Modeling and dynamic analysis of rotating composite shaft

Structural modeling and dynamical analysis of rotating composite shaft are conducted in this paper. A thin-walled composite shaft structure model, which includes the transverse shear deformation of the shaft, rigid disks and the flexible bearings, is presented and then used to predict natural frequencies and dynamical stability. Based on the thin-walled composite beam theory referred to as variational asymptotically method (VAM), the displacement and strain fields of the shaft are described. Hamilton’s principle is employed to derive the equations of motion of the shaft system. Galerkin’s method is used to discretize and solve the governing equations. The validity of the model is proved by comparing the results with those in literatures and convergence examination. The effects of fiber orientation, ratios of length over radius, ratios of radius over thickness and shear deformation on natural frequency and critical speeds are investigated. Finally the unbalance transient responses of the composite shaft system are also given by using the time-integration method

Primary resonance of a rotating composite shaft with geometrical nonlineary

The primary resonance of a simply supported rotating composite shafts with geometrical nonlineary is studied. The composite shaft is modeled as a thin-walled Euler-Bernoulli beam. A variational-asymptotical method (VAM) applied to anisotropic thin-walled closed-cross-sectional beams is used to describe the displacement and strain fields of the composite shafts. The geometrical nonlineary is considered in the relationships of strain and displacement of the shaft. The nonlinear extensional-bending-torsional equations of motion for the composite shaft are derived by using the Hamilton principle. In order to emphatically study nonlinear transverse bending vibration, the effects of extensional and torsional deformations are ignored. By means of the method of multiple scales the approximation solution of primary resonance of transverse bending vibration is obtained. The Galerkin method is employed to reduce the governing equations to the ordinary differential equations. By using fourth-order Runge-Kutta method the time histories, phase diagrams and power spectrums are plotted. The study shows the effect of the external damping, ply angle, eccentricity, ratios of length over radius, ratios of radius over thickness and rotating speed on nonlinear dynamic behavior of the shaft. Specifically, the numerical simulation results show that the shaft exhibits the complex dynamic behavior including periodic, quasi-periodic and chaotic motion

Inhibitors of Phosphatidylinositol 3′-Kinases Promote Mitotic Cell Death in HeLa Cells

The phosphatidylinositol 3-kinase (PI3K) pathway plays an important role in many biological processes, including cell cycle progression, cell growth, survival, actin rearrangement and migration, and intracellular vesicular transport. However, the involvement of the PI3K pathway in the regulation of mitotic cell death remains unclear. In this study, we treated HeLa cells with the PI3K inhibitors, 3-methyladenine (3-MA, as well as a widely used autophagy inhibitor) and wortmannin to examine their effects on cell fates using live cell imaging. Treatment with 3-MA decreased cell viability in a time- and dose-dependent manner and was associated with caspase-3 activation. Interestingly, 3-MA-induced cell death was not affected by RNA interference-mediated knockdown (KD) of beclin1 (an essential protein for autophagy) in HeLa cells, or by deletion of atg5 (an essential autophagy gene) in mouse embryonic fibroblasts (MEFs). These data indicate that cell death induced by 3-MA occurs independently of its ability to inhibit autophagy. The results from live cell imaging studies showed that the inhibition of PI3Ks increased the occurrence of lagging chromosomes and cell cycle arrest and cell death in prometaphase. Furthermore, PI3K inhibitors promoted nocodazole-induced mitotic cell death and reduced mitotic slippage. Overexpression of Akt (the downstream target of PI3K) antagonized PI3K inhibitor-induced mitotic cell death and promoted nocodazole-induced mitotic slippage. These results suggest a novel role for the PI3K pathway in regulating mitotic progression and preventing mitotic cell death and provide justification for the use of PI3K inhibitors in combination with anti-mitotic drugs to combat cancer

SdCT-GAN: Reconstructing CT from Biplanar X-Rays with Self-driven Generative Adversarial Networks

Computed Tomography (CT) is a medical imaging modality that can generate more informative 3D images than 2D X-rays. However, this advantage comes at the expense of more radiation exposure, higher costs, and longer acquisition time. Hence, the reconstruction of 3D CT images using a limited number of 2D X-rays has gained significant importance as an economical alternative. Nevertheless, existing methods primarily prioritize minimizing pixel/voxel-level intensity discrepancies, often neglecting the preservation of textural details in the synthesized images. This oversight directly impacts the quality of the reconstructed images and thus affects the clinical diagnosis. To address the deficits, this paper presents a new self-driven generative adversarial network model (SdCT-GAN), which is motivated to pay more attention to image details by introducing a novel auto-encoder structure in the discriminator. In addition, a Sobel Gradient Guider (SGG) idea is applied throughout the model, where the edge information from the 2D X-ray image at the input can be integrated. Moreover, LPIPS (Learned Perceptual Image Patch Similarity) evaluation metric is adopted that can quantitatively evaluate the fine contours and textures of reconstructed images better than the existing ones. Finally, the qualitative and quantitative results of the empirical studies justify the power of the proposed model compared to mainstream state-of-the-art baselines

Effect of sequential treatment with syndrome differentiation on acute exacerbation of chronic obstructive pulmonary disease and "AECOPD Risk-Window": study protocol for a randomized placebo-controlled trial

BACKGROUND: Frequent chronic obstructive pulmonary disease (COPD) exacerbation is a major cause of hospital admission and mortality. It has been reported that Traditional Chinese Medicine (TCM) may relieve COPD symptoms and reduce the incidence of COPD exacerbations, thus improving life quality of COPD patients. The acute exacerbation of COPD risk-window (AECOPD-RW) is the period after an exacerbation and before the patient returns to baseline. In the AECOPD-RW, patients are usually at increased risk of a second exacerbation, which may lead to hospital admission and high mortality. It may be beneficial for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients to receive interventions during AECOPD-RW. During exacerbations the treatment principle is to eliminate exogenous pathogens, whereas the AECOPD-RW treatment principle focuses on enhancing body resistance. METHODS/DESIGN: A prospective, multi-center, single-blinded, double-dummy and randomized controlled clinical trial is being conducted to test the therapeutic effects of a sequential two stage treatment, which includes eliminating pathogen and strengthening vital qi with syndrome differentiation. A total of 364 patients will be enrolled in this study with 182 in each treatment group (TCM and control). Patients received medication (or control) according to their assigned group. TCM for AECOPD were administered twice daily to patients with AECOPD over 7 to 21 days, followed by TCM for AECOPD-RW over 28 days. All patients were followed for six months. The clinical symptoms, the modified medical research council dyspnea (MMRC) scale and exacerbations were used as the primary outcome measures. Pulmonary function, quality of life and mortality rate were used as secondary outcome measures. DISCUSSION: It is hypothesized that sequentially eliminating pathogens and strengthening vital qi treatments with syndrome differentiation will have beneficial effects on reducing the frequency and duration of acute exacerbation, relieving symptoms and improving quality of life for COPD patients. TRIAL REGISTRATION: This study is registered at ClinicalTrials.gov, ChiCTR-TRC-11001460

The changes of the interspace angle after anterior correction and instrumentation in adolescent idiopathic scoliosis patients

<p>Abstract</p> <p>Background</p> <p>In idiopathic scoliosis patients, after anterior spinal fusion and instrumentation, the discs (interspace angle) between the lowest instrumented vertebra (LIV) and the next caudal vertebra became more wedged. We reviewed these patients and analyzed the changes of the angle.</p> <p>Methods</p> <p>By reviewing the medical records and roentgenograms of adolescent idiopathic scoliosis patients underwent anterior spinal fusion and instrumentation, Cobb angle of the curve, correction rate, coronal balance, LIV rotation, interspace angle were measured and analyzed.</p> <p>Results</p> <p>There were total 30 patients included. The mean coronal Cobb angle of the main curve (thoracolumbar/lumbar curve) before and after surgery were 48.9° and 11.7°, respectively, with an average correction rate of 76.1%. The average rotation of LIV before surgery was 2.1 degree, and was improved to 1.2 degree after surgery. The interspace angle before surgery, on convex side-bending films, after surgery, at final follow up were 3.2°, -2.3°, 1.8° and 4.9°, respectively. The difference between the interspace angle after surgery and that preoperatively was not significant (P = 0.261), while the interspace angle at final follow-up became larger than that after surgery, and the difference was significant(P = 0.012). The interspace angle after surgery was correlated with that on convex side-bending films (r = 0.418, P = 0.022), and the interspace angle at final follow-up was correlated with that after surgery (r = 0.625, P = 0.000). There was significant correlation between the loss of the interspace angle and the loss of coronal Cobb angle of the main curve during follow-up(r = 0.483, P = 0.007).</p> <p>Conclusion</p> <p>The interspace angle could be improved after anterior correction and instrumentation surgery, but it became larger during follow-up. The loss of the interspace angle was correlated with the loss of coronal Cobb angle of the main curve during follow-up.</p

Mesenchymal stem cells improve mouse non-heart-beating liver graft survival by inhibiting Kupffer cell apoptosis via TLR4-ERK1/2-Fas/FasL-caspase3 pathway regulation

Abstract Background Liver transplantation is the optimal treatment option for end-stage liver disease, but organ shortages dramatically restrict its application. Donation after cardiac death (DCD) is an alternative approach that may expand the donor pool, but it faces challenges such as graft dysfunction, early graft loss, and cholangiopathy. Moreover, DCD liver grafts are no longer eligible for transplantation after their warm ischaemic time exceeds 30 min. Mesenchymal stem cells (MSCs) have been proposed as a promising therapy for treatment of certain liver diseases, but the role of MSCs in DCD liver graft function remains elusive. Methods In this study, we established an arterialized mouse non-heart-beating (NHB) liver transplantation model, and compared survival rates, cytokine and chemokine expression, histology, and the results of in vitro co-culture experiments in animals with or without MSC infusion. Results MSCs markedly ameliorated NHB liver graft injury and improved survival post-transplantation. Additionally, MSCs suppressed Kupffer cell apoptosis, Th1/Th17 immune responses, chemokine expression, and inflammatory cell infiltration. In vitro, PGE2 secreted by MSCs inhibited Kupffer cell apoptosis via TLR4-ERK1/2-caspase3 pathway regulation. Conclusion Our study uncovers a protective role for MSCs and elucidates the underlying immunomodulatory mechanism in an NHB liver transplantation model. Our results suggest that MSCs are uniquely positioned for use in future clinical studies owing to their ability to protect DCD liver grafts, particularly in patients for whom DCD organs are not an option according to current criteria

Metallic vanadium disulfide nanosheets as a platform material for multifunctional electrode applications

Nano-thick metallic transition metal dichalcogenides such as VS$_{2}$ are essential building blocks for constructing next-generation electronic and energy-storage applications, as well as for exploring unique physical issues associated with the dimensionality effect. However, such 2D layered materials have yet to be achieved through either mechanical exfoliation or bottom-up synthesis. Herein, we report a facile chemical vapor deposition route for direct production of crystalline VS$_{2}$ nanosheets with sub-10 nm thicknesses and domain sizes of tens of micrometers. The obtained nanosheets feature spontaneous superlattice periodicities and excellent electrical conductivities (~3$\times$10$^{3}$ S cm$^{-1}$), which has enabled a variety of applications such as contact electrodes for monolayer MoS$_{2}$ with contact resistances of ~1/4 to that of Ni/Au metals, and as supercapacitor electrodes in aqueous electrolytes showing specific capacitances as high as 8.6$\times$10$^{2}$ F g$^{-1}$. This work provides fresh insights into the delicate structure-property relationship and the broad application prospects of such metallic 2D materials.Comment: 23 pages, 5 figue

Proteomic analysis of regenerating mouse liver following 50% partial hepatectomy

<p>Abstract</p> <p>Background</p> <p>Although 70% (or 2/3) partial hepatectomy (PH) is the most studied model for liver regeneration, the hepatic protein expression profile associated with lower volume liver resection (such as 50% PH) has not yet been reported. Therefore, the aim of this study was to determine the global protein expression profile of the regenerating mouse liver following 50% PH by differential proteomics, and thereby gaining some insights into the hepatic regeneration mechanism(s) under this milder but clinically more relevant condition.</p> <p>Results</p> <p>Proteins from sham-operated mouse livers and livers regenerating for 24 h after 50% PH were separated by SDS-PAGE and analyzed by nanoUPLC-Q-Tof mass spectrometry. Compared to sham-operated group, there were totally 87 differentially expressed proteins (with 50 up-regulated and 37 down-regulated ones) identified in the regenerating mouse livers, most of which have not been previously related to liver regeneration. Remarkably, over 25 differentially expressed proteins were located at mitochondria. Several of the mitochondria-resident proteins which play important roles in citric acid cycle, oxidative phosphorylation and ATP production were found to be down-regulated, consistent with the recently-proposed model in which the reduction of ATP content in the remnant liver gives rise to early stress signals that contribute to the onset of liver regeneration. Pathway analysis revealed a central role of c-Myc in the regulation of liver regeneration.</p> <p>Conclusions</p> <p>Our study provides novel evidence for mitochondria as a pivotal organelle that is connected to liver regeneration, and lays the foundation for further studies on key factors and pathways involved in liver regeneration following 50% PH, a condition frequently used for partial liver transplantation and conservative liver resection.</p