BACKGROUND & AIMS: :It is well-recognised that steady-state isometric muscle force is decreased following active shortening (force depression, FD) and increased following active stretch (force enhancement, FE). It has also been demonstrated that passive muscle force is increased following active stretch (passive FE). Several studies have reported that FD increases with shortening amplitude and that FE and passive FE increase with stretch amplitude. Here, we investigate whether these trends continue with further increases in shortening or stretch amplitude. Experiments were performed using in situ cat soleus muscles (n=8 for FD; n=7 for FE and passive FE). FD, FE and passive FE were measured after shortening or stretch contractions that covered as wide a range of amplitudes as practically possible without damaging the muscles. FD increased approximately linearly with shortening amplitude, over the full range of amplitudes investigated. This is consistent with the hypothesis that FD arises from a stress-induced inhibition of crossbridges. FE increased with stretch amplitude only up to a point, and then levelled off. Passive FE, and the transient increase in force at the end of stretch, showed relationships to stretch amplitude that were qualitatively very similar to the relationship for FE, increasing only until the same critical stretch amplitude had been reached. We conclude that FE and passive FE do not increase with stretch amplitude under all circumstances. This finding has important consequences for determining the mechanisms underlying FE and passive FE because any mechanism that is proposed to explain them must be able to predict it.

背景与目标： ：众所周知，稳态等距肌肉力量在主动缩短（力量压迫，FD）后降低，而在主动伸展（力量增强，FE）后增加。还已经证明，主动拉伸（被动FE）后，被动肌肉的力量会增加。几项研究报告说，FD随着幅度的减小而增加，而FE和被动FE随拉伸幅度而增加。在这里，我们调查这些趋势是否继续缩短或拉伸幅度的进一步增加。使用原位猫的比目鱼肌进行实验（FD为n = 8； FE和被动FE为n = 7）。 FD，FE和被动FE是在收缩或拉伸收缩后测量的，收缩或拉伸收缩实际上覆盖了尽可能宽的幅度范围，而不会损坏肌肉。在所研究的整个振幅范围内，FD随振幅的减小而近似线性地增加。这与FD由应力诱导的跨桥抑制作用引起的假设相一致。 FE随拉伸幅度仅增加到一个点，然后趋于平稳。被动有限元，以及拉伸结束时力的瞬时增加，表明与拉伸幅度的关系在质量上与有限元的关系非常相似，仅在达到相同的临界拉伸幅度之前才增加。我们得出结论，在所有情况下，有限元和无源有限元都不会随拉伸幅度的增加而增加。这一发现对确定有限元和被动有限元的机制具有重要意义，因为提议用来解释它们的任何机制都必须能够对其进行预测。

BACKGROUND & AIMS: :Angiostensin II (Ang II) regulates the migration and proliferation of vascular smooth muscle cells. Recent studies indicate that intermediate-conductance Ca2+ -activated K+ (IKca) channels have an important role in cell migration and proliferation. It is not known, however, whether the action of Ang II is linked to IKca channel regulation. Here, we investigated the modulation of IKca channels by Ang II in artery smooth muscle cells. Functional IKca channel expression in cultured embryonic rat aorta smooth muscle (A10) cells was studied using the patch-clamp technique. These cells predominantly express IKca channels. In contrast, large-conductance Ca2+ -activated K+ (BKca) currents were rarely observed in excised patches. Ang II increased the IKca current in a contration-dependent manner. Losartan (1.0 microM), an AT1 selective antagonist, abolished the activation of IKca channels by Ang II. Pretreatment with 100 microM myristoylated protein kinase C inhibitor peptide 20-28 or 10 microM GF109203X completely abolished the AngII-induced activation of IKca currents, whereas the action of Ang II was not prevented in the presence of 100 microM Rp-cyclic 3', 5'-hydrogen phosphotiate adenosine triethylammonium, a protein kinase A inhibitor, or 1.0 microM KT-5823, a protein kinase G inhibitor. A membrane permeant analogue of diacylglycerol 1, 2-dioctanoyl-sn-glycerol (10 microM) induced the activation of IKca currents. These data suggest that Ang II activates IKca channels through the activation of protein kinase C, and the AT1 receptor is involved in the regulation of these channels.

背景与目标： ：血管紧张素II（Ang II）调节血管平滑肌细胞的迁移和增殖。最近的研究表明，中导Ca2激活的K（IKca）通道在细胞迁移和增殖中具有重要作用。但是，尚不清楚Ang II的作用是否与IKca通道调节有关。在这里，我们研究了血管平滑肌细胞中Ang II对IKca通道的调节作用。使用膜片钳技术研究了在培养的大鼠大鼠主动脉平滑肌（A10）细胞中功能性IKca通道的表达。这些细胞主要表达IKca通道。相反，在切除的斑块中很少观察到大电导的Ca2激活的K（BKca）电流。 Ang II以依赖冲突的方式增加了IKca电流。 Losartan（1.0 microM），一种AT1选择性拮抗剂，取消了Ang II对IKca通道的激活。用100 microM肉豆蔻酰化的蛋白激酶C抑制剂肽20-28或10 microM GF109203X进行的预处理完全消除了AngII诱导的IKca电流激活，而在存在100 microM Rp-环3'，5的情况下并未阻止Ang II的作用。 -磷酸磷酸氢腺苷三乙铵，一种蛋白激酶A抑制剂，或1.0 microM KT-5823，一种蛋白激酶G抑制剂。二酰基甘油1、2-二辛酰基-sn-甘油（10 microM）的膜渗透类似物诱导了IKca电流的激活。这些数据表明，Ang II通过蛋白激酶C的激活来激活IKca通道，而AT1受体参与了这些通道的调节。

BACKGROUND & AIMS: :Gliomas are highly lethal neoplasms that cannot be cured by currently available therapies. Temozolomide is a recently introduced alkylating agent that has yielded a significant benefit in the treatment of high-grade gliomas. However, either de novo or acquired chemoresistance occurs frequently and has been attributed to increased levels of O6-methylguanine-DNA methyltransferase or to the loss of mismatch repair capacity. However, very few gliomas overexpress O6-methylguanine-DNA methyltransferase or are mismatch repair-deficient, suggesting that other mechanisms may be involved in the resistance to temozolomide. The purpose of the present study was to generate temozolomide-resistant variants from a human glioma cell line (SNB-19) and to use large-scale genomic and transcriptional analyses to study the molecular basis of acquired temozolomide resistance. Two independently obtained temozolomide-resistant variants exhibited no cross-resistance to other alkylating agents [1,3-bis(2-chloroethyl)-1-nitrosourea and carboplatin] and shared genetic alterations, such as loss of a 2p region and loss of amplification of chromosome 4 and 16q regions. The karyotypic alterations were compatible with clonal selection of preexistent resistant cells in the parental SNB-19 cell line. Microarray analysis showed that 78 out of 17,000 genes were differentially expressed between parental cells and both temozolomide-resistant variants. None are implicated in known resistance mechanisms, such as DNA repair, whereas interestingly, several genes involved in differentiation were down-regulated. The data suggest that the acquisition of resistance to temozolomide in this model resulted from the selection of less differentiated preexistent resistant cells in the parental tumor.

背景与目标： ：胶质瘤是高度致死性的肿瘤，目前尚无法治愈。替莫唑胺是最近引入的烷基化剂，已在治疗高级神经胶质瘤中产生了显着的益处。然而，从头或获得性化学抗性经常发生，并且归因于O6-甲基鸟嘌呤-DNA甲基转移酶水平的增加或失配修复能力的丧失。但是，极少的神经胶质瘤过表达O6-甲基鸟嘌呤-DNA甲基转移酶或错配修复缺陷，提示其他机制可能与对替莫唑胺的抗性有关。本研究的目的是从人类神经胶质瘤细胞系（SNB-19）产生抗替莫唑胺的变体，并使用大规模的基因组和转录分析来研究获得的替莫唑胺抗性的分子基础。两个独立获得的替莫唑胺抗性变体对其他烷基化剂[1,3-双（2-氯乙基）-1-亚硝基脲和卡铂]无交叉抗性，并且共有遗传变异，例如2p区域丢失和扩增丢失染色体4和16q区域。核型改变与亲本SNB-19细胞系中先前存在的抗性细胞的克隆选择相容。基因芯片分析显示，在17,000个基因中，有78个在亲代细胞和两种替莫唑胺耐药变体之间差异表达。没有人参与已知的抗性机制，例如DNA修复，而有趣的是，参与分化的几个基因被下调。数据表明，在该模型中获得对替莫唑胺的抗药性是由于在亲本肿瘤中选择了分化程度较低的抗药性细胞而引起的。

BACKGROUND & AIMS: :The purpose of this study was to test the hypothesis that runners having different running economies show differences in the mechanical and morphological properties of their muscle-tendon units (MTU) in the lower extremities. Twenty eight long-distance runners (body mass: 76.8+/-6.7 kg, height: 182+/-6 cm, age: 28.1+/-4.5 years) participated in the study. The subjects ran on a treadmill at three velocities (3.0, 3.5 and 4.0 m s(-1)) for 15 min each. The V(O(2)) consumption was measured by spirometry. At all three examined velocities the kinematics of the left leg were captured whilst running on the treadmill using a high-speed digital video camera operating at 250 Hz. Furthermore the runners performed isometric maximal voluntary plantarflexion and knee extension contractions at eleven different MTU lengths with their left leg on a dynamometer. The distal aponeuroses of the gastrocnemius medialis (GM) and vastus lateralis (VL) were visualised by ultrasound during plantarflexion and knee extension, respectively. The morphological properties of the GM and VL (fascicle length, angle of pennation, and thickness) were determined at three different lengths for each MTU. A cluster analysis was used to classify the subjects into three groups according to their V(O(2)) consumption at all three velocities (high running economy, N=10; moderate running economy, N=12; low running economy, N=6). Neither the kinematic parameters nor the morphological properties of the GM and VL showed significant differences between groups. The most economical runners showed a higher contractile strength and a higher normalised tendon stiffness (relationship between tendon force and tendon strain) in the triceps surae MTU and a higher compliance of the quadriceps tendon and aponeurosis at low level tendon forces. It is suggested that at low level forces the more compliant quadriceps tendon and aponeurosis will increase the force potential of the muscle while running and therefore the volume of active muscle at a given force generation will decrease.

背景与目标： ：这项研究的目的是检验以下假设：具有不同运行经济状况的跑步者在下肢的肌腱单位（MTU）的机械和形态特性上存在差异。参加研究的有28名长跑运动员（体重：76.8 /-6.7公斤，身高：182 / -6厘米，年龄：28.1 /-4.5岁）。受试者分别以三种速度（3.0、3.5和4.0 m s（-1））在跑步机上跑步15分钟。 V（O（2））消耗量通过肺活量测定法进行测量。在所有三个检查的速度下，使用在250 Hz下运行的高速数码摄像机在跑步机上跑步时，捕获左腿的运动学信息。此外，跑步者在其左腿放在测力计上以11种不同的MTU长度进行等距最大自愿足底屈曲和膝盖伸展收缩。分别在足底屈曲和膝关节屈伸期间通过超声观察腓肠肌的远端腱膜（GM）和股外侧肌（VL）。对于每个MTU，在三种不同的长度下确定了GM和VL的形态学特性（纤维束长度，垂垂角度和厚度）。根据所有三个速度（高运行经济性，N = 10；中等运行经济性，N = 12；低运行经济性，N = 6）。 GM和VL的运动学参数和形态学特性均未显示组之间的显着差异。最经济的跑步者在肱三头肌MTU中表现出更高的收缩强度和更高的标准化肌腱刚度（肌腱力与肌腱应变之间的关系），在低水平的肌腱力下，股四头肌和腱膜的顺应性更高。建议在低水平的力量下，股四头肌和腱膜的顺应性会增加跑步时肌肉的力量，因此在给定的力量产生下，活跃肌肉的体积会减少。

BACKGROUND & AIMS: OBJECTIVE:The aim of the present investigation was to characterize the effects of supraphysiological doses of the anabolic androgenic steroid nandrolone decanoate (ND) on the fertility of female rats, as well as on the morphology of their uterus. STUDY DESIGN:Female Wistar rats (n=15) received a subcutaneous injection of ND (15 mg/kg) once daily during a 2-week period, while the control animals (n=10) were administered vehicle alone (arachidis oleum) in the same manner. Estrus behavior was evaluated 4 weeks after termination of this treatment and in cases where signs of receptivity were present, the female rat was given the opportunity to copulate with a male. After breeding, the female animals were sacrificed and their uteri examined histomorphologically. RESULTS:All ND-treated animals exhibited abnormal vaginal smears, whereas all of the control smears were normal. Most (73%) of the treated females demonstrated normal estrus behavior (i.e., willingness) on the day of mating, but none got pregnant; whereas all of the control rats became pregnant. The female rats receiving the ND showed an enhanced rate of weight gain and the myometrium thickness of their uteri was significantly increased, while the endometrium was significantly thinner. Furthermore, ND caused a significant proportion of the treated animals to display tortuous and irregularly branching endometrial glands, as well as a lack of the physiologically normal infiltration of eosinophilic leukocytes into the endometrium (endometrial eosinophilic homing), a finding that has not been reported previously. CONCLUSION:The present findings indicate that high doses of ND cause morphological and physiological alterations in the uterus of female rats that are associated with a suppression of their reproductive capacity.

背景与目标： 目的：本研究的目的是表征同化雄性类固醇癸酸nandrolone癸酸酯的超生理剂量对雌性大鼠生育能力以及子宫形态的影响。
研究设计：Wistar雌性大鼠（n = 15）在2周内每天一次皮下注射ND（15 mg / kg），而对照组（n = 10）单独给予媒介物（花生油）。同样的方式。终止该治疗4周后评估发情行为，并且在出现接受迹象的情况下，给予雌性大鼠与雄性交配的机会。繁殖后，将雌性动物处死并对其子宫进行组织形态学检查。
结果：所有接受ND治疗的动物均表现出异常的阴道涂片，而所有对照涂片均正常。接受治疗的大多数女性（73％）在交配当天表现出正常的发情行为（即意愿），但没有人怀孕；而所有对照大鼠都怀孕了。接受ND的雌性大鼠体重增加率增加，子宫肌层厚度明显增加，而子宫内膜明显变薄。此外，ND导致相当一部分被治疗的动物表现出曲折和不规则分支的子宫内膜腺体，并且缺乏正常的嗜酸性白细胞进入子宫内膜的生理正常浸润（子宫内膜嗜酸性归巢），这一发现以前未见报道。 。
结论：本研究结果表明，高剂量的ND可导致雌性大鼠子宫形态和生理改变，从而抑制其生殖能力。

BACKGROUND & AIMS: Epoxyeicosatrienoic acids (EETs) are endothelium-derived arachidonic acid metabolites of cytochrome P450. They dilate coronary arteries, open K+ channels, and hyperpolarize vascular smooth muscles. However, the mechanisms of these smooth muscle actions remain unknown. This study examined the effects of EETs on the large-conductance Ca(2+)-activated K+ channel (KCa) in smooth muscle cells of small bovine coronary arteries. In cell-attached patch-clamp experiments, 11,12-EET produced a 0.5- to 10-fold increase in the activity of the KCa channels when added in concentrations of 1, 10, and 100 nmol/L. In the inside-out excised membrane patch mode, 11,12-EET was without effect on the activity of the KCa channel unless GTP (0.5 mmol/L) or GTP and ATP (1 mmol/L) were added to the bath solution. In the presence of GTP and ATP, the increase in the KCa channel activity with 11,12-EET in inside-out patches was comparable to that in cell-attached patches. This effect of 11,12-EET in inside-out patches was blocked by the addition of GDP-beta-S (100 mumol/L). In outside-out patches, 11,12-EET also increased the KCa channel activity when GTP and ATP were added to the pipette solution. The addition of a specific anti-Gs alpha antibody (100 nmol/L) in the pipette solution completely blocked the activation of the KCa channels induced by 11,12-EET. An anti-G beta gamma or anti-Gi alpha antibody was without effect. We conclude that 11,12-EET activates the KCa channels by a Gs alpha-mediated mechanism. This mechanism contributes to the effects of EETs as endothelium-derived hyperpolarizing factors to hyperpolarize and relax arterial smooth muscle.

背景与目标： 环氧二十碳三烯酸（EET）是内皮细胞色素P450的花生四烯酸代谢产物。它们扩张冠状动脉，打开K通道，并使血管平滑肌超极化。但是，这些平滑肌动作的机制仍然未知。这项研究检查了EETs对小牛冠状动脉平滑肌细胞中大电导Ca（2）激活的K通道（KCa）的影响。在贴有细胞的膜片钳实验中，当以1、10和100 nmol / L的浓度添加时，11,12-EET使KCa通道的活性增加0.5至10倍。在由内而外的切膜模式下，除非将GTP（0.5 mmol / L）或GTP和ATP（1 mmol / L）添加到浴液中，否则11,12-EET对KCa通道的活性没有影响。在存在GTP和ATP的情况下，由内而外的贴片中11,12-EET的KCa通道活性的增加与细胞附着的贴片中的KCa通道活性的增加相当。通过添加GDP-β-S（100 mumol / L），阻止了由内而外的11,12-EET的这种作用。在外向斑块中，将GTP和ATP添加到移液器中时，11,12-EET也增加了KCa通道活性。在移液器中添加特异性抗Gsα抗体（100 nmol / L）完全阻断了11,12-EET诱导的KCa通道的激活。抗Gβγ或抗Giα抗体无效。我们得出的结论是11,12-EET通过Gs alpha介导的机制激活了KCa通道。这种机制有助于将EETs作为内皮源的超极化因子来使动脉平滑肌超极化和松弛。

BACKGROUND & AIMS: :The distinction between ectopic hamartomatous thymoma and sarcoma is difficult, and preoperative biopsy and intraoperative histopathological examination fail to give a definitive diagnosis. It is important to recognise ectopic hamartomatous thymoma as one of the differential diagnoses of a cervical tumour.

背景与目标： ：异位错构瘤性胸腺瘤和肉瘤之间的区别很困难，术前活检和术中组织病理学检查不能做出明确的诊断。重要的是要认识到异位错构瘤性胸腺瘤是宫颈肿瘤的鉴别诊断之一。

BACKGROUND & AIMS: :The vascular endothelial growth factor (VEGF) family of cytokines is involved in the maintenance of existing adult blood vessels as well as in angiogenesis, the sprouting of new vessels. To study the proangiogenic activation of VEGF receptors (VEGFRs) by VEGF family members in skeletal muscle, we develop a computational model of VEGF isoforms (VEGF(121), VEGF(165)), their cell surface receptors, and the extracellular matrix in in vivo tissue. We build upon our validated model of the biochemical interactions between VEGF isoforms and receptor tyrosine kinases (VEGFR-1 and VEGFR-2) and nonsignaling neuropilin-1 coreceptors in vitro. The model is general and could be applied to any tissue; here we apply the model to simulate the transport of VEGF isoforms in human vastus lateralis muscle, which is extensively studied in physiological experiments. The simulations predict the distribution of VEGF isoforms in resting (nonexercising) muscle and the activation of VEGFR signaling. Little of the VEGF protein in muscle is present as free, unbound extracellular cytokine; the majority is bound to the cell surface receptors or to the extracellular matrix. However, interstitial sequestration of VEGF(165) does not affect steady-state receptor binding. In the absence of neuropilin, VEGF(121) and VEGF(165) behave similarly, but neuropilin enhances the binding of VEGF(165) to VEGFR-2. This model is the first to study VEGF tissue distribution and receptor activation in human muscle, and it provides a platform for the design and evaluation of therapeutic approaches.

背景与目标： ：细胞因子的血管内皮生长因子（VEGF）家族与现有成人血管的维护以及血管生成，新血管的萌发有关。为了研究骨骼肌中VEGF家族成员对VEGF受体（VEGFRs）的促血管生成激活作用，我们建立了VEGF同种型（VEGF（121），VEGF（165）），它们的细胞表面受体和细胞外基质的计算模型。体内组织。我们建立在我们的体外VEGF同工型和受体酪氨酸激酶（VEGFR-1和VEGFR-2）和非信号神经pilin-1共受体之间的生化相互作用的验证模型的基础上。该模型是通用模型，可以应用于任何组织。在这里，我们应用该模型来模拟VEGF同工型在人股外侧肌中的运输，这在生理实验中已得到广泛研究。模拟预测了静息（非运动）肌肉中VEGF亚型的分布和VEGFR信号的激活。肌肉中很少有VEGF蛋白以游离的，未结合的细胞外细胞因子的形式存在。大多数与细胞表面受体或细胞外基质结合。但是，间质隔离VEGF（165）不会影响稳态受体结合。在没有神经纤毛蛋白的情况下，VEGF（121）和VEGF（165）的行为相似，但是神经纤毛蛋白会增强VEGF（165）与VEGFR-2的结合。该模型是第一个研究人肌肉中VEGF组织分布和受体激活的模型，它为设计和评估治疗方法提供了平台。

BACKGROUND & AIMS: :Insulin resistance affecting skeletal muscle metabolism is present in the prehypertensive state. The aim of our study was to test the hypothesis that blood pressure value is related to skeletal muscle composition, measured by (31)P magnetic resonance (MR) spectroscopy, and to insulin sensitivity in the offspring of hypertensive parents (OH) and healthy controls. Study groups consisted of 10 healthy young lean OH with normal glucose tolerance, confirmed with oral glucose tolerance test, and 13 controls matched for age, sex, and body mass index. Insulin action was estimated as glucose disposal (M), glucose metabolic clearance rate (MCR), and insulin sensitivity index (M/I) during a 10-hour hyperinsulinemic euglycemic clamp. The sum of immunoreactive insulin values from the oral glucose tolerance test was calculated. (31)P MR spectroscopy was performed on a whole-body MR scanner (Siemens Vision, Erlangen, Germany) operating at 1.5 T and equipped with actively shielded gradient coils. There were no differences in common metabolic and anthropometric parameters between OH and controls except for the blood pressure, which was in the range of normal to high-normal level in OH. Mean blood pressure was significantly higher in OH (95.73 +/- 4.39 vs 83.76 +/- 3.95 mm Hg; P < .001). Trend toward insulin resistance was registered in OH with significantly lower M/I (0.74 +/- 0.47 vs 1.42 +/- 0.65 mg x kg(-1) x min(-1) x mIU(-1) x L(-1); P < .05). There were no significant differences in total serum magnesium (sMg) levels between OH and controls, although a positive correlation exists between sMg and insulin sensitivity expressed as M (r = 0.63, P < .01), MCR (r = 0.54, P < .01), and M/I (r = 0.51, P < .05). No differences in signal intensities of phosphocreatine (PCr), phosphomonoesters, phosphodiesters, inorganic phosphates (Pi), adenosine triphosphates (Patp and betaATP), and calculated concentrations of intracellular ionized magnesium (Mgi) and H(+) ions between the groups were detected. Systolic blood pressure correlates positively with PCr/Patp (r = 0.43, P < .05), Pi/Patp (r = 0.413, P < .05), and Pi/betaATP (r = 0.48, P < .05). Diastolic blood pressure correlates positively only with the ratio Pi/betaATP (r = 0.42, P < .05). The sum of immunoreactive insulin values correlates with PCr/betaATP (r = 0.53, P < .01) and with Pi/betaATP (r = 0.6, P < .01). In conclusion, increase in blood pressure and insulin resistance were confirmed in offspring of OH. Insulin sensitivity is related to sMg and the elevation of blood pressure is associated with the activation of energy metabolism in skeletal muscle. The relationship between muscle energetic characteristics and markers of insulin resistance suggests that the alteration of energy metabolism may be present in early stages of metabolic syndrome.

背景与目标： ：在高血压前状态下，会影响骨骼肌新陈代谢的胰岛素抵抗。我们研究的目的是检验以下假设：血压值与通过（31）P磁共振（MR）光谱法测量的骨骼肌成分以及高血压父母（OH）和健康对照的后代的胰岛素敏感性有关。研究组包括10名健康正常的年轻瘦肉OH，其葡萄糖耐量正常，经口服葡萄糖耐量试验确认，另有13个对照的年龄，性别和体重指数匹配。在10小时高胰岛素正常血糖钳制期间，胰岛素作用估计为葡萄糖处置（M），葡萄糖代谢清除率（MCR）和胰岛素敏感性指数（M / I）。计算来自口服葡萄糖耐量试验的免疫反应性胰岛素值的总和。 （31）P MR光谱是在全身MR扫描仪（Siemens Vision，Erlangen，德国）上以1.5 T操作并配备有源屏蔽梯度线圈进行的。 OH和对照组之间的共同代谢和人体测量学参数没有差异，除了血压处于OH正常水平到高正常水平的范围之内。 OH中的平均血压显着升高（95.73 /-4.39与83.76 /-3.95 mm Hg； P <.001）。在OH中出现胰岛素抵抗的趋势，M / I显着降低（0.74 /-0.47对1.42 /-0.65 mg x kg（-1）x min（-1）x mIU（-1）x L（-1）; P <.05）。尽管sMg与胰岛素敏感性之间呈正相关，以M（r = 0.63，P <.01），MCR（r = 0.54，P < .01）和M / I（r = 0.51，P <.05）。两组之间没有发现磷酸肌酸（PCr），磷酸单酯，磷酸二酯，无机磷酸盐（Pi），三磷酸腺苷（Patp和betaATP）的信号强度差异以及计算出的细胞内离子化镁（Mgi）和H（）离子浓度。收缩压与PCr / Patp（r = 0.43，P <.05），Pi / Patp（r = 0.413，P <.05）和Pi / betaATP（r = 0.48，P <.05）正相关。舒张压仅与Pi / betaATP比率呈正相关（r = 0.42，P <.05）。免疫反应性胰岛素值的总和与PCr / betaATP（r = 0.53，P <.01）和Pi / betaATP（r = 0.6，P <.01）相关。总之，在OH的后代中证实了血压升高和胰岛素抵抗。胰岛素敏感性与sMg有关，而血压升高与骨骼肌能量代谢的激活有关。肌肉能量特性与胰岛素抵抗标志物之间的关系表明，能量代谢的改变可能在代谢综合征的早期出现。

BACKGROUND & AIMS: :Thyroid hormone (TH) regulates such crucial biological functions as normal growth, development and metabolism of nearly all vertebrate tissues. In skeletal muscle, TH plays a critical role in regulating the function of satellite cells, the bona fide skeletal muscle stem cells. Deiodinases (D2 and D3) have been found to modulate the expression of various TH target genes in satellite cells. Regulation of the expression and activity of the deiodinases constitutes a cell-autonomous, pre-receptor mechanism that controls crucial steps during the various phases of myogenesis. Here, we review the roles of deiodinases in skeletal muscle stem cells, particularly in muscle homeostasis and upon regeneration. We focus on the role of T3 in stem cell functions and in commitment towards lineage progression. We also discuss how deiodinases might be therapeutically exploited to improve satellite-cell-mediated muscle repair in skeletal muscle disorders or injury.

背景与目标： 甲状腺激素（TH）调节至关重要的生物学功能，例如几乎所有脊椎动物组织的正常生长，发育和代谢。在骨骼肌中，TH在调节卫星细胞（真正的骨骼肌干细胞）的功能中起着至关重要的作用。已发现脱碘酶（D2和D3）可调节卫星细胞中各种TH靶基因的表达。脱碘酶的表达和活性的调节构成了细胞自主的前受体机制，该机制在肌生成的各个阶段中控制关键步骤。在这里，我们回顾了脱碘酶在骨骼肌干细胞中的作用，特别是在肌肉稳态和再生中。我们专注于T3在干细胞功能中的作用以及对谱系进展的承诺。我们还将讨论如何在骨骼肌疾病或损伤中治疗性利用脱碘酶来改善卫星细胞介导的肌肉修复。

BACKGROUND & AIMS: :Accurate muscle geometry (muscle length and moment arm) is required to estimate muscle function when using musculoskeletal modelling. In shoulder, muscles are often modelled as a collection of independent line segments, leading to non-physiological muscles trajectory, especially for the rotator cuff muscles. To prevent this, a surface mesh model was developed and validated against 7 MRI positions in one participant. Mean moment arm errors was 11.4% for the line vs. 8.8% for the mesh model. While the model with independent lines led to some non-physiological trajectories, the mesh model gave lower misestimations of muscle lengths and moment arms.

背景与目标： ：使用肌肉骨骼模型时，需要准确的肌肉几何形状（肌肉长度和力矩臂）来估计肌肉功能。在肩部，肌肉通常被建模为独立线段的集合，从而导致非生理性的肌肉运动轨迹，特别是对于肩袖肌。为了防止这种情况，开发了一个表面网格模型，并针对一位参与者的7个MRI位置进行了验证。直线的平均力矩臂误差为11.4％，而网格模型为8.8％。尽管具有独立线的模型导致了一些非生理轨迹，但网格模型给出了较低的肌肉长度和弯矩臂错误估计。

BACKGROUND & AIMS: :Decline in MM and MS with aging, defined as sarcopenia, is related with physical disability, poor quality of life and death. Its mechanisms are not fully understood. Testosterone increases muscle protein synthesis. However, the effects of in utero androgen exposure to MM and MS in older adults have not been studied. In utero androgen exposure is inversely related with 2D:4D ratio. The aim of this study was to investigate the relationship between 2D:4D ratio as an indicator of in utero androgen exposure and MM and MS in elderly patients. A total of 151 older adults were included. Calf-circumference (CC) and skeletal muscle mass index (SMI) were used for the assessment of MM and hand grip strength for the assessment of MS. Mean age ± SD of the patients was 73.72 ± 6.23. Fifty-two (34.4%) of patients were male, 99 (65.6%) were female. Right and left 2D:4D were significantly and negatively correlated with hand grip strength (r=-0.365, p=0.018 and r=-0.434, p=0.005, respectively), CC (r=-0.422, p=0.002 and r=-0.459, p=0.001, respectively) and SMI (r=-0.354, p=0.018 and r=-0.348, p=0.022, respectively) in men. In women, right and left 2D:4D were significantly and negatively correlated with hand grip strength (r=-0.252, p=0.022 and r=-0.234, p=0.033, respectively), CC (r=-0.229, p=0.024 and r=-0.302, p=0.003, respectively) and SMI (r=-0.382, p<0.001 and r=-0.431, p<0.001, respectively). In this study, we found that 2D:4D ratio was significantly and negatively correlated with parameters depicting MM and MS which may suggest the possible role of in utero androgen exposure in the development of MM and MS loss in the elderly.

背景与目标： ：衰老的MM和MS的下降（定义为肌肉减少症）与身体残疾，不良的生活和死亡质量有关。其机制尚不完全清楚。睾丸激素可增加肌肉蛋白质的合成。但是，尚未研究子宫内雄激素暴露于老年人的MM和MS的影响。在子宫内，雄激素暴露与2D：4D比率成反比。这项研究的目的是调查老年患者子宫内雄激素暴露的指标2D：4D比值与MM和MS之间的关系。总共包括151位老年人。小腿围（CC）和骨骼肌质量指数（SMI）用于MM评估，手握力用于MS评估。患者的平均年龄±SD为73.72±6.23。男性（52）（34.4％），女性（99）（65.6％）。左右2D：4D与握力强度显着负相关（r = -0.365，p = 0.018和r = -0.434，p = 0.005），CC（r = -0.422，p = 0.002和r = -0.459，p = 0.001）和SMI（r = -0.354，p = 0.018和r = -0.348，p = 0.022）。在女性中，左右2D：4D与握力强度显着负相关（分别为r = -0.252，p = 0.022和r = -0.234，p = 0.033），CC（r = -0.229，p = 0.024）和r = -0.302，p = 0.003）和SMI（r = -0.382，p <0.001和r = -0.431，p <0.001）。在这项研究中，我们发现2D：4D比率与描述MM和MS的参数显着负相关，这可能表明子宫内雄激素暴露在老年人MM和MS丢失发展中的可能作用。

BACKGROUND & AIMS: INTRODUCTION:Fatiguing of respiratory muscles reduces peripheral muscle perfusion. Further, acute hypoxia enhances respiratory muscle fatigue. This study investigated the effects of inspiratory muscle loading (IML) on resting locomotor muscle perfusion in hypoxia compared to normoxia. METHODS:Ten subjects completed two study days of fatiguing IML (blinded, randomized) in normobaric hypoxia (targeted oxygen saturation 80%) and normoxia, respectively. Contrast-enhanced ultrasound (CEUS) of the gastrocnemius muscle and popliteal doppler ultrasonography were used to monitor muscle perfusion. Based on CEUS and monitored cardiac output, perfusion surrogate parameters (CLPaer and CLPap) were established. RESULTS:Muscle perfusion declines early during IML in normoxia (CLPaer: -54±25%, p<0.01; CLPap: -58±32%, p<0.01) and hypoxia (CLPaer: -43±23%, p<0.01; CLPap: -41±20%, p<0.01). Hypoxia compared to normoxia increased cardiac output before (+23±19%, p<0.01 ANOVA) and during (+22±20%, p<0.01 ANOVA) IML, while local muscle perfusion during IML remained unchanged (CLPaer: p=0.41 ANOVA; CLPap: p=0.29 ANOVA). CONCLUSION:Acute hypoxia compared to normoxia does not affect locomotor muscle perfusion during fatiguing IML.

背景与目标： 引言：呼吸肌疲劳会减少周围肌肉的灌注。此外，急性缺氧会增强呼吸肌疲劳。这项研究调查了吸氧量（IML）与低氧相比低氧对静息运动肌灌注的影响。
方法：十名受试者分别完成了常压低氧（目标血氧饱和度为80％）和常氧性疲劳IML（盲，随机）疲劳研究的两天。腓肠肌的造影增强超声（CEUS）和pop肌多普勒超声检查可监测肌肉灌注情况。基于CEUS和监测的心输出量，建立灌注替代参数（CLPaer和CLPap）。
结果：常氧（CLPaer：-54±25％，p <0.01; CLPap：-58±32％，p <0.01）和缺氧（CLPaer：-43±23％，p <0.01）在IML早期肌肉灌注下降。 CLPap：-41±20％，p ＜0.01）。与常氧相比，低氧增加了IML之前（23±19％，p <0.01 ANOVA）和期间（22±20％，p <0.01 ANOVA）的心输出量，而IML期间的局部肌肉灌注保持不变（CLPaer：p = 0.41 ANOVA； CLPap：p ＝ 0.29 ANOVA）。
结论：与常氧相比，急性缺氧并不影响IML疲劳期间运动肌的灌注。

BACKGROUND & AIMS: :The purpose of this study was to compare fatigue, strength, body composition, muscle thickness, and muscle quality between Hodgkin's lymphoma survivors (HLS) and apparently healthy subjects matched by age, gender, and physical activity levels (CON). Twelve HLS (32.16 ± 8.06) and 36 CON (32.42 ± 7.64) were enrolled in the study. Fatigue was assessed using the 20-item Multidimensional Fatigue Inventory, muscle strength using an isokinetic dynamometer, body composition using dual-energy X-ray absorptiometry, and thickness and muscle quality using B-mode ultrasound. Differences between HLS and CON were analyzed using independent samples t tests. No significant differences were observed between groups for any demographic characteristics: age ( P = .922), weight ( P = .943), height ( P = .511), body mass index ( P = .796), fat mass ( P = .688), fat-free mass ( P = .520), and percent body fat ( P = .446). No significant differences were observed for strength (peak torque; P = .552), relative peak torque ( P = .200), muscle thickness ( P > .05) and muscle quality ( P > .05). However, self-perceived fatigue was significantly higher in HLS than in CON ( P = .009). It appears that when HLS are matched by age and physical activity levels to CON, no significant difference in body composition, muscle thickness, muscle quality, or strength is observed. Self-perceived fatigue, as predicted, is higher in HLS, which may have implications and should be considered when prescribing exercise training to this cancer population.

背景与目标： ：本研究的目的是比较霍奇金淋巴瘤幸存者（HLS）与显然健康的受试者之间的疲劳，强度，身体成分，肌肉厚度和肌肉质量，并根据年龄，性别和身体活动水平（CON）进行比较。十二项HLS（32.16±8.06）和36 CON（32.42±7.64）被纳入研究。使用20个项目的多维疲劳清单评估疲劳，使用等速测功机评估肌肉强度，使用双能X射线吸收法评估身体成分，并使用B型超声评估厚度和肌肉质量。使用独立样本t检验分析了HLS和CON之间的差异。两组之间在任何人口统计学特征上均未观察到显着差异：年龄（P = .922），体重（P = .943），身高（P = .511），体重指数（P = .796），脂肪质量（P = .688），不含脂肪的质量（P = .520）和体内脂肪百分比（P = .446）。在强度（峰值扭矩； P = .552），相对峰值扭矩（P = .200），肌肉厚度（P> .05）和肌肉质量（P> .05）方面，均未观察到显着差异。但是，HLS的自我感觉疲劳明显高于CON（P = .009）。看起来，当HLS通过年龄和身体活动水平与CON相匹配时，在身体组成，肌肉厚度，肌肉质量或强度上均未观察到显着差异。正如预期的那样，HLS中的自我感觉疲劳较高，这可能会产生影响，因此在对此人群进行运动训练时应考虑这一点。

BACKGROUND & AIMS: :Satellite cells, localized within muscles in vivo, are Pax7+ muscle stem cells supporting skeletal muscle growth and regeneration. Unfortunately, their amplification in vitro, required for their therapeutic use, is associated with reduced regenerative potential. In the present study, we investigated if human myogenic reserve cells (MRC) obtained in vitro, represented a reliable cell source for muscle repair. For this purpose, primary human myoblasts were freshly isolated and expanded. After 2 days of differentiation, 62 ± 2.9% of the nuclei were localized in myotubes and 38 ± 2.9% in the mononucleated non-fusing MRC. Eighty percent of freshly isolated human MRC expressed a phenotype similar to human quiescent satellite cells (CD56+/Pax7+/MyoD-/Ki67- cells). Fourteen days and 21 days after cell transplantation in immunodeficient mice, live human cells were significantly more numerous and the percentage of Pax7+/human lamin A/C+ cells was 2 fold higher in muscles of animals injected with MRC compared to those injected with human myoblasts, despite that percentage of spectrin+ and lamin A/C+ human fibers in both groups MRC were similar. Taken together, these data provide evidence that MRC generated in vitro represent a promising source of cells for improving regeneration of injured skeletal muscles.

背景与目标： ：卫星细胞位于体内肌肉中，是支持骨骼肌生长和再生的Pax7肌肉干细胞。不幸的是，其治疗用途所需的体外扩增与降低的再生潜力有关。在本研究中，我们调查了体外获得的人肌原性储备细胞（MRC）是否代表肌肉修复的可靠细胞来源。为此目的，新鲜分离并扩增了原代人成肌细胞。分化2天后，有62％±2.9％的细胞核位于肌管中，有38％±2.9％的细胞位于单核非融合性MRC中。 80％的新鲜分离出的人类MRC表现出与人类静止卫星细胞（CD56 / Pax7 / MyoD- / Ki67-细胞）相似的表型。在免疫缺陷小鼠中，细胞移植后第14天和第21天，活人细胞明显增多，并且与注射人成肌细胞的动物相比，注射MRC的动物的肌肉中Pax7 /人层粘连A / C细胞的百分比高2倍，尽管两组中的血影蛋白和层状A / C人纤维百分比均相似。综上所述，这些数据提供了证据，证明体外产生的MRC代表了改善受损骨骼肌再生的有希望的细胞来源。