A study on calculation method for mechanical impedance of air spring

This paper proposes an approximate analytic method of obtaining the mechanical impedance of air spring. The sound pressure distribution in cylindrical air spring is calculated based on the linear air wave theory. The influences of different boundary conditions on the acoustic pressure field distribution in cylindrical air spring are analysed. A 1-order ordinary differential matrix equation for the state vector of revolutionary shells under internal pressure is derived based on the non-moment theory of elastic thin shell. Referring to the transfer matrix method, a kind of expanded homogeneous capacity high precision integration method is introduced to solve the non-homogeneous matrix differential equation. Combined the solved stress field of shell with the calculated sound pressure field in air spring under the displacement harmonic excitation, the approximate analytical expression of the input and transfer mechanical impedance for the air spring can be achieved. The numerical simulation with the Comsol Multiphysics software verifies the correctness of theoretical analysis result

Research on active control strategy of vibration in complex environment

FxLMS algorithm has been widely used in active vibration control field theoretically. This paper is aimed at the complex situations in actual environment including interference and occasional divergence due to algorithm. Firstly the effects to control process and result caused by those situations are analyzed, then select different means based on different characteristics of the effects to deal with them, and integrate all those means to derive a new optimal control strategy which is suitable to actual applications. The experiment shows that the improved control strategy can response effectively different occasional situations without any weakness of normal control, and it can promote the practical application ability of the algorithm and is able to adapt to complex environments in active vibration control

Comparative analysis of phosphoproteomic in the intestine of Sepia lycidas under different salinity environments

Cuttlefish are sensitive to the breeding environment, and the low-salinity environment significantly impacts their growth and immunity. So far, it is difficult to breed this species artificially. This study was conducted in Sepia lycidas. And the aim was to investigate the differences in protein phosphorylation in the intestine of S. lycidas under different salinity conditions. Firstly, 999 phosphoproteins (specific peptide ≥ 1), 1928 phosphopeptides, and 2727 phosphorylation sites were identified. Among them were 284 down-regulated expression phosphorylation sites (corresponding to 115 phosphoproteins) and 674 up-regulated expression phosphorylation sites (corresponding to 408 phosphoproteins) in the intestine under a low salinity environment compared with that under a natural salinity environment. Next, GO analysis found that more phosphoproteins corresponding to differentially expressed phosphorylation sites were related to anatomical structure development, multicellular organism development, regulation of the cellular process, etc. The molecular functions of these proteins mainly contain protein binding, transferase activity, catalytic activity, and heterocyclic compound binding. And they are mainly involved in the cellular components of intracellular anatomical structure, organelle, and cytoplasm. KEGG enrichment analysis of the differential phosphoproteins suggested that many significantly enriched pathways were related to the phosphatidylinositol signaling system, cell junction (adherens junction and tight junction), and inositol phosphate metabolism. Finally, changes in environmental salinity can affect the intestinal structure, metabolism, and immune homeostasis of S. lycidas

Pro-Angiogenic Role of LncRNA HULC in Microvascular Endothelial Cells via Sequestrating miR-124

Background/Aims: HULC is a multifunctional lncRNA that has pro-angiogenic function in various cancers. The present study was designed to see the role of lncRNA HULC in normal endothelial cells angiogenesis. Methods: Cell viability, apoptosis, migration, tube formation and expression levels of angiogenesis-related proteins were respectively assessed in human microvascular endothelial HMEC-1 cells after lncRNA HULC was silenced by shRNA transfection. Cross-regulation between lncRNA HULC and miR-124, and between miR-124 and MCL-1 were detected by qRT-PCR, sequence analysis, and luciferase reporter assay. Results: Silence of lncRNA HULC significantly reduced viability, migration, tube formation and protein levels of VEGF, VEGFR2, CD144 and eNOS in HMEC-1 cells. Meanwhile, silence of lncRNA HULC induced apoptosis in HMEC-1 cells, as Bcl-2 was down-regulated, Bax was up-regulated, and caspase-3 and -9 were cleaved. miR-124 expression was negatively regulated by lncRNA HULC, and HULC worked as a molecular sponge for miR-124, in having miR-124 exhausted. Besides, MCL-1 was a target gene of miR-124. Rescue assay results showed that the effects of lncRNA HULC silence on HMEC-1 cells growth, migration and angiogenesis were abolished by miR-124 suppression. Similarly, the effects of miR-124 on HMEC-1 cells were abolished by MCL-1 overexpression. Furthermore, MCL-1 activated PI3K/AKT and JAK/STAT signaling pathways. Conclusion: These findings suggest a pro-angiogenic role of lncRNA HULC in endothelial cells. The pro-angiogenic actions of lncRNA HULC may be through sponging miR-124, preventing MCL-1 from degradation by miR-124

Complex Networks Approach for Analyzing the Correlation of Traditional Chinese Medicine Syndrome Evolvement and Cardiovascular Events in Patients with Stable Coronary Heart Disease

This is a multicenter prospective cohort study to analyze the correlation of traditional Chinese medicine (TCM) syndrome evolvement and cardiovascular events in patients with stable coronary heart disease (CHD). The impact of syndrome evolvement on cardiovascular events during the 6-month and 12-month follow-up was analyzed using complex networks approach. Results of verification using Chi-square test showed that the occurrence of cardiovascular events was positively correlated with syndrome evolvement when it evolved from toxic syndrome to Qi deficiency, blood stasis, or sustained toxic syndrome, when it evolved from Qi deficiency to blood stasis, toxic syndrome, or sustained Qi deficiency, and when it evolved from blood stasis to Qi deficiency. Blood stasis, Qi deficiency, and toxic syndrome are important syndrome factors for stable CHD. There are positive correlations between cardiovascular events and syndrome evolution from toxic syndrome to Qi deficiency or blood stasis, from Qi deficiency to blood stasis, or toxic syndrome and from blood stasis to Qi deficiency. These results indicate that stable CHD patients with pathogenesis of toxin consuming Qi, toxin leading to blood stasis, and mutual transformation of Qi deficiency and blood stasis are prone to recurrent cardiovascular events

A Unilateral Negative Feedback Loop Between miR-200 microRNAs and Sox2/E2F3 Controls Neural Progenitor Cell-Cycle Exit and Differentiation

MicroRNAs have emerged as key posttranscriptional regulators of gene expression during vertebrate development. We show that the miR-200 family plays a crucial role for the proper generation and survival of ventral neuronal populations in the murine midbrain/hindbrain region, including midbrain dopaminergic neurons, by directly targeting the pluripotency factor Sox2 and the cell-cycle regulator E2F3 in neural stem/progenitor cells. The lack of a negative regulation of Sox2 and E2F3 by miR-200 in conditional Dicer1 mutants (En1(+/Cre); Dicer1(flox/flox) mice) and after miR-200 knockdown in vitro leads to a strongly reduced cell-cycle exit and neuronal differentiation of ventral midbrain/hindbrain (vMH) neural progenitors, whereas the opposite effect is seen after miR-200 overexpression in primary vMH cells. Expression of miR-200 is in turn directly regulated by Sox2 and E2F3, thereby establishing a unilateral negative feedback loop required for the cell-cycle exit and neuronal differentiation of neural stem/progenitor cells. Our findings suggest that the posttranscriptional regulation of Sox2 and E2F3 by miR-200 family members might be a general mechanism to control the transition from a pluripotent/multipotent stem/progenitor cell to a postmitotic and more differentiated cell

Calpain Activator Dibucaine Induces Platelet Apoptosis

Calcium-dependent calpains are a family of cysteine proteases that have been demonstrated to play key roles in both platelet glycoprotein Ibα shedding and platelet activation and altered calpain activity is associated with thrombotic thrombocytopenic purpura. Calpain activators induce apoptosis in several types of nucleated cells. However, it is not clear whether calpain activators induce platelet apoptosis. Here we show that the calpain activator dibucaine induced several platelet apoptotic events including depolarization of the mitochondrial inner transmembrane potential, up-regulation of Bax and Bak, down-regulation of Bcl-2 and Bcl-XL, caspase-3 activation and phosphatidylserine exposure. Platelet apoptosis elicited by dibucaine was not affected by the broad spectrum metalloproteinase inhibitor GM6001. Furthermore, dibucaine did not induce platelet activation as detected by P-selectin expression and PAC-1 binding. However, platelet aggregation induced by ristocetin or α-thrombin, platelet adhesion and spreading on von Willebrand factor were significantly inhibited in platelets treated with dibucaine. Taken together, these data indicate that dibucaine induces platelet apoptosis and platelet dysfunction

Gastrodin attenuates renal injury and collagen deposition via suppression of the TGF-β1/Smad2/3 signaling pathway based on network pharmacology analysis

Background: Gastrodin has been widely used clinically in China as an antihypertensive drug. However, its effect on hypertensive renal injury is yet to be elucidated. The current study aimed to investigate the effects of gastrodin on hypertensive renal injury and its underlying mechanisms by network pharmacology analysis and validation in vivo and in vitro.Methods: A total of 10 spontaneously hypertensive rats (SHRs) were randomly categorized into the following two groups: SHR and SHR + Gastrodin groups. Wistar Kyoto (WKY) rats were used as the control group (n = 5). The SHR + Gastrodin group was intragastrically administered gastrodin (3.5 mg/kg/day), and the rats in both WKY and SHR groups were intragastrically administered an equal amount of double-distilled water for 10 weeks. Hematoxylin-eosin, Masson’s trichrome, and Sirius red staining were used to detect the pathological changes and collagen content in the renal tissues. Network pharmacology analysis was performed to explore its potential targets and related pathways. In vitro, the CCK-8 assay was used to determine the cell viability. Immunohistochemistry and western-blotting analyses were employed to assess the protein expression associated with renal fibrosis and transforming growth factor-β1 (TGF-β1) pathway-related proteins in the renal tissues or in TGF-β1-stimulated rat kidney fibroblast cell lines (NRK-49F).Results: Gastrodin treatment attenuates renal injury and pathological alterations in SHRs, including glomerular sclerosis and atrophy, epithelial cell atrophy, and tubular dilation. Gastrodin also reduced the accumulation of collagen in the renal tissues of SHRs, which were confirmed by downregulation of α-SMA, collagen I, collagen III protein expression. Network pharmacology analysis identified TGFB1 and SMAD2 as two of lead candidate targets of gastrodin on against hypertensive renal injury. Consistently, gastrodin treatment downregulated the increase of the protein expression of TGF-β1, and ratios of both p-Smad2/Smad2 and p-Samd3/Smad3 in renal tissues of SHRs. In vitro, gastrodin (25–100 μM) treatment significantly reversed the upregulation of α-SMA, fibronectin, collagen I, as well as p-Smad2 and p-Smad3 protein expressions without affecting the cell viability of TGF-β1 stimulated NRK-49F cells.Conclusion: Gastrodin treatment significantly attenuates hypertensive renal injury and renal fibrosis and suppresses TGF-β1/Smad2/3 signaling in vivo and in vitro

Alterations of hemostatic parameters in the early development of allogeneic hematopoietic stem cell transplantation-related complications

Thrombotic events are common and potentially fatal complications in patients receiving hematopoietic stem cell transplantation (HSCT). Early diagnosis is crucial but remains controversial. In this study, we investigated the early alterations of hemostatic parameters in allogeneic HSCT recipients and determined their potential diagnostic values in transplantation-related thrombotic complications and other post-HSCT events. Results from 107 patients with allogeneic HSCT showed higher levels of plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and tissue-plasminogen activator (t-PA) and a lower level of plasma protein C after transplantation. No change was found for prothrombin time, antithrombin III, d-dimer, and activated partial thromboplastin time following HSCT. Transplantation-related complications (TRCs) in HSCT patients were defined as thrombotic (n = 8), acute graft-versus-host disease (aGVHD, n = 45), and infectious (n = 38). All patients with TRCs, especially the patients with thrombotic complications, presented significant increases in the mean and maximum levels of PAI-1 during the observation period. Similarly, a high maximum t-PA level was found in the thrombotic group. In contrast, apparent lower levels of mean and minimum protein C were observed in the TRC patients, especially in the aGVHD group. Therefore, the hemostatic imbalance in the early phase of HSCT, reflecting prothrombotic state and endothelial injury due to the conditioning therapy or TRCs, might be useful in the differential diagnosis of the thrombotic complication from other TRCs