Search

To improve the accuracy of modal analysis for a four-stage centrifugal-pump rotor system with a balancing disc based on the concentrated-mass analytical method, a simplified concentrated mass mathematical model and an ANSYS simulation model are established. The results from these two models are compared to determine factors that cause significant differences in the mode shapes. Subsequently, an optimized mathematical model based on the corrected mass moment of an inertia matrix and stiffness correction coefficients is proposed, and the effectiveness of this optimized mathematical model is validated using a four-stage centrifugal pump with back blades. The results show that the natural frequencies obtained from the ANSYS simulations are consistently higher than those obtained using the analytical method. The simplification of the moment of inertia at the impeller and balancing disc contributes primarily to the calculated errors. The optimized mathematical model reduces the errors in the natural frequencies from 12.96%, 12.13%, 9.96%, 5.85%, and 8.74% to 2.45%, 1.56%, 0.65%, 5.34%, and 2.28%, respectively. The optimization of natural frequencies offers better performance at lower-order modes, whereas its effects on higher-order modes are less significant. The optimization method is applicable to centrifugal pumps with back blades and reduces the error in theoretical calculations, based on reductions in the concentrated mass from 13.11%, 12.85%, 9.91%, and 7.2% to 3.7%, 3.86%, 0.57%, and 2.87%, respectively, thus further confirming the feasibility of the optimized model design. [ABSTRACT FROM AUTHOR]

Background: Toxoplasmosis affects a quarter of the world's population. Toxoplasma gondii (T.gondii) is an intracellular parasitic protozoa. Macrophages are necessary for proliferation and spread of T.gondii by regulating immunity and metabolism. Family with sequence similarity 96A (Fam96a; formally named Ciao2a) is an evolutionarily conserved protein that is highly expressed in macrophages, but whether it play a role in control of T. gondii infection is unknown. Methodology/principal findings: In this study, we utilized myeloid cell-specific knockout mice to test its role in anti-T. gondii immunity. The results showed that myeloid cell-specific deletion of Fam96a led to exacerbate both acute and chronic toxoplasmosis after exposure to T. gondii. This was related to a defectively reprogrammed polarization in Fam96a-deficient macrophages inhibited the induction of immune effector molecules, including iNOS, by suppressing interferon/STAT1 signaling. Fam96aregulated macrophage polarization process was in part dependent on its ability to fine-tuning intracellular iron (Fe) homeostasis in response to inflammatory stimuli. In addition, Fam96a regulated the mitochondrial oxidative phosphorylation or related events that involved in control of T. gondii. Conclusions/significance: All these findings suggest that Fam96a ablation in macrophages disrupts iron homeostasis and inhibits immune effector molecules, which may aggravate both acute and chronic toxoplasmosis. It highlights that Fam96a may autonomously act as a critical gatekeeper of T. gondii control in macrophages. Author summary: An important feature of macrophages is their ability to adopt many different phenotypes and functions in response to extracellular or intracellular cues. Functionally well-adapted macrophages are required for the defense against T. gondii. Here, we found that Fam96a expressed in macrophages played a role in control of T. gondii infection. Mechanically speaking, Fam96a regulated intracellular iron homeostasis, which affected immune effector molecules. Our study reveals that Fam96a may autonomously act as a critical gatekeeper of intracellular parasitic control by coupling Fe metabolism to adaptative remodeling of macrophage function. It provides a novel target for prevention and treatment of toxoplasmosis and other intracellular pathogens in the future. [ABSTRACT FROM AUTHOR]

The heterotrimeric G protein subunit Gsα couples receptors to activate adenylyl cyclase and is required for the intracellular cAMP response and protein kinase A (PKA) activation. Gsα is ubiquitously expressed in many cell types; however, the role of Gsα in neural crest cells (NCCs) remains unclear. Here we report that NCCs-specific Gsα knockout mice die within hours after birth and exhibit dramatic craniofacial malformations, including hypoplastic maxilla and mandible, cleft palate and craniofacial skeleton defects. Histological and anatomical analysis reveal that the cleft palate in Gsα knockout mice is a secondary defect resulting from craniofacial skeleton deficiencies. In Gsα knockout mice, the morphologies of NCCs-derived cranial nerves are normal, but the development of dorsal root and sympathetic ganglia are impaired. Furthermore, loss of Gsα in NCCs does not affect cranial NCCs migration or cell proliferation, but significantly accelerate osteochondrogenic differentiation. Taken together, our study suggests that Gsα is required for neural crest cells-derived craniofacial development. [ABSTRACT FROM AUTHOR]