Chordae tendineae, referred to as heart tendinous cords, act as tendons connecting the papillary muscles to the valves in the heart. Their role is analogous to tendons in the musculoskeletal system. Despite being exposed to millions of cyclic tensile stretches over a human\'s lifetime, chordae tendineae rarely suffer from overuse injuries. On the other hand, musculoskeletal tendinopathy is very common and remains challenging in clinical treatment. The objective of this study was to investigate the mechanism behind the remarkable durability and resistance to overuse injuries of chordae tendineae, as well as to explore their effects on flexor tenocyte biology. The messenger RNA expression profiles of chordae tendineae were analyzed using RNA sequencing and verified by quantitative reverse transcription polymerase chain reaction  and immunohistochemistry. Interestingly, we found that periostin (Postn) and fibroblast growth factor 7 (FGF7) were expressed at significantly higher levels in chordae tendineae, compared to flexor tendons. We further treated flexor tenocytes in vitro with periostin and FGF7 to examine their effects on the proliferation, migration, apoptosis, and tendon-related gene expression of flexor tenocytes. The results displayed enhanced cell proliferation ability at an early stage and an antiapoptotic effect on tenocytes, while treated with periostin and/or FGF7 proteins. Furthermore, there was a trend of promoted tenocyte migration capability. These findings indicated that Postn and FGF7 may represent novel cytokines to target flexor tendon healing. Clinical significance: The preliminary discovery leads to a novel idea for treating tendinopathy in the musculoskeletal system using specific molecules identified from chordae tendineae.

This study aimed to investigate the association between biomarkers and overuse injuries in well-trained wrestlers. Seventy-six well-trained wrestlers on a national team completed two blood sample collections, two clinical overuse injuries diagnoses, and a questionnaire survey at a 2-week interval. Multivariate logistic regression analysis and receiver operating characteristic curve were used to screen for related factors and construct the prediction probability model of overuse injuries. Using a restricted cubic spline further clarifies the relationship between biomarker levels and the risk of overuse injuries. Creatine kinase (CK), cortisol, rheumatoid factor, testosterone in men, and C-reactive protein (CRP) levels in the overuse injuries group were significantly different compared to those in the non-overuse injuries group. The diagnostic efficiency of the prediction probability model was more valuable than any single variable (area under the curve=0.96, Specificity=0.91, Sensitivity=0.89, high accuracy). A J-shaped relationship was noted between biomarkers (cortisol, CRP, and CK) and the risk of overuse injuries (cutoff point: 17.95 μg·dL-1, 4.72 mg·L-1, and 344 U·L-1; p for nonlinearity:<0.001, 0.025, and 0.043, respectively). In conclusion, a predictive model based on biomarkers (cortisol, CRP, and CK) predicted the overuse injuries risk of well-trained wrestlers. High levels of these three biomarkers were associated with a higher risk of overuse injuries, and a J-shaped relationship was observed between them.

UNASSIGNED: Patellar tendinopathy (PT), or jumper\'s knee, is a chronic painful overuse patellar tendon injury. For PT, prevention is more important than treatment. However, there is still a lack of strong evidence to confirm the effectiveness of prevention.
UNASSIGNED: This study will analyze by meta-analysis the effect of a prophylactic program on high PT risk people (but without PT) in reducing PT occurrence.
UNASSIGNED: PubMed, Embase, the Cochrane Library, Scopus, and Ebscohost, from inception to January 11, 2022.
UNASSIGNED: A study comparing the effects of prophylactic programs and controls on the risk of PT was included in the analysis. After a database search with search terms ((patellar tendinopathy) OR (jumper\'s knee) OR (patellar tendinitis) OR (patellar tendinosis) OR (patellar tendonitis)) AND ((Prevent*) OR (prophyla*)), a total of 1444 items were obtained. Of these, 11 studies with 6091 participants were eligible for inclusion in this meta-analysis.
UNASSIGNED: Systematic review and meta-analysis.
UNASSIGNED: Level 2.
UNASSIGNED: The first author\'s name, publication year, study design, country, population, mean age, sex, prophylactic program, control, study duration, and the frequency or incidence of PT in each group were extracted.
UNASSIGNED: A total of 11 articles were included in the analysis. Overall, no significant difference was considered in the risk of PT between the prophylactic program and control groups based on the random-effect model (odds ratio [OR], 0.85; 95% CI, 0.67, 1.08; P = 0.18). In the recruit subgroup, there was even a tendency to elevate the risk of PT occurrence after prophylaxis was executed (OR, 1.89; 95% CI, 0.68, 5.28; P = 0.22). In athletes, the prophylactic program tended to decrease the risk of PT compared with the control (OR, 0.81; 95% CI, 0.63, 1.04; P = 0.10); however, the difference was not statistically significant. Trial sequential analysis results suggested that prophylaxis may still be effective for athletes, but this needs to be confirmed with a larger sample size.
UNASSIGNED: The risk of PT cannot be reduced with the current prophylactic program. However, for athletes, the negative results may be due to insufficient sample size.

In the field of obstetrics and gynaecology, sonographers are often exposed to health and safety risks that may have significant consequences: it has been reported that up to 90% of sonographers experience work-related musculoskeletal disorders. These have the potential to be career-ending. This topic warrants routine evaluation, which is the aim of this editorial. We intend to achieve this by presenting a summary of risks, their outcomes, and strategies to optimise health and wellness in the workplace of sonographers in obstetrics and gynaecology. We believe this discussion is of utmost importance to sonographers, their employers, and regulatory bodies.

Although the overuse injury rate of the Achilles tendon (AT) for running is high, the effect of shoe conditions on AT loading remains unclear. Hence, this study aims to determine the mechanical properties of AT during running under different shoe conditions (minimalist vs. conventional shoes).
This work is a controlled laboratory study.
Sixteen healthy male rearfoot strike runners were recruited to complete over ground running trials at 3.33 m/s (±5%) under two shoe conditions (minimalist shoes: INOV-8 Bare-XF 210; conventional shoes: NIKE AIR ZOOM PEGASUS 34). Sagittal plane ankle kinematics and ground reaction forces were simultaneously recorded. Ankle joint mechanics (ankle joint angle and moment) and the mechanical properties (peak force, impulse, stress, strain, and their corresponding peak rate) of the AT were calculated.
In comparison with conventional shoes, wearing minimalist shoes showed significant changes (p < 0.05): (1) decreased strike angle (48.92 ± 9.01 vs. 41.04 ± 8.69°); (2) increased ankle moment (2.34 ± 0.44 vs. 2.55 ± 0.46 Nm/kg); (3) increased peak AT force (5.85 ± 1.22 vs. 6.24 ± 1.13 BW), AT force impulse (0.65 ± 0.13 vs. 0.70 ± 0.13 BW·s), peak AT loading rate (109.94 ± 9.33 vs. 118.84 ± 26.62 BW/s), and average loading rate (48.42 ± 15.64 vs. 54.90 ± 17.47 BW/s); (4) decreased time to peak AT force (126.31 ± 20.68 vs. 117.77 ± 17.62 ms); (5) increased AT stress (66.96 ± 14.59 vs. 71.89 ± 14.74 MPa), strain (8.19 ± 1.77 vs. 8.78 ± 1.80 %), peak AT stress rate (66.96 ± 14.59 vs. 71.89 ± 14.74 MPa/s), and strain rate (148.71 ± 48.52 vs. 167.28 ± 42.82 %/s).
Increased AT force, loading rate, and stress were observed in runners who habitually wear conventional shoes with rearfoot strike patterns when they wore minimalist shoes. Hence, we recommend a gradual transition to minimalist shoes for runners who habitually wear conventional shoes with rearfoot strike patterns.

This study was to investigate the mechanism of intestinal physical and immune barriers in the occurrence of high-intensive exercise-induced gastrointestinal symptoms.
An overtraining model of male C57BL/6 mice was established by running-to-exhaustive exercise. Then, the mice were sacrificed, and a series of evaluation indicators, including the routine blood analysis as well as histological examinations, inflammatory factors, ultrastructure observation, and intestinal permeability of the gut, were measured based on this model. The expressions of inflammatory factors tumor necrosis factor α, interferon-γ, and interleukin (IL)-6 as well as the tight junction and adherence junction proteins ZO-1, Occludin, Claudin-1, and E-cadherin were measured, respectively. Furthermore, the mRNA level of IL-22 and the proportion of ILC3 and IL-22 produced in CD4 T cells in lamina propria lymphocytes (LPL) were analyzed by flow cytometry. Besides, the liver glycogen and the expressions of sirtuins-3 and hypoxia-inducible factor-1a, which were associated with the intestinal metabolism phenotype, were analyzed by Western blotting.
Exhaustive exercise induced a disrupted intestinal barrier integrity, an aggravated intestinal inflammation, increased gut permeability, and the reduced IL-22 mRNA level. Compared with the nonexercise mice, the IL-22 produced in LPL was reduced followed by exhaustive exercise, whereas the proportion of IL-22 produced in CD4 T cells was still unchanged. Significantly, the proportion of ILC3 in the LPL was decreased obviously, including the NCR ILC3. Furthermore, the intestinal metabolism phenotype assessment showed lower liver glycogen and blood glucose as well as higher blood lactic acid and hypoxia-inducible factor-1a, respectively.
The data indicated that the acute high-intensity running-induced gastrointestinal symptom is closely associated with a reduced percentage of ILC3 and IL-22 level in the LPL, possibly due to the glycogen exhaustion and intestinal mucosa hypoperfusion.

The pathogenesis of patellar tendon fibrosis caused by overuse remains unclear. In an effort to further investigate effective treatments for patellar tendon fibrosis attributed to overuse, it is necessary to construct a reliable animal model.
A rabbit patellar tendon fibrosis model was developed with the use of electrical stimulation to induce jumping. The pathogenesis and development of patellar tendon fibrosis were subsequently investigated with this model.
Controlled laboratory study.
A total of 32 New Zealand White rabbits were randomly divided into a jumping group and a control group. Rabbits in the control group did not receive any treatment, while those in the jumping group jumped 150 times daily, 5 days per week. At 2, 4, 6, and 8 weeks after the initiation of treatment, the patellar tendons of 4 rabbits from each group were harvested and subjected to hematoxylin and eosin staining, immunohistochemical staining, and real-time polymerase chain reaction. The influence of jumping training on the expressions of histology- and fibrosis-related factors in the patellar tendon was assessed.
The histological changes of patellar tendon fibrosis in the jumping group were most pronounced at 4 weeks. When compared with the control group at corresponding time points, the mRNA and protein expressions of TGF-β1, CTGF, COL-I, and COL-III were upregulated significantly in the patellar tendon after jumping training for 4 weeks (P < .05). Intragroup comparison at different time points indicated that the mRNA and protein expressions of TGF-β1, COL-I, and COL-III were the highest at 4 weeks in the jumping group (P < .01).
It was found that patellar tendon fibrosis occurred because of overuse and the peak changes occurred at 4 weeks. Jumping load increased the secretions of TGF-β1 and Smad3 in the patellar tendon, with CTGF upregulation and higher synthesis of COL-I and COL-III, which were considered the pathogenesis of fibrosis.
This study simulated the effects of jumping load on tendon fibrosis at different time points. Moreover, the time course relationship between jumping training and patellar tendon fibrosis in the rabbit model was determined, which provided a new animal model for the study of patellar tendon fibrosis.

BACKGROUND: Enthesis injury is a common problem in athletes and workers, which is considered closely related to overuse. However, the early pathophysiologic changes of osteotendinous junction are not well understood, and moreover, few studies investigated the relationship between intensity and pathological changes. The purpose of this study was to evaluate microstructural changes induced by different loading intensities and to find out the threshold intensity.
METHODS: Forty-eight New Zealand White rabbits were randomly divided into six groups. One control group, the others were electrically stimulated to contract repetitively for 2 h per day, three days a week. 30% of peak tetanic force (7.06 N) was adopted to stimulate the rabbits in the 100% cyclic loading group. Other groups were stimulated with 20%, 40%, 60% and 80% of this force. After four weeks, prepared samples were stained with hematoxylin and eosin.
RESULTS: After 4 weeks of cyclic loading, the shape and the distribution of tendon cells in patellar enthesis changed, the arrangement of collagen fibers became disordered and the tidemark had become irregular or even disappeared. Different stimulus intensity caused a significant change of cell density in different groups (F = 10.19, P < 0.001). The cell densities of tendon were 34.3 ± 7.9 cells/100 μm2 (L60), 38.2 ± 5.9 cells/100 μm2 (L80), 43.8 ± 10.3 cells/100 μm2 (L100) respectively, which had significant difference with CON group 22.5 ± 3.5 cells/100 μm2. The thickness of fibrocartilage zone had no significant difference among the groups.
CONCLUSIONS: The changes of histomorphology with the increasing exercise intensity elucidated that the degree of enthesis microdamage was directly related to the intensity of exercises. The findings demonstrated that 18% (used in L60 group) of peak tetanic force was the threshold intensity which could induce pathological changes in enthesis in four weeks.

Achilles tendinopathy is a significant clinical disease characterized by activity-related pain, focal movement limitation, and intratendinous imaging changes. However, treatment of Achilles tendinopathy has been based mainly on theoretical rationale and clinical experience because of its unclear underlying pathogenesis and mechanism. The purpose of the study was to develop a simple but reproducible overuse-induced animal model of Achilles tendinopathy in mice to better understand the underlying mechanism and prevent calcific Achilles tendinopathy. A total of 80 C57/B6 mice (8 or 9 weeks old) were employed and randomly divided into control and experimental groups. Unilateral Achilles tenotomy was performed on the right hind limbs in the experiment group. 12 weeks after unilateral Achilles tenotomy, the onset of Achilles tendinopathy in the contralateral Achilles tendon was determined by radiological assessment, histologic analysis, electron microscopy observation, and biomechanical test. The onset of calcific Achilles tendinopathy in contralateral Achilles tendon was confirmed after 12 weeks of unilateral tenotomy. The contralateral Achilles tendon in the experimental group was characterized as hypercellularity, neovascularization, and fused collagen fiber disarrangement, compared with the control group. Importantly, intra-tendon endochondral ossification and calcaneus deformity were featured in contralateral Achilles tendon. In addition, poor biomechanical properties in the contralateral Achilles tendon revealed the incidence of Achilles tendinopathy. We hereby introduce a novel, simple, but reproducible spontaneous contralateral calcific Achilles tendinopathy model in mice, which represents overuse conditions during tendinopathy development in humans. It should be a useful tool to further study the underlying pathogenesis of calcific Achilles tendinopathy.

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