Some structural and functional properties of nerves and muscles in the oviduct of the pink bollworm moth,Pectinophora gossypiella (Saund.)

The oviduct of the pink bollworm is innervated by an intrinsic neural network arising from 4 nerves from the terminal ganglion. The nerve tracts in this network often contained elliptical swellings, each with a central nucleus.

A distinct surface topography was evident in the muscular sheath of the common and lateral oviduct. A very thin muscular envelope consisting of an inner band of circular fibers and an outer layer of longitudinal fibers was also found in the ovarioles. Although conventional A and I bands were recognized, the z-disk was composed of an irregular and loose meshwork, suggesting that the visceral muscles of the reproductive tract possess super-contracting properties. Even when the oviduct and the ovarioles were isolated from the central nervous system, an endogenous rhythmic activity was evident.

Two types of spontaneous excitatory postsynaptic potentials were detected in the oviduct. The type most frequently observed had a complex of multiple spikes with a duration of 18–32 msec. The other type had a saw-tooth shape and a duration of 80–160 msec. Spontaneous action potentials with a plateau-type configuration and a duration of 280–320 msec were also observed. After the removal of the terminal ganglion, endogenous electrical activity distinct from the events just described was found in the midand upper common oviduct. Such discharges seem to originate from the intrinsic neural network and had durations similar to those found for neurosecretory cells.     

Electron-microscopic study of innervation of smooth muscle cells surrounding collecting tubules of the fish kidney

Summary The fine structure of the collecting tubules of the trout and killifish kidney was studied. These tubules are surrounded by layers of smooth muscle cells which are commonly innervated. The nerve terminals contain synaptic vesicles and, occasionally, a few dense-cored granules as well. Capillaries occur in the connective tissue space between these smooth muscle cells and the collecting tubule. Epithelial cells of the collecting tubules contain abundant mitochondria and a well developed membrane system displaying parallel arrays, and were considered to be actively involved in the transport of materials. In the trout, the collecting tubules contain peculiar cells in addition to regular tubule cells. The fine structure of these peculiar cells is highly reminiscent of that of gill chloride cells. The significance of these findings may be summarized as follows: If the smooth muscles around the collecting tubule contract under neural influence, intratubular pressure may be increased and, thus affect glomerular filtration rate. The contraction of these muscles may also cause the collapse of peritubular capillaries, affecting the transport activity of tubule cells.     

原花青素对小鼠后肢缺血肌肉的作用及miR-133b的表达变化

肢体缺血后的氧化应激反应将导致肌肉损伤,刺激肌卫星细胞（satellite cells,SCs）的成肌分化,从而完成损伤修复,而肌源性miRNAs参与其中。原花青素（proanthocyanidins,PC）来源于植物多酚提取物,具有抗氧化应激的作用。但原花青素对缺血肌肉的作用和机制尚不明确。本文研究原花青素对小鼠后肢缺血肌肉的作用,探讨miR 133b在其中的表达及作用。雄性C57/BL6小鼠经左后肢缺血后随机分为：对照组（H₂O）、低浓度PC（low dose PC,LDPC）组（1 mg/kg）和高浓度PC（high dose PC,HDPC）组（20 mg/kg）。对缺血肢体运动功能评分：7 d时,对照组为1.33±0.14,LDPC组为1.50±0.15,HDPC组为2.08±0.23;14 d时,对照组为2.17±0.31,LDPC组为2.00±0.37,HDPC组为3.83±0.17。说明高浓度PC可促进缺血肢体运动功能恢复（P<0.05）。测定各组的氧化应激产物丙二醛含量,在7 d时：血浆中,对照组为32.85±7.61 nmol/μL,LDPC组为35.90±7.45 nmol/μL,HDPC组为10.46±2.49 nmol/μL;缺血肌肉中,对照组为39.75±7.61 nmol/μg,LDPC组为28.75±7.05 nmol/μg,HDPC组为15.80±3.63 nmol/μg。表明高浓度PC可有效降低后肢缺血小鼠体内氧化应激水平（P<0.05）。HE染色结果显示,高浓度组再生肌纤维比例（7 d,53.88%±8.13%;21 d,39.30%±0.37%）均明显高于（P<0.05）对照组（7 d,10.61%±3.00%;21 d,22.61%±3.16%）和低浓度组（7 d,14.57%±2.94%;21 d,18.74%±4.73%）。RT-qPCR检测缺血肌肉中miR-133b-3p含量,与对照组相比,高浓度组的miR-133b-3p表达上调（3.26倍,P<0.05）。生物信息学分析发现,PPP2CA、PPP2CB和MKP-1可能是miR-133b-3p的靶基因。Western印迹检测发现,与对照组相比,高浓度组PCNA、MyoD和ERK2表达升高,而p-ERK2表达下降（P<0.05）。以上结果说明,高浓度原花青素可降低缺血后的氧化应激反应,促进缺血肌肉再生,而miR-133b-3p和ERK信号通路可能参与其中。     

The miR-182/SORT1 axis regulates vascular smooth muscle cell calcification in vitro and in vivo

Arterial calcification is a common feature of cardiovascular disease. Sortilin is involved in the development of atherosclerosis, but the specific mechanism is unclear. In this study, we established calcification models in vivo and in vitro by using vitamin D₃ and β-glycerophosphate, respectively. In vivo, the expression of SORT1 was up-regulated and the expression of miR-182 was down-regulated in calcified arterial tissues. Meanwhile there was a negative correlation between SORT1 expression and miR-182 levels. In vitro, downregulating SORT1 expression using shRNA inhibited β-glycerophosphoric induced vascular smooth muscle cells (VSMCs) calcification. Moreover, reduced sortilin levels followed transfection of miR-182 mimics, whereas there was a significant increase in sortilin levels after transfection of miR-182 inhibitors. A luciferase reporter assay confirmed that SORT1 is the direct target of miR-182. Our study suggests that SORT1 plays a vital role in the development of arterial calcification and is regulated by miR-182.     

Modification of a three-compartment muscle fatigue model to predict peak torque decline during intermittent tasks

This study aimed to test whether adding a rest recovery parameter, r, to the analytical three-compartment controller (3CC) fatigue model (Xia and Frey Law, 2008) will improve fatigue estimates during intermittent contractions. The 3CC muscle fatigue model uses differential equations to predict the flow of muscle between three muscle states: Resting (M_R), Active (M_A), and Fatigued (M_F). This model uses a feedback controller to match the active state to target loads and two joint-specific parameters: F, fatigue rate controlling flow from active to fatigued compartments) and R, the recovery rate controlling flow from the fatigued to the resting compartments. This model does well to predict intensity-endurance time curves for sustained isometric tasks. However, previous studies find when rest intervals are present that the model over predicts fatigue. Intermittent rest periods would allow for the occurrence of subsequent reactive vasodilation and post-contraction hyperemia. We hypothesize a modified 3CC-r fatigue model will improve predictions of force decay during intermittent contractions with the addition of a rest recovery parameter, r, to augment recovery during rest intervals, representing muscle re-perfusion. A meta-analysis compiling intermittent fatigue data from 63 publications reporting decline in peak torque (% torque decline) were used for comparison. The original model over-predicted fatigue development from 19 to 29% torque decline; the addition of a rest multiplier significantly improved fatigue estimates to 6–10% torque decline. We conclude the addition of a rest multiplier to the three-compartment controller fatigue model provides a physiologically consistent modification for tasks involving rest intervals, resulting in improved estimates of muscle fatigue.     

Cross-bridge mechanism of residual force enhancement after stretching in a skeletal muscle

A muscle model that uses a modified Langevin equation with actomyosin potentials was used to describe the residual force enhancement after active stretching. Considering that the new model uses cross-bridge theory to describe the residual force enhancement, it is different from other models that use passive stretching elements. Residual force enhancement was simulated using a half sarcomere comprising 100 myosin molecules. In this paper, impulse is defined as the integral of an excess force from the steady isometric force over the time interval for which a stretch is applied. The impulse was calculated from the force response due to fast and slow muscle stretches to demonstrate the viscoelastic property of the cross-bridges. A cross-bridge mechanism was proposed as a way to describe the residual force enhancement on the basis of the impulse results with reference to the compliance of the actin filament. It was assumed that the period of the actin potential increased by 0.5% and the amplitude of the potential decreased by 0.5% when the half sarcomere was stretched by 10%. The residual force enhancement after 21.0% sarcomere stretching was 6.9% of the maximum isometric force of the muscle; this value was due to the increase in the number of cross-bridges.     

Vascular smooth muscle cells direct extracellular dysregulation in aortic stiffening of hypertensive rats

Aortic stiffening is an independent risk factor that underlies cardiovascular morbidity in the elderly. We have previously shown that intrinsic mechanical properties of vascular smooth muscle cells (VSMCs) play a key role in aortic stiffening in both aging and hypertension. Here, we test the hypothesis that VSMCs also contribute to aortic stiffening through their extracellular effects. Aortic stiffening was confirmed in spontaneously hypertensive rats (SHRs) vs. Wistar‐Kyoto (WKY) rats in vivo by echocardiography and ex vivo by isometric force measurements in isolated de‐endothelized aortic vessel segments. Vascular smooth muscle cells were isolated from thoracic aorta and embedded in a collagen I matrix in an in vitro 3D model to form reconstituted vessels. Reconstituted vessel segments made with SHR VSMCs were significantly stiffer than vessels made with WKY VSMCs. SHR VSMCs in the reconstituted vessels exhibited different morphologies and diminished adaptability to stretch compared to WKY VSMCs, implying dual effects on both static and dynamic stiffness. SHR VSMCs increased the synthesis of collagen and induced collagen fibril disorganization in reconstituted vessels. Mechanistically, compared to WKY VSMCs, SHR VSMCs exhibited an increase in the levels of active integrin β1‐ and bone morphogenetic protein 1 (BMP1)‐mediated proteolytic cleavage of lysyl oxidase (LOX). These VSMC‐induced alterations in the SHR were attenuated by an inhibitor of serum response factor (SRF)/myocardin. Therefore, SHR VSMCs exhibit extracellular dysregulation through modulating integrin β1 and BMP1/LOX via SRF/myocardin signaling in aortic stiffening.