Global bounded solutions to the Boltzmann equation for a polyatomic gas

In this paper we consider the Boltzmann equation modelling the motion of a polyatomic gas where the integration collision operator in comparison with the classical one involves an additional internal energy variable $I\in\mathbb{R}_+$ and a parameter $\delta\geq 2$ standing for the degree of freedom. In perturbation framework, we establish the global well-posedness for bounded mild solutions near global equilibria on torus. The proof is based on the $L^2\cap L^\infty$ approach. Precisely, we first study the $L^2$ decay property for the linearized equation, then use the iteration technique for the linear integral operator to get the linear weighted $L^\infty$ decay, and in the end obtain $L^\infty$ bounds as well as exponential time decay of solutions for the nonlinear problem with the help of the Duhamel's principle. Throughout the proof, we present a careful analysis for treating the extra effect of internal energy variable $I$ and the parameter $\delta$.Comment: 31 pages. All comments are welcom

Global mild solution with polynomial tail for the Boltzmann equation in the whole space

We are concerned with the Cauchy problem on the Boltzmann equation in the whole space. The goal is to construct global-in-time bounded mild solutions near Maxwellians with the perturbation admitting a polynomial tail in large velocities. The proof is inspired by the Caflisch's decomposition together with an $L^2- L^\infty$ interplay technique developed by Guo. The full range of both hard and soft potentials under the Grad's cutoff assumption can be covered. In contrast with the torus case, the main difficulty to be overcome in case of the whole space is the slower time decay of solutions.Comment: 39 pages. All comments are welcom

Remote silicate supply regulates spring phytoplankton bloom magnitude in the Gulf of Maine

© The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Zang, Z., Ji, R., Liu, Y., Chen, C., Li, Y., Li, S., & Davis, C. S. Remote silicate supply regulates spring phytoplankton bloom magnitude in the Gulf of Maine. Limnology and Oceanography Letters, 7, (2022): 277-285, https://doi.org/10.1002/lol2.10245.Spring phytoplankton blooms in the Gulf of Maine (GoM) are sensitive to climate-related local and remote forcing. Nutrient supply through the slope water intrusion has been viewed as critical in regulating the GoM spring blooms, with an assumption that nitrogen is the primary limiting nutrient. In recent years, this paradigm has been challenged, with silicate being recognized as another potential limiting nutrient, but the source of silicate and its associated water mass remain difficult to be determined. In this study, a time series of spring bloom magnitude was constructed using a self-organizing map algorithm, and then correlated with the fluctuation of water composition in the deep Northeast Channel. The results reveal the importance of silicate supply from previously less-recognized deep Scotian Shelf Water inflow. This study offers a new hypothesis for spring bloom regulation, providing a better understanding of mechanisms controlling the spring bloom magnitude in the GoM.This study was supported by NOAA Coastal and Ocean Climate Application (COCA) Program (NA17OAR4310273) and NSF Northeast US Shelf-Long-Term Ecological Research (NES-LTER) Program (OCE-1655686)

Transient receptor potential channel 1 deficiency impairs host defense and proinflammatory responses to bacterial infection by regulating protein kinase Cα signaling

Transient receptor potential channel 1 (TRPC1) is a nonselective cation channel that is required for Ca2+ homeostasis necessary for cellular functions. However, whether TRPC1 is involved in infectious disease remains unknown. Here, we report a novel function for TRPC1 in host defense against Gram-negative bacteria. TRPC1-/- mice exhibited decreased survival, severe lung injury, and systemic bacterial dissemination upon infection. Furthermore, silencing of TRPC1 showed decreased Ca2+ entry, reduced proinflammatory cytokines, and lowered bacterial clearance. Importantly, TRPC1 functioned as an endogenous Ca2+ entry channel critical for proinflammatory cytokine production in both alveolar macrophages and epithelial cells. We further identified that bacterium-mediated activation of TRPC1 was dependent on Toll-like receptor 4 (TLR4), which induced endoplasmic reticulum (ER) store depletion. After activation of phospholipase Cγ (PLC-γ), TRPC1 mediated Ca2+ entry and triggered protein kinase Cα (PKC-α) activity to facilitate nuclear translocation of NF-kB/Jun N-terminal protein kinase (JNK) and augment the proinflammatory response, leading to tissue damage and eventually mortality. These findings reveal that TRPC1 is required for host defense against bacterial infections through the TLR4-TRPC1-PKCγ signaling circuit.Fil: Zhou, Xikun. University Of North Dakota; Estados Unidos. West China Hospital Of Sichuan University; ChinaFil: Ye, Yan. University Of North Dakota; Estados UnidosFil: Sun, Yuyang. University Of North Dakota; Estados UnidosFil: Li, Xuefeng. West China Hospital Of Sichuan University; China. University Of North Dakota; Estados UnidosFil: Wang, Wenxue. University Of North Dakota; Estados UnidosFil: Privratsky, Breanna. University Of North Dakota; Estados UnidosFil: Tan, Shirui. University Of North Dakota; Estados UnidosFil: Zhou, Zongguang. West China Hospital Of Sichuan University; ChinaFil: Huang, Canhua. West China Hospital Of Sichuan University; ChinaFil: Wei, Yu-Quan. West China Hospital Of Sichuan University; ChinaFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute Of Environmental Health Sciences; Estados UnidosFil: Singh, Brij B.. University Of North Dakota; Estados UnidosFil: Wu, Min. University Of North Dakota; Estados Unido

Vitamin E Inhibits Osteoclastogenesis in Protecting Osteoporosis

The most common orthopedic condition affecting senior adults is osteoporosis, which is defined by a decrease in bone mass and strength as well as microstructural degradation that leads to fragility fractures. Bone remodeling is a well-planned, ongoing process that replaces deteriorated, old bone with new, healthy bone. Bone resorption and bone creation work together during the cycle of bone remodeling to preserve the bone’s volume and microarchitecture. The only bone-resorbing cells in the human body, mononuclear preosteoclasts fuse to form osteoclasts, are multinucleated cells. In numerous animal models or epidemiological studies, vitamin E’s anti-osteoporotic characteristics have been extensively described. This review aims to summarize recent developments in vitamin E’s molecular features as a bone-protective agent. In RANKL/RANK/OPG signaling pathway, vitamin E inhibits synthesis of RANKL, stimulation of c-Fos, and increase level of OPG. Vitamin E also inhibits inflammatory cytokines, such as TNF-α, IL-1, IL-6, IL-27, and MCP-1, negative regulating the JAK–STAT, NF-κB, MAPK signaling pathways. Additionally, vitamin E decreases malondialdehyde and increases superoxide dismutase, GPx and heme oxygenase-1, in suppressing osteoclasts. In this article, we aim to give readers the most recent information on the molecular pathways that vitamin E uses to enhance bone health