The Optimal Collision Avoidance Trajectory Planning of Redundant Manipulators in the Process of Grinding Ceramic Billet Surface

The intelligent manufacturing system (IMS) is widely used in the surface machining of the workpiece. In the process of ceramic surface grinding, the intelligent machine (manipulator) in IMS is required to automatically plan the collision avoidance trajectory in a complex environment. This paper presents an optimal trajectory planning method of the use of redundant manipulators in the surface grinding of ceramic billet, which is based on trajectory evaluation. The collision avoidance trajectory can be optimized, taking into account several parameters in the trajectory, including the length of the collision avoidance path, the weighted sum of the strokes of all joints, and the duration of the collision avoidance trajectory. Firstly, get the planning task. Secondly, set the planning parameters and obtain a number of collision avoidance trajectories. Finally, the evaluation function is used to evaluate the collision avoidance trajectories and get the optimal collision avoidance trajectory. The performance of the proposed optimal collision avoidance trajectory planning method is validated in different evaluation functions

Jiedu Tongluo granules ameliorates post-stroke depression rat model via regulating NMDAR/BDNF signaling pathway

Post-stroke depression (PSD) is one of the most common stroke complications, which seriously affects stroke’s therapeutic effect and brings great pain for patients. The pathological mechanism of PSD has not been revealed. Jiedu Tongluo granules (JDTLG) is an effective traditional Chinese medicine for PSD treatment which is widely used in clinical treatment. JDTLG has a significant therapeutic effect against PSD, but the mechanism is still unclear. The PSD rat model was established by carotid artery embolization combined with chronic sleep deprivation followed by treating with JDTLG. Neurobehavioral and neurofunctional experiments were engaged in studying the neural function of rats. Histomorphology, proteomics, and western blotting researches were performed to investigate the potential molecular mechanisms related to JDTLG therapy. Oral treatment of JDTLG could significantly improve the symptoms of neurological deficit and depression symptoms of PSD rats. Proteomic analysis identified several processes that may involve the regulation of JDTLG on the PSD animal model, including energy metabolism, nervous system, and N-methyl-D-aspartate receptor (NMDAR)/brain-derived neurotrophic factor (BDNF) signal pathway. Our results showed that JDTLG could reduce glutamate (Glu) level and increase gamma-aminobutyric acid (GABA) level via regulating the NMDAR/BDNF pathway, which may play a vital role in the occurrence and development of PSD

Impact characteristics and erosion mechanism of solid particles in a centrifugal pump

To study the impact and erosion mechanism of solid particles in centrifugal pumps, the standard k–ε turbulence model and SIMPLE algorithm are adopted in this paper. Based on the discrete phase model (DPM) of the Lagrange method and McLaury erosion model, the flow impact characteristics and erosion mechanism of solid particles impacting the surface of flow passage components in a single-stage centrifugal pump were numerically simulated, and the test data were compared with the numerical simulation results of the external characteristics of the pump in clean water. The results show that the erosion mechanism of the pressure surface of the blade is mostly the impact erosion caused by high-speed particles with large impact angles, and the impact angle and impact velocity are larger near the tail of the pressure surface. The impact angle of solid particles on the shroud and hub is relatively small, but the erosion mechanism is still impact erosion. The erosion mechanism of the volute wall is mostly the cutting friction erosion caused by the low-velocity particles with small impact angles, and it is only impacted by the particles with large angles near the volute tongue, which is impact erosion. Overall, the average impact angle and impact velocity of the particles on the pressure surface of the blade are higher than those on the volute, so the erosion of the pressure surface is more serious than that of the volute in theory. The research results have certain theoretical reference value for improving the wear resistance of a centrifugal pump

Remote sensing and environmental assessment of wetland ecological degradation in the Small Sanjiang Plain, Northeast China

IntroductionThe plain marsh wetland ecosystems are sensitive to changes in the natural environment and the intensity of human activities. The Sanjiang Plain is China’s largest area of concentrated marsh wetland, the Small Sanjiang Plain is the most important component of the Sanjiang Plain. However, with the acceleration of the urbanization and development of large-scale agricultural reclamation activities in the Small Sanjiang Plain in Northeast China, the wetland has been seriously damaged. In light of this degradation this study examines the Small Sanjiang Plain.MethodsFrom the four aspects of area, structure, function, and human activities, we try to construct a wetland degradation comprehensive index (WDCI) in cold region with expert scoring methods and analytic hierarchy process (AHP), coupled with network and administrative unit. The objective was to reveal the degradation of wetlands in Northeast China over three decades at a regional scale.ResultsThe results showed that (1) the overall wetland area decreased between 1990 and 2020 by 39.26×103 hm2. Within this period a significant decrease of 336.56×103 hm2 occurred between 1990 and 200 and a significant increase of 214.62×103 hm2 occurred between 2010 and 2020. (2) In terms of structural changes, the fractal dimension (FRAC) has the same trend as the Landscape Fragmentation Index (LFI) with little change. (3) In terms of functional changes, the average above-ground biomass (AGB) increased from 1029.73 kg/hm2 to 1405.38 kg/hm2 between 1990 and 2020 in the study area. (4) In terms of human activities, the average human disturbance was 0.52, 0.46, 0.57 and 0.53 in 1990, 2000, 2010 and 2020, with the highest in 2010. (5) The composite wetland degradation index shows that the most severe wetland degradation was 49.61% in 2010 occurred between 1990 and 2020. (6) Among the severely deteriorated trajectory types in 2010–2020, mild degradation → serious degradation accounted for the largest area of 240.23×103 hm2, and the significant improvement trajectory type in 1990–2000 accounted for the largest area of 238.50×103 hm2.DiscussionIn brief, we conclude that the degradation of the Small Sanjiang Plain wetland was caused mainly by construction, overgrazing, deforestation, and farmland reclamation. This study can also provide new views for monitoring and managing wetland degradation by remote sensing in cold regions

Prognosis for patients with apical hypertrophic cardiomyopathy: A multicenter cohort study based on propensity score matching

Background: Apical hypertrophic cardiomyopathy (AHCM) is a subtype of HCM, and few studies on the prognosis in AHCM are available.Aims: This study aimed to explore the clinical prognosis for AHCM and non-AHCM patients through clinical data based on propensity score matching (PSM) in a large cohort of Chinese HCM patients.Methods: The cohort study included 2268 HCM patients, 226 AHCM and 2042 non-AHCM patients from 13 tertiary hospitals, who were treated between 1996 and 2021. Fifteen demographic and clinical variables of 226 AHCM patients and 2042 non-AHCM patients were matched using 1:2 PSM. A Cox proportional hazard regression model was constructed to assess the effect of AHCM on mortality.Results: During a median follow-up of 5.1 (2.4–8.4) years, 353 (15.6%) of the 2268 HCM patients died, of whom 205 died due to cardiovascular mortality/cardiac transplantation and 94 experienced sudden cardiac death (SCD). In the matched cohort, the ACHM patients had lower rates of all-cause mortality (P = 0.003), cardiovascular mortality/cardiac transplantation (P = 0.03), and SCD (P = 0.02) than the non-AHCM patients. Furthermore, the Cox proportional hazard regression model showed that AHCM was an independent prognostic predictor of all-cause HCM mortality (P = 0.004) and a univariable prognostic predictor of cardiovascular mortality/cardiac transplantation (P = 0.03) and for SCD (P = 0.03). However, AHCM was not significant in multivariable Cox regression models in relation to cardiovascular mortality/cardiac transplantation and SCD.Conclusion: AHCM had a favorable prognosis both before and after matching, with lower all-cause mortality, cardiovascular mortality/cardiac transplantation, and SCD than non-AHCM

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving Asxl1(-/-) mice lived for up to 42 days and developed features of myelodysplastic syndrome (MDS), including dysplastic neutrophils and multiple lineage cytopenia. Asxl1(-/-) mice had a reduced hematopoietic stem cell (HSC) pool, and Asxl1(-/-) HSCs exhibited decreased hematopoietic repopulating capacity, with skewed cell differentiation favoring granulocytic lineage. Asxl1(+/-) mice also developed mild MDS-like disease, which could progress to MDS/myeloproliferative neoplasm, demonstrating a haploinsufficient effect of Asxl1 in the pathogenesis of myeloid malignancies. Asxl1 loss led to an increased apoptosis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human MDS. Furthermore, Asxl1(-/-) Lin(-)c-Kit(+) cells exhibited decreased global levels of H3K27me3 and H3K4me3 and altered expression of genes regulating apoptosis (Bcl2, Bcl2l12, Bcl2l13). Collectively, we report a novel ASXL1 murine model that recapitulates human myeloid malignancies, implying that Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis. Future work is necessary to clarify the contribution of microenvironment to the hematopoietic phenotypes observed in the constitutional Asxl1(-/-) mice

Consecutive epigenetically-active agent combinations act in ID1-RUNX3-TET2 and HOXA pathways for Flt3ITD+ve AML

Co-occurrence of Flt3ITD and TET2 mutations provoke an animal model of AML by epigenetic repression of Wnt pathway antagonists, including RUNX3, and by hyperexpression of ID1, encoding Wnt agonist. These affect HOXA over-expression and treatment resistance. A comparable epigenetic phenotype was identified among adult AML patients needing novel intervention. We chose combinations of targeted agents acting on distinct effectors, at the levels of both signal transduction and chromatin remodeling, in relapsed/refractory AML's, including Flt3ITD+ve, described with a signature of repressed tumor suppressor genes, involving Wnt antagonist RUNX3, occurring along with ID1 and HOXA over-expressions. We tracked patient response to combination of Flt3/Raf inhibitor, Sorafenib, and Vorinostat, pan-histone deacetylase inhibitor, without or with added Bortezomib, in consecutive phase I trials. A striking association of rapid objective remissions (near-complete, complete responses) was noted to accompany induced early pharmacodynamic changes within patient blasts in situ, involving these effectors, significantly linking RUNX3/Wnt antagonist de-repression (80%) and ID1 downregulation (85%), to a response, also preceded by profound HOXA9 repression. Response occurred in context of concurrent TET2 mutation/hypomorphy and Flt3ITD+ve mutation (83% of complete responses). Addition of Bortezomib to the combination was vital to attainment of complete response in Flt3ITD+ve cases exhibiting such Wnt pathway dysregulation

Integrative Analyses Identify Potential Key Genes and Calcium-Signaling Pathway in Familial Atrioventricular Nodal Reentrant Tachycardia Using Whole-Exome Sequencing

BackgroundAtrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia. Growing evidence suggests that family aggregation and genetic factors are involved in AVNRT. However, in families with a history of AVNRT, disease-causing genes have not been reported.ObjectiveTo investigate the genetic contribution of familial AVNRT using a whole-exome sequencing (WES) approach.MethodsBlood samples were collected from 20 patients from nine families with a history of AVNRT and 100 control participants, and we systematically analyzed mutation profiles using WES. Gene-based burden analysis, integration of previous sporadic AVNRT data, pedigree-based co-segregation, protein-protein interaction network analysis, single-cell RNA sequencing, and confirmation of animal phenotype were performed.ResultsAmong 95 related reference genes, seven candidate pathogenic genes have been identified both in sporadic and familial AVNRT, including CASQ2, AGXT, ANK2, SYNE2, ZFHX3, GJD3, and SCN4A. Among the 37 reference genes from sporadic AVNRT, five candidate pathogenic genes were identified in patients with both familial and sporadic AVNRT: LAMC1, ryanodine receptor 2 (RYR2), COL4A3, NOS1, and ATP2C2. To identify the common pathogenic mechanisms in all AVNRT cases, five pathogenic genes were identified in patients with both familial and sporadic AVNRT: LAMC1, RYR2, COL4A3, NOS1, and ATP2C2. Considering the unique internal candidate pathogenic gene within pedigrees, three genes, TRDN, CASQ2, and WNK1, were likely to be the pathogenic genes in familial AVNRT. Notably, the core calcium-signaling pathway may be closely associated with the occurrence of AVNRT, including CASQ2, RYR2, TRDN, NOS1, ANK2, and ATP2C2.ConclusionOur pedigree-based studies demonstrate that RYR2 and related calcium signaling pathway play a critical role in the pathogenesis of familial AVNRT using the WES approach