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Rotate vector (RV) reducers are typical deceleration elements that moderate and increase torsion. They are widely applied in industrial robots and automatic machinery with the superiorities of compact structure, high precision, and overload resistance performance. However, the RV reducers also have disadvantages, such as low bearing capacity and short service life. As the core drive mechanism in an RV reducer, the bearing capacity for a cycloid-pin gear drive system directly affects the performance of the entire deceleration system. Therefore, the bearing capacity of an RV reducer should be improved by increasing the capacity of a cycloid-pin gear. In this paper, the design of a cycloid-pin gear is optimized to improve its bearing capacity. The tooth profile equations for cycloid gear and the meshing gap are derived based on the gear meshing principle. The bearing capacity for cycloid-pin gear is modeled by combining the contact strength theory with the multi-tooth contact bearing analysis. The effects of eccentricity, the radius of pin tooth distribution circle, pin teeth number, pin tooth radius, cycloid thickness, modification value of moved distance and equidistance on total volume, contact stress, and torsional stiffness are systematically researched. Then, a single-, double-, and three-objective optimization model is proposed based on the load-bearing capacity for cycloid-pin gear by taking these three factors as the objective function. Moreover, the parameters are optimized with the genetic algorithm, and the analyses for three optimizations are compared and discussed. The theoretical models are confirmed by the simulation analysis through ANSYS software. The results show that the bearing capacity for the cycloid-pin gear system can be largely enhanced after optimization.

Rotate vector (RV) reducers are the two-stage deceleration device comprising involute and cycloid-pin gear transmission mechanisms. As the typical deceleration elements, they are widely applied in industrial robots, digitally controlled machine tools and automation fields due to their compact structure and high precision. However, a reducer may lose precision after a long-term operation. Moreover, pitting and metal peeling of internal components may also occur, leading to a fatigue failure. Therefore, it is necessary to conduct investigations on lifespan evaluation for RV reducers. In this study, the CRV-80E reducer is taken as the research object. Firstly, according to its transmission characteristics, the lifespan evaluation model for a standard RV reducer is established based on fatigue strength theory and Palmgren-Miner linear cumulative damage law, with the internal crankshaft bearing is considered as the key component. Then, the simulations are carried out on crankshaft bearing by the ANSYS Workbench and SKF SimPro. The contact stress, deformation on bearing rollers, and the rated lifespan of the reducer are simulated. Finally, the accelerated life test is conducted on an RV reducer by increasing the external load with the positioning precision as an output and criterion. After the test, the reducer is disassembled, and metal peeling failure is observed on the crankshaft bearing while other parts are relatively intact. The test results validate the feasibility and accuracy of the service life evaluation model and simulation analysis. This study provides a new research approach for researchers and manufacturers and a design reference for engineers to improve the lifespan of RV reducers by optimizing crankshaft bearings, which have a certain academic value. [ABSTRACT FROM AUTHOR]

BackgroundInterstitial lung disease (ILD) is a rare clinical presentation of primary myelofibrosis (PMF).Case presentationWe report a case of ILD as the main manifestation on admission. A 58-year-old man was diagnosed with PMF owing to worsening anemia following treatment failure for conventional interstitial pneumonia.ResultsAnemia and interstitial pneumonia both significantly improved following treatment with a Janus kinase 2 gene inhibitor. In this report, we discuss the possible mechanisms underlying PMF complicated with ILD.

Phthalic acid esters (PAEs) are widely used as plasticizers and have been suggested to engender adverse effects on glucose metabolism. However, epidemiological data regarding the PAE mixture on type 2 diabetes (T2DM), as well as the mediating role of oxidative stress are scarce. This case-control study enrolled 206 T2DM cases and 206 matched controls in Guangdong Province, southern China. The concentrations of eleven phthalate metabolites (mPAEs) and the oxidative stress biomarker 8-hydroxy-2′-deoxyguanosine (8-OHdG) in urine were determined. Additionally, biomarkers of T2DM in paired serum were measured to assess glycemic status and levels of insulin resistance. Significantly positive associations were observed for mono-(2-ethylhexyl) phthalate (MEHP) and Mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) with T2DM (P < 0.001). Restricted cubic spline modeling revealed a non-linear dose-response relationship between MEHHP and T2DM (Pnon-linear = 0.001). The Bayesian kernel machine regression and quantile g-computation analyses demonstrated a significant positive joint effect of PAE exposure on T2DM risk, with MEHHP being the most significant contributor. The mediation analysis revealed marginal evidence that oxidative stress mediated the association between the mPAEs mixture and T2DM, while 8-OHdG respectively mediated 26.88 % and 12.24 % of MEHP and MEHHP on T2DM risk individually (Pmediation < 0.05). Di(2-ethylhexyl) phthalate (DEHP, the parent compound for MEHP and MEHHP) was used to further examine the potential molecular mechanisms by in silico analysis. Oxidative stress may be crucial in the link between DEHP and T2DM, particularly in the reactive oxygen species metabolic process and glucose import/metabolism. Molecular simulation docking experiments further demonstrated the core role of Peroxisome Proliferator Activated Receptor alpha (PPARα) among the DEHP-induced T2DM. These findings suggest that PAE exposure can alter oxidative stress via PPARα, thereby increasing T2DM risk.