The link between tendon stem/progenitor cells (TSPCs) senescence and tendon aging has been well recognized. However, the cellular and molecular mechanisms of TSPCs senescence are still not fully understood. In present study, we investigated the role of Aquaporin 1 (AQP1) in TSPCs senescence. We showed that AQP1 expression declines with age during tendon aging. In aged TSPCs, overexpression of AQP1 significantly attenuated TSPCs senescence. In addition, AQP1 overexpression also restored the age-related dysfunction of self-renewal, migration and tenogenic differentiation. Furthermore, we demonstrated that the JAK-STAT signaling pathway is activated in aged TSPCs, and AQP1 overexpression inhibited the JAK-STAT signaling pathway activation which indicated that AQP1 attenuates senescence and age-related dysfunction of TSPCs through the repression of JAK−STAT signaling pathway. Taken together, our findings demonstrated the critical role of AQP1 in the regulation of TSPCs senescence and provided a novel target for antagonizing tendon aging.

The Chinese pangolin (Manis pentadactyla) has long suffered from intense exploitation driven by consumer demand for medicinal use and food. Effective conservation management is hampered by insufficient data on pangolin status and distribution. We integrated ecological niche modelling with long-term ecological records at the local scale (e.g. from local historical documents, grey and published literature and interviews) to estimate the magnitude of potential distribution change of the Chinese pangolin in eastern China (Fujian, Jiangxi and Zhejiang provinces) over time. Our results suggest that the range of the species decreased by 52.20% between the 1970s and early 2000s and that the population is now mainly confined to the Wuyi Mountains. This reduction in potential distribution range is attributable to anthropogenic pressures. According to our conservation prioritization analysis, the priority conservation area for the Chinese pangolin in eastern China is 51 268.4 km2, 5.62% of which is covered by nature reserves. There are 18 nature reserves and 46 prefectures which are priority areas for conservation in China. The priority-level nature reserves and prefectures in eastern China are mainly located in the centre of the Wuyi Mountains, and areas declared important tend to be around the Wuyi Mountains. We propose several actions to improve the conservation status of this species: establish or enlarge nature reserves, ensure local governments at the prefecture level prioritize conservation management and encourage local communities to participate in pangolin conservation.

Diminished regeneration or healing capacity of tendon occurs during aging. It has been well demonstrated that tendon stem/progenitor cells (TSPCs) play a vital role in tendon maintenance and repair. Here, we identified an accumulation of senescent TSPCs in tendon tissue with aging. In aged TSPCs, the activity of JAK-STAT signaling pathway was increased. Besides, genetic knockdown of JAK2 or STAT3 significantly attenuated TSPC senescence in aged TSPCs. Pharmacological inhibition of JAK-STAT signaling pathway with AG490 similarly attenuated cellular senescence and senescence-associated secretory phenotype (SASP) of aged TSPCs. In addition, inhibition of JAK-STAT signaling pathway also restored the age-related dysfunctions of TSPCs, including self-renewal, migration, actin dynamics, and stemness. Together, our findings reveal the critical role of JAK-STAT signaling pathway in the regulation of TSPC aging and suggest an ideal therapeutic target for the age-related tendon disorders.

Aging is a key dangerous factor for the occurrence and severity of tendon injury, but the exact cognition of the relationship is elusive at present. More previous studies suggest age-related changes occur at tendon mechanical properties, structure and composition, but the pathological alternations may be overlooked, which might be a cause for the structure and function variations, and even speed up the progress of age-related disorders. Recently, the presence of tendon stem/progenitor cells (TSPCs) would provide new insights for the pathogenesis of tendon aging. In this review, the tendon mechanical properties, structure and composition are presented in brief, then, the pathological changes of the aging tendon are described firstly, and the latest researches on alterations of TSPCs in the pathogenesis of tendon aging have also been analyzed. At a cellular level, the hypothetical model of altered TSPCs fate for tendon aging is also proposed. Moreover, the regulation of TSPCs as a potential way of the therapies for age-related tendon diseases is discussed. Therefore, reversing the impaired function of TSPCs and promoting the tenogenic differentiation of TSPCs could become hot spots for further study and give the opportunity to establish new treatment strategies for age-related tendon injuries.

Understanding historical context can help clarify the ecological and biogeographic characteristics of species population changes. The sable (Martes zibellina) population has decreased dramatically in Northeast China since the l950s, and understanding the changes in its distribution over time is necessary to support conservation efforts. To achieve this goal, we integrated ecological niche modeling and historical records of sables to estimate the magnitude of change in their distribution over time. Our results revealed a 51.71% reduction in their distribution in 2000–2016 compared with the potential distribution in the 1950s. This reduction was related to climate change (Pearson's correlation: Bio1, −.962, p < .01; Bio2, −.962, p < .01; Bio5, .817, p < .05; Bio6, .847, p < .05) and human population size (−.956, p < .01). The sable population tended to migrate in different directions and elevations over time in different areas due to climate change: In the Greater Khingan Mountains, they moved northward and to lower elevations; in the Lesser Khingan Mountains, they moved northward; and in the Changbai Mountains, they move southward and to higher elevations. Active conservation strategies should be considered in locations where sable populations have migrated or may migrate to.

Background The structural and functional properties of tendon decline with age, and these changes contribute to tendon disorder. Tendon stem/progenitor cells (TSPCs) play a vital role in tendon repair, regeneration and homeostasis maintaining. Although studies have demonstrated that tendon aging is closely associated with the altered TSPCs function on senescence, the cellular and molecular mechanisms of TSPCs senescence remain largely unknown. This study was designed to investigate the role of Wnt5a in TSPCs senescence. Methods TSPCs were isolated from 2-month-old and 20-month-old male C57BL/6 mice. The expression of Wnt5a was determined by RNA sequencing, qRT-PCR and western blotting. TSPCs were then treated with Wnt5a shRNA or recombinant Wnt5a or AG490 or IFN-γ or Ror2-siRNA. Western blotting, β-gal staining, qRT-PCR, immunofluorescence staining and cell cycle analysis were used for confirming the role of Wnt5a in TSPCs senescence. Results We found a canonical to noncanonical Wnt signaling shift due to enhanced expression of Wnt5a in aged TSPCs. Functionally, we demonstrated that inhibition of Wnt5a attenuated TSPCs senescence, age-related cell polarity and the senescence-associated secretory phenotype (SASP) expression in aged TSPCs. Mechanistically, the JAK–STAT signaling pathway was activated in aged TSPCs, while Wnt5a knockdown inhibited the JAK–STAT signaling pathway, suggesting that Wnt5a modulates TSPCs senescence via JAK–STAT signaling pathway. Moreover, knockdown of Ror2 inhibited Wnt5a-induced activation of the JAK–STAT signaling pathway, which indicates that Wnt5a potentiates JAK–STAT signaling pathway through Ror2, and Ror2 acts as the functional receptor of Wnt5a in TSPCs senescence. Conclusion Our results demonstrate a critical role of noncanonical Wnt5a signaling in TSPCs senescence, and Wnt5a could be an attractive therapeutic target for antagonizing tendon aging.

We present here a generalized Girard-Waring identity constructed from recursive sequences. We also present the construction of Binet Girard-Waring identity and classical Girard-Waring identity by using the generalized Girard-Waring identity and divided differences. The application of the generalized Girard-Waring identity to the transformation of recursive sequences of numbers and polynomials is discussed.

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