Offshore and coastal common bottlenose dolphins of the western South Atlantic face‐to‐face: What the skull and the spine can tell us

The taxonomy of Tursiops truncatus in the western South Atlantic is not resolved. Two different hypotheses have been proposed: (1) offshore and coastal ecotypes with a parapatric distribution, and (2) two species, T. truncatus and T. gephyreus, living in sympatry. To test these hypotheses, we examined a total of 100 physically mature skulls and 35 vertebral columns from the suggested overlap zone in southern Brazil. In all skulls, 24 measurements, four alveoli counts and two categorical variables were analyzed. Vertebral formula was determined and five measurements were taken from selected vertebrae. Multivariate analyses were conducted for skull and vertebral data. Results revealed the presence of two well‐separated groups. Specimens of Group1 had smaller skulls and shorter body lengths, but more vertebrae, than Group2. The morphological characteristics of each group corresponded well with two ecotypes of common bottlenose dolphins reported in other ocean basins. Therefore, we assigned the specimens of Group1 to the offshore ecotype, and Group2 to the coastal ecotype. Differences in the geographic locations and ratio of strandings supported the parapatric hypothesis. The significant morphological differentiation observed suggests the presence of different subspecies, but an additional independent line of evidence is needed to hypothesize whether they represent different species.     

FOXO1 delays skeletal muscle regeneration and suppresses myoblast proliferation

Unloading stress, such as bed rest, inhibits the regenerative potential of skeletal muscles; however, the underlying mechanisms remain largely unknown. FOXO1 expression, which induces the upregulated expression of the cell cycle inhibitors p57 and Gadd45α, is known to be increased in the skeletal muscle under unloading conditions. However, there is no report addressing FOXO1-induced inhibition of myoblast proliferation. Therefore, we induced muscle injury by cardiotoxin in transgenic mice overexpressing FOXO1 in the skeletal muscle (FOXO1-Tg mice) and observed regeneration delay in skeletal muscle mass and cross-sectional area in FOXO1-Tg mice. Increased p57 and Gadd45α mRNA levels, and decreased proliferation capacity were observed in C2C12 myoblasts expressing a tamoxifen-inducible active form of FOXO1. These results suggest that decreased proliferation capacity of myoblasts by FOXO1 disrupts skeletal muscle regeneration under FOXO1-increased conditions, such as unloading.     

关节镜下清理术联合腓骨截骨术治疗膝关节骨性关节炎的疗效及对炎性因子的影响

目的:探讨采用关节镜下清理术联合腓骨截骨术治疗膝关节骨性关节炎(KOA)的疗效及对炎性因子的影响。方法:选取2015年3月～2017年12月期间右江民族医学院附属河池医院收治的KOA患者99例,根据手术方式的不同将患者分为A组(n=46,关节镜下清理术治疗)和B组(n=53,关节镜下清理术联合腓骨截骨术治疗),比较两组患者手术时间、术中出血量、住院时间,比较两组术前、术后6个月、术后1年疼痛情况、膝关节功能恢复情况、膝关节相关角,比较两组术前、术后1个月炎性因子变化,记录两组术后并发症发生情况。结果:B组手术时间长于A组(P0.05),两组术中出血量、住院时间比较无差异(P0.05)。B组术后6个月、术后1年视觉疼痛模拟(VAS)评分低于A组,美国特种外科医院(HSS)、膝关节评分及美国膝关节协会(KSS)评分则高于A组(P0.05)。两组患者术后1个月白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)均较术前降低,且B组低于A组(P0.05)。B组术后6个月、术后1年膝关节相关角[股骨干与股骨双髁连线夹角(F角)、股骨胫骨角(FT角)、胫股关节间隙角(JS角)]均低于术前以及A组同时间点(P0.05)。两组术后并发症发生率比较差异无统计学意义(P0.05)。结论:KOA患者经关节镜下清理术、腓骨截骨术联合治疗后,疗效显著,可有效改善患者疼痛及膝关节功能,降低炎性因子水平,手术方案安全且可改善患者下肢力线。     

Effects of IGF‐1 isoforms on muscle growth and sarcopenia

The decline in skeletal muscle mass and strength occurring in aging, referred as sarcopenia, is the result of many factors including an imbalance between protein synthesis and degradation, changes in metabolic/hormonal status, and in circulating levels of inflammatory mediators. Thus, factors that increase muscle mass and promote anabolic pathways might be of therapeutic benefit to counteract sarcopenia. Among these, the insulin‐like growth factor‐1 (IGF‐1) has been implicated in many anabolic pathways in skeletal muscle. IGF‐1 exists in different isoforms that might exert different role in skeletal muscle. Here we study the effects of two full propeptides IGF‐1Ea and IGF‐1Eb in skeletal muscle, with the aim to define whether and through which mechanisms their overexpression impacts muscle aging. We report that only IGF‐1Ea expression promotes a pronounced hypertrophic phenotype in young mice, which is maintained in aged mice. Nevertheless, examination of aged transgenic mice revealed that the local expression of either IGF‐1Ea or IGF‐1Eb transgenes was protective against age‐related loss of muscle mass and force. At molecular level, both isoforms activate the autophagy/lysosome system, normally altered during aging, and increase PGC1‐α expression, modulating mitochondrial function, ROS detoxification, and the basal inflammatory state occurring at old age. Moreover, morphological integrity of neuromuscular junctions was maintained and preserved in both MLC/IGF‐1Ea and MLC/IGF‐1Eb mice during aging. These data suggest that IGF‐1 is a promising therapeutic agent in staving off advancing muscle weakness.     

(Pro)renin receptor accelerates development of sarcopenia via activation of Wnt/YAP signaling axis

To extend life expectancy and ensure healthy aging, it is crucial to prevent and minimize age‐induced skeletal muscle atrophy, also known as sarcopenia. However, the disease's molecular mechanism remains unclear. The age‐related Wnt/β‐catenin signaling pathway has been recently shown to be activated by the (pro)renin receptor ((P)RR). We report here that (P)RR expression was increased in the atrophied skeletal muscles of aged mice and humans. Therefore, we developed a gain‐of‐function model of age‐related sarcopenia via transgenic expression of (P)RR under control of the CAG promoter. Consistent with our hypothesis, (P)RR‐Tg mice died early and exhibited muscle atrophy with histological features of sarcopenia. Moreover, Wnt/β‐catenin signaling was activated and the regenerative capacity of muscle progenitor cells after cardiotoxin injury was impaired due to cell fusion failure in (P)RR‐Tg mice. In vitro forced expression of (P)RR protein in C2C12 myoblast cells suppressed myotube formation by activating Wnt/β‐catenin signaling. Administration of Dickkopf‐related protein 1, an inhibitor of Wnt/β‐catenin signaling, and anti‐(P)RR neutralizing antibody, which inhibits binding of (P)RR to the Wnt receptor, significantly improved sarcopenia in (P)RR‐Tg mice. Furthermore, the use of anti‐(P)RR neutralizing antibodies significantly improved the regenerative ability of skeletal muscle in aged mice. Finally, we show that Yes‐associated protein (YAP) signaling, which is coordinately regulated by Wnt/β‐catenin, contributed to the development of (P)RR‐induced sarcopenia. The present study demonstrates the use of (P)RR‐Tg mice as a novel sarcopenia model, and shows that (P)RR‐Wnt‐YAP signaling plays a pivotal role in the pathogenesis of this disease.     

Glutamine Metabolism Regulates Proliferation and Lineage Allocation in Skeletal Stem Cells

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Mechanisms Preserving Insulin Action during High Dietary Fat Intake

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