeutic success (https://pubmed.ncbi.nlm.nih.gov/29609224/). Encouragingly, systemically acting treatments—including GLP-1 receptor agonists, metformin, and anti-inflammatory drugs originally developed for metabolic or cardiovascular conditions—are emerging as promising options for specific OA subgroups (https://pubmed.ncbi.nlm.nih.gov/39476339/, https://pubmed.ncbi.nlm.nih.gov/40179178/).

🔄 In addition to the concept that systemic factors can influence OA, there is growing evidence that shows the effects of knee pain and damage on the rest of the organism, illustrating a bidirectional relationship. This concept has also been demonstrated in studies showing that knee injury and pain might cause changes to the cardiovascular system (https://www.oarsijournal.com/article/S1063-4584(24)00059-1/fulltext) , brain (https://pubmed.ncbi.nlm.nih.gov/36593507/, https://pubmed.ncbi.nlm.nih.gov/36374499/) adipose tissue (https://pubmed.ncbi.nlm.nih.gov/40279436/) and other organ systems (figure 1, bottom). These data suggest that systemic factors can drive OA and, in turn, OA can have systemic consequences (figure)). This bidirectional relationship reinforces the idea of OA as a chronic, multi-organ condition rather than an isolated joint disorder.

17/01/2026

Hot off the Press 🔥

𝗗𝗼𝗲𝘀 𝘁𝗵𝗲 𝗦𝗶𝘇𝗲 𝗼𝗳 𝗖𝗲𝗿𝘃𝗶𝗰𝗮𝗹 𝗗𝗶𝘀𝗰 𝗛𝗲𝗿𝗻𝗶𝗮𝘁𝗶𝗼𝗻 𝗔𝗳𝗳𝗲𝗰𝘁 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗣𝗮𝗿𝗮𝗺𝗲𝘁𝗲𝗿𝘀 𝗶𝗻 𝗖𝗲𝗿𝘃𝗶𝗰𝗮𝗹 𝗥𝗮𝗱𝗶𝗰𝘂𝗹𝗼𝗽𝗮𝘁𝗵𝘆

Cervical radiculopathy is a common clinical condition characterized by neck pain and radiating arm symptoms, most frequently caused by cervical disc herniation. Epidemiological studies estimate its prevalence at approximately 5–6 per 1,000 individuals, with disc-related nerve root irritation being a major underlying mechanism (https://pubmed.ncbi.nlm.nih.gov/32710604/, https://pubmed.ncbi.nlm.nih.gov/8186959/). Traditionally, symptom severity and treatment decisions have been assumed to correlate with the degree of mechanical nerve root compression visible on magnetic resonance imaging (MRI). However, increasing evidence suggests that inflammatory and neuroimmune processes may play an equally important, if not dominant, role in the development and persistence of radicular symptoms (https://pubmed.ncbi.nlm.nih.gov/17204882/, https://pubmed.ncbi.nlm.nih.gov/24614255/). Despite the widespread use of MRI in clinical decision-making, the prognostic value of disc herniation size remains uncertain.

📘 Against this background, a brand-new multicentre retrospective cohort study by Gül and colleagues (https://pubmed.ncbi.nlm.nih.gov/41464802/) examined whether the size of cervical disc herniation influences clinical presentation and one-year outcomes in patients with cervical radiculopathy.

✅ The analysis combined data from two well-established prospective trials: the NECK trial (https://pubmed.ncbi.nlm.nih.gov/30583108/), which focused on surgically treated patients undergoing anterior cervical discectomy with or without implants, and the CASINO trial (https://pubmed.ncbi.nlm.nih.gov/40528016/), which compared surgical and conservative management strategies. In total, 206 patients with MRI-confirmed cervical disc herniation were included.

📋 Baseline MRI scans were used to classify disc herniations according to their size. Due to small subgroup numbers, herniations were dichotomised into “small” (slight bulging or small herniation) and “large” (moderate or severe herniation, pro/extrusion with less than ¼ of the canal and severe herniation with pro/extrusion more than ¼ of the canal). Clinical outcomes were assessed at baseline and after one year using validated measures, including the Neck Disability Index (NDI), Visual Analogue Scale (VAS) scores for arm and neck pain, and the EuroQol Visual Analogue Scale (EQ-VAS).

📊 The results demonstrated no significant association between disc herniation size and baseline symptom severity across all clinical parameters (OR 1.010, p = 0.323). Furthermore, herniation size did not predict clinical outcomes at one year, regardless of whether patients were treated surgically or conservatively. Improvements in pain, disability, and self-perceived health were observed in both treatment groups, but these improvements were independent of the initial size of the disc herniation.

💡 This finding reinforces the idea that symptom progression may primarily be driven by immunological processes, rather than mechanical compression. Neuroinflammatory mechanisms are increasingly recognised to play a key role in the pathogenesis and the clinical course of radiculopathy. The majority of high-quality studies on neuroinflammation and disc herniation have focused on the lumbar spine (https://pubmed.ncbi.nlm.nih.gov/35357731/, https://pubmed.ncbi.nlm.nih.gov/38900144/, https://pubmed.ncbi.nlm.nih.gov/32169419/) resulting in a relative scarcity of cervical-specific data. Nonetheless, it is hypothesised that similar neuroimmune and biomechanical mechanisms underlie both lumbar and cervical radiculopathy.

Illustration: https://www.nejm.org/doi/full/10.1056/NEJMcp043887

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