The planetary boundary layer (PBL) mediates the exchange of heat, momentum, and mass between a planetary surface and its overlying atmosphere, where turbulent processes govern vertical energy transport. Given the stark disparities in atmospheric properties across Venus, Earth, Mars, and Jupiter, it remains an open question whether the conventional Reynolds number (Re) remains a valid metric for cross-planetary comparisons of boundary layer turbulence. Using published mission datasets, atmospheric profiles, and peer-reviewed literature, we compile key dynamical parameters—atmospheric density, dynamic viscosity, characteristic wind speed, and characteristic length scale—to derive representative Re values for these four planetary bodies. These estimates are then benchmarked against observed and numerically simulated turbulence regimes. The calculated Re values follow the descending order: Jupiter (10 10 ) > Venus (10 9 ) > Earth (10 8 ) > Mars (10 7 ). While values for Jupiter and Earth align well with documented turbulent behaviors, Venus exhibits a high Re alongside weak surface winds and subdued turbulence. Conversely, Mars yields the lowest Re despite hosting vigorous convective boundary layer turbulence. These divergences indicate that Re does not scale linearly with actual turbulence intensity across distinct planetary regimes. Consequently, while Re provides a useful quantitative baseline for cross-planetary scaling, it cannot serve as a standalone criterion for assessing boundary-layer turbulence strength. This work does not attempt to derive a universal scaling law. Instead, using publicly available data, it systematically delineates the conditions under which a single Reynolds-number criterion holds and where it breaks down across planetary scales.

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The shoulder is the most mobile joint within the human body, yet its shallow bony socket makes it structurally vulnerable to sports-related injuries. This paper examines shoulder injuries across three representative sports: swimming, basketball and strength training. Swimming mainly produces chronic overuse injuries caused by millions of cyclic arm strokes, which place repeated stress on the rotator cuff tendons. Basketball creates mixed injury patterns combining cumulative overhead strain from shooting and blocking with acute traumatic damage from physical contact and falls. Strengthtraining-related shoulder harm arises from heavy external loading, flawed movement technique and poorly managed training volume. The paper compares injury mechanisms, athletic consequences, rehabilitation pathways and sport-specific preventive measures across the three sports. Common pathological conditions include rotator cuff damage, shoulder impingement and glenohumeral instability, and all three require careful, sport-adapted rehabilitation before an athlete can return to full training and competition. Generic rehabilitation and prevention advice cannot fit all athletic contexts. Targeted measures, such as correcting stroke technique, rebuilding shoulder stability and controlling training load, can effectively reduce injury incidence, support functional recovery and sustain long-term athletic performance.

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Chronic stress is an important risk factor for depression and is associated with sutained glucocorticoid signaling and impaired hippocampal function. Prolonged exposure to corticosterone, a major glucocorticoid, can distrpt adult hippocampal neurogenesis (AHN) in the dentate gyrus (DG) and reduce brain-derived neurotrophic factor (BDNF), which contributes to the differentiation and maturation of adult-born neurons through TrkB signaling. This review focuses on the studies showing that chronic CORT exposure increases neuronal autophagy in the DG and reduces BDNF levels, and disccus the current evidence linking CORT-induced neural autophagy to BDNF loss. While inhibition of autophagy can restore BDNF and partially rescue impaired AHN, whether GR mediates CORT-induced autophagy in DG neurons remain unanswered. In addition, GR signaling may influence BDNF through autophagy-independent mechanisms, including direct regulation of BDNF transcription. Together, the current studies supports a potential model in which GR-mediated autophay coontributes to intracellular BDNF loss following chornic CORT. This propsoed mechanism provides a direction for further examing how prolonged glucocorticoid signaling participates in impaired AHN.

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Low back pain (LBP) has become one of the most common musculoskeletal health problems among adolescents worldwide. It not only affects daily activities, athletic performance and sleep quality, but also tends to become chronic in adulthood. This article, from the perspective of evidence-based medicine, focuses on the high school student group and systematically sorts out the common risk factors and mechanisms of action of lower back pain. It is classified into two major categories based on modifiability: non-modifable factors (genetic susceptibility, gender) and interventionable factors (prolonged sitting, poor posture, excessive use of electronic devices, academic pressure and psychological factors, improper carrying of schoolbags, insufficient physical activity, sleep disorders), and the mechanisms by which it causes disease through pathways such as biomechanical imbalance, neuroendocrine disorders, and central sensitization are clarified. On this basis, the focus is on discussing strategies such as core stability training, hamstring and hip flexibility training, as people as phased rehabilitation and comprehensive school intervention. The analgesic and functional improvement effects are evaluated by combining randomized controlled trials and meta-analysis quantitative evidence. Existing evidence indicates that scientific exercise rehabilitation can significantly reduce pain scores, improve lumbar function, and is safe, economical, and easy to promote in schools. It can provide a reference for the early identification and precise prevention of lower back pain among high school students.

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