JAS静态牵伸结合拮抗肌针刺治疗脑卒中后肌张力增高的疗效观察

目的探讨膝关节活动系统(JAS)静态牵伸结合拮抗肌针刺治疗脑卒中后肌张力增高的疗效。方法 60例脑卒中后肌张力增高患者,采用随机数字表法分为实验组和对照组,各30例。对照组采用JAS静态牵伸方法治疗,实验组在对照组基础上配合拮抗肌针刺治疗。比较两组患者不同时间段腱反射、肌张力和阵挛临床痉挛指数(CSI)评分;不同时间段肢体运动功能(Fugl-Meyer)评分;治疗前后日常生活活动能力评分;治疗效果。结果实验组治疗后腱反射、肌张力和阵挛CSI评分分别为(2.13±0.57)、(4.20±0.62)、(1.50±0.57)分,随访期腱反射、肌张力和阵挛CSI评分分别为(2.22±0.75)、(4.27±1.04)、(1.60±0.62)分,均低于治疗前的(2.97±1.07)、(5.33±2.19)、(2.50±0.90)分,差异有统计学意义(P<0.05)。对照组治疗后腱反射、肌张力和阵挛CSI评分分别为(2.43±1.01)、(4.80±1.34)、(1.97±0.81)分,随访期腱反射、肌张力和阵挛CSI评分分别为(2.60±0.65)、(4.87±1.05)、(2.10±0.92)分,与治疗前的(2.83±1.05)、(5.20±2.20)、(2.57±0.94)分比较,差异无统计学意义(P>0.05)。实验组治疗后及随访期腱反射、肌张力和阵挛CSI评分低于对照组,差异有统计学意义(P<0.05)。实验组治疗后及随访期Fugl-Meyer评分分别为(80.97±3.32)、(82.13±2.71)分,均低于治疗前的(38.63±5.57)分,差异有统计学意义(P<0.05)。对照组治疗后及随访期Fugl-Meyer评分分别为(66.87±4.56)、(65.97±4.25)分,均低于治疗前的(43.73±7.05)分,差异有统计学意义(P<0.05)。实验组治疗后及随访期FuglMeyer评分均高于对照组,差异有统计学意义(P<0.05)。实验组和对照组治疗后日常生活活动能力评分为(75.91±12.61)、(62.53±15.43)分,均高于治疗前的(44.72±11.23)、(44.86±11.64)分,实验组治疗后日常生活活动能力评分高于对照组,差异有统计学意义(P<0.05)。实验组治疗总有效率96.67%高于对照组50.00%,差异有统计学意义(P<0.05)。结论采用JAS静态牵伸结合拮抗肌针刺治疗脑卒中后肌张力增高,能有效改善患者的上下肢痉挛情况,提高日常生活能力,值得临床推广应用。     

Circular RNA PPP1CC promotes Porphyromonas gingivalis-lipopolysaccharide-induced pyroptosis of vascular smooth muscle cells by activating the HMGB1/TLR9/AIM2 pathway

ObjectivePorphyromonas gingivalis (Pg) plays a critical role in the occurrence and development of atherosclerosis. Lipopolysaccharide from Pg (Pg-LPS) could lead to pyroptosis of vascular smooth muscle cells (VSMCs) and induce instability of atherosclerotic plaque. Therefore, pyroptosis of VSMCs could promote the process of atherosclerosis. However, the exact mechanism of Pg-LPS-induced pyroptosis of VSMCs is unclear.MethodsWe determined pyroptosis and expression of interleukin (IL)-1β and IL-18 in VSMCs using 4′,6-diamidino-2-phenylindole staining and ELISA after stimulation by Pg-LPS. We established a knockdown plasmid containing the circular (circ)RNA PPP1CC and transfected it into VSMCs. Luciferase assays were performed to reveal the association between microRNAs miR-103a-3p and miR-107 and circRNA PPP1CC.ResultsStimulation of Pg-LPS led to pyroptosis of VSMCs. Knockdown of circRNA PPP1CC relieved the Pg-LPS-induced pyroptosis of VSMCs and suppressed the expression of HMGB1, TLR9, AIM2, and cleaved caspase-1. Luciferase assays showed that PPP1CC directly targeted and competitively adsorbed miR-103a-3p and miR-107, weakening the inhibitory effect of these microRNAs on the expression of HMGB1.ConclusionKnockdown of circRNA PPP1CC relieved Pg-LPS-induced pyroptosis of VSMCs. Pyroptosis of VSMCs appears to promote atherosclerosis and may represent a novel therapeutic target for its treatment.     

Immunoelectron Microscopic Localization of Plasminogen Activator Inhibitor Type 1 (PAI-1) in Smooth Muscle Cells from Morphologically Normal and Atherosclerotic Human Arteries

Vascular wall fibrinolytic system proteins are believed to play a pivotal role in atherogenesis. Tissue-type plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA) influence persistence of luminal thrombi and proteolysis of extracellular matrix, respectively. The major physiologic inhibitor of t-PA and u-PA is plasminogen activator inhibitor type 1 (PAI-1). All three of these fibrinolytic system proteins have been detected in vascular endothelial cells, smooth muscle cells, and macrophages by light microscopic immunohistochemistry. This study was undertaken to delineate, by immunoelectron microscopy, the loci of PAI-1 in smooth muscle cells from intact morphologically normal and atherosclerotic human arteries as well as in isolated and cultured smooth muscle cells from arteries. In intact vessels, PAI-1 immunoreactivity was associated with contractile filaments in cells in both normal and atherosclerotic tissues. Lipid-laden smooth muscle cells in atherosclerotic vessels were mainly of the synthetic phenotype and displayed lesser amounts of PAI-1 associated with rough endoplasmic reticulum and contractile filaments. Isolated smooth muscle cells exhibited either a contractile or synthetic phenotype. In the cells with a contractile phenotype, PAI-1 was associated with the contractile elements, whereas in the cells with a synthetic phenotype, the PAI-1 was associated predominantly with elements of the endoplasmic reticulum. Because PAI-1 is associated predominantly with contractile filaments in smooth muscle cells, the net amount of immunodetectable PAI-1 appears to be greater in contractile compared with synthetic phenotype cells.     

Intermittent Claudication and Muscle Fiber Fine Structure: Morphometric Data on Mitochondrial Volumes

The mitochondrial volume densities (V mit) of the different fiber types (type 1, type 2A, type 2B) were estimated in bilaterally obtained biopsies from 22 patients with unilateral intermittent claudication. These data, which were obtained from structurally intact fibers, were compared with clinical data from the same subject In both the asymptomatic and symptomatic legs, V mit 1 > V mit 2A > V mit 2B. Furthermore, V mit 1 covariated with Vmit 2A and V mit 2A with V mit 2B in the asymptomatic legs (as in healthy subjects) but not in the symptomatic legs. V mit 2 (mainly Vmit 2A) covariated with the age of the subjects in both legs. V mit Tot was higher in the symptomatic legs than in the asymptomatic legs. This was mainly due to increase in the oxidative fibers, type 1 and type 2A. Usually, V mit in the asymptomatic legs covariated sig-nificantly with the results of the functional tests (initial pain and maximum walking tolerance), while only V mit 2A in the symptomatic legs showed such a corre lation. However, the difference between the two legs concerning V mit 1 was also correlated to the walking tolerance. Patients with high stenosis or occlusion showed higher Vmit Tot than did those with low obstacles. The results conclusively show that a fiber type-specific adaptation to ischemia occurs through an increase of mitochondrial content of oxidative fibers, which suggests that hypoxia may influence the control of synthesis or degradation of mitochondrial proteins.     

Membrane-bound Cytoplasmic Crystals,Similar to Those in Alveolar Soft Part Sarcoma,in a Human Muscle Spindle

Membrane-bound cytoplasmic crystals were found in the intrafusal fibers of a muscle spindle from a patient with neurogenic atrophy. The crystals have a periodicity of 10 nm and an intersecting axis angle of approximately 80°. This makes the crystals similar to those described in alveolar soft part sarcoma (ASPS). Because the crystals in ASPS may not be quite as specific as previously believed, and because similar crystals have been described in various other neoplasms, the present findings should not be taken as evidence for a muscle spindle derivation for ASPS.     

Costamere remodeling with muscle loading and unloading in healthy young men

Costameres are mechano-sensory sites of focal adhesion in the sarcolemma that provide a structural anchor for myofibrils. Their turnover is regulated by integrin-associated focal adhesion kinase (FAK). We hypothesized that changes in content of costamere components (beta 1 integrin, FAK, meta-vinculin, gamma-vinculin) with increased and reduced loading of human anti-gravity muscle would: (i) relate to changes in muscle size and molecular parameters of muscle size regulation [p70S6K, myosin heavy chain (MHC)1 and MHCIIA]; (ii) correspond to adjustments in activity and expression of FAK, and its negative regulator, FRNK; and (iii) reflect the temporal response to reduced and increased loading. Unloading induced a progressive decline in thickness of human vastus lateralis muscle after 8 and 34 days of bedrest (−4% and −14%, respectively; n = 9), contrasting the increase in muscle thickness after 10 and 27 days of resistance training (+5% and +13%; n = 6). Changes in muscle thickness were correlated with changes in cross-sectional area of type I muscle fibers (r = 0.66) and beta 1 integrin content (r = 0.76) at the mid-point of altered loading. Changes in meta-vinculin and FAK-pY397 content were correlated (r = 0.85) and differed, together with the changes of beta 1 integrin, MHCI, MHCII and p70S6K, between the mid- and end-point of resistance training. By contrast, costamere protein level changes did not differ between time points of bedrest. The findings emphasize the role of FAK-regulated costamere turnover in the load-dependent addition and removal of myofibrils, and argue for two phases of muscle remodeling with resistance training, which do not manifest at the macroscopic level.     

Possible Involvement of Altered RGD Sequence in Reduced Adhesive and Spreading Activities of Advanced Glycation End Product-Modified Fibronectin to Vascular Smooth Muscle Cells

Although fibronectin (FN) modified by advanced glycation end products (AGEs) has been shown to contribute to the development of diabetic vascular complications through its reduced adhesive activity to vascular cells, little is known about changes in the cell binding domain of AGE-modified FN. Here we examined the mechanism of reduced adhesive and spreading activities of AGE-modified FN to vascular smooth muscle cells (SMCs), particularly the contribution of modification of Arg-Gly-Asp (RGD) sequence. Incubation with glucose caused not only the formation of N-carboxymethyllysine and pentosidine, but also polymerization of FN in a dose- and time-dependent manner. AGE-modified FN had significantly low adhesive and spreading activities to cultured SMCs. On the other hand, multimeric FN formed by disulfide bonds did not show any effect on either cell adhesion or spreading. The adhesive activity of type I collagen, one of the RGD sequence-containing proteins, to SMCs also decreased by AGE-modification. The inhibitory effect of AGE-modification on cell adhesion was significantly greater in type I collagen than in FN. Although the extent of AGE-modification of type I collagen was indistinguishable from that of FN, AGE-modification decreased the arginine content of type I collagen by 69.5% and of FN by 30.6%, compared with their non-glycated forms. The addition of RGD peptides caused a decrease in adhesion of SMCs to non-glycated FN, but not to AGE-modified FN. Modification of RGD sequence with glyoxal eliminated its inhibitory effect on cell adhesion. Our results suggest that a marked decrease in adhesive and spreading activities of AGE-modified FN to SMCs might largely be due to a modification of its RGD sequence by AGE, thus suggesting a potential link between AGE modification of FN and the pathogenesis of diabetic angiopathy.