Optimal decay rates to the contact wave for 1-D compressible Navier-Stokes equations

This paper investigates the decay rates of the contact wave in one-dimensional Navier-Stokes equations. We study two cases of perturbations, with and without zero mass condition, i.e., the integration of initial perturbations is zero and non-zero, respectively. For the case without zero mass condition, we obtain the optimal decay rate $(1+t)^{-\frac{1}{2}}$ for the perturbation in $L^\infty$ norm, which provides a positive answer to the conjecture in \cite{HMX}. We applied the anti-derivative method, introducing the diffusion wave to carry the initial excess mass, diagonalizing the integrated system, and estimating the energy of perturbation in the diagonalized system. Precisely, due to the presence of diffusion waves, the decay rates for errors of perturbed system are too poor to get the optimal decay rate. We find the dissipation structural in the diagonalized system, see \cref{ds}. This observation makes us able to fully utilize the fact that the sign of the derivative of the contact wave is invariant and to control the terms with poor decay rates in energy estimates. For the case with zero mass condition, there are also terms with poor decay rates. In this case, note that there is a cancellation in the linearly degenerate field so that the terms with poor decay rates will not appear in the second equation of the diagonalized system. Thanks to this cancellation and a Poincar\'e type of estimate obtained by a critical inequality introduced by \cite{HLM}, we get the decay rate of $\ln^{\frac{1}{2}} (2+t)$ for $L^2$ norm of anti-derivatives of perturbation and $(1+t)^{-\frac{1}{2}}\ln^{\frac{1}{2}}(2+t)$ for the $L^2$ norm of perturbation itself, the decay rates are optimal, which is consistent with the results obtained by using pointwise estimate in \cite{XZ} for the system with artificial viscosity

Vanishing viscosity limit to the planar rarefaction wave with vacuum for 3-D full compressible Navier-Stokes equations with temperature-dependent transport coefficients

In this paper, we construct a family of global-in-time solutions of the 3-D full compressible Navier-Stokes (N-S) equations with temperature-dependent transport coefficients (including viscosity and heat-conductivity), and show that at arbitrary times {and arbitrary strength} this family of solutions converges to planar rarefaction waves connected to the vacuum as the viscosity vanishes in the sense of $L^\infty(\R^3)$. We consider the Cauchy problem in $\R^3$ with perturbations of the infinite global norm, particularly, periodic perturbations. To deal with the infinite oscillation, we construct a suitable ansatz carrying this periodic oscillation such that the difference between the solution and the ansatz belongs to some Sobolev space and thus the energy method is feasible. The novelty of this paper is that the viscosity and heat-conductivity are temperature-dependent and degeneracies caused by vacuum. Thus the a priori assumptions and two Gagliardo-Nirenberg type inequalities are essentially used. Next, more careful energy estimates are carried out in this paper, by studying the zero and non-zero modes of the solutions, we obtain not only the convergence rate concerning the viscosity and heat conductivity coefficients but also the exponential time decay rate for the non-zero mode.Comment: The version has been updated and the results have been extende

LeTetR Positively Regulates 3-Hydroxylation of the Antifungal HSAF and Its Analogs in \u3ci\u3eLysobacter enzymogenes\u3c/i\u3e OH11

The biocontrol agent Lysobacter enzymogenes OH11 produces several structurally distinct antibiotic compounds, including the antifungal HSAF (Heat Stable Antifungal Factor) and alteramides, along with their 3-dehydroxyl precursors (3-deOH). We previously showed that the 3-hydroxylation is the final step of the biosynthesis and is also a key structural moiety for the antifungal activity. However, the procedure through which OH11 regulates the 3-hydroxylation is still not clear. In OH11, the gene orf3232 was predicted to encode a TetR regulator (LeTetR) with unknown function. Here, we deleted orf3232 and found that the LeTetR mutant produced very little HSAF and alteramides, while the 3-deOH compounds were not significantly affected. The production of HSAF and alteramides was restored in orf3232-complemented mutant. qRT-PCR showed that the deletion of orf3232 impaired the transcription of a putative fatty acid hydroxylase gene, orf2195, but did not directly affect the expression of the HSAF biosynthetic gene cluster (hsaf ). When an enzyme extract from E. coli expressing the fatty acid hydroxylase gene, hsaf -orf7, was added to the LeTetR mutant, the production of HSAF and alteramides increased by 13–14 fold. This study revealed a rare function of the TetR family regulator, which positively controls the final step of the antifungal biosynthesis and thus controls the antifungal activity of the biocontrol agent

Spermidine-Regulated Biosynthesis of Heat-Stable Antifungal Factor (HSAF) in Lysobacter enzymogenes OH11

Heat-Stable Antifungal Factor (HSAF) and its analogs are antifungal natural products produced by the biocontrol agent Lysobacter enzymogenes. The production of HSAF is greatly influenced by environmental stimuli and nutrients, but the underlying molecular mechanism is mostly unclear. Here, we found that HSAF production in L. enzymogenes OH11 is strictly controlled by spermidine, which is the most prevalent triamine in bacteria. When added into OH11 cultures, spermidine regulated the production of HSAF and analogs in a concentration-dependent manner. To verify the role of spermidine, we deleted LeSDC and LeADC genes, encoding S-adenosylmethionine decarboxylase and arginine decarboxylase, respectively, that are the key enzymes for spermidine biosynthesis. Both deletion mutants produced barely detectable spermidine and HSAF including its analogs, whereas the antifungals production was restored by exogenous spermidine. The results showed that the OH11 cells must maintain a proper spermidine homeostasis for the antifungals production. Indeed, the expression level of the key HSAF biosynthetic genes was significantly impaired in LeSDC and LeADC mutants, and exogenous spermidine restored the gene expression level in the mutants. Ornithine is a key substrate for HSAF biosynthesis, and OH11 genome contains arg1 and arg2 genes, encoding arginases that convert arginine to ornithine. While the expression of arg1 and arg2 was affected slightly upon mutation of LeSDC and LeADC, exogenous spermidine significantly increased the arginase gene expression in LeSDC and LeADC mutants. Together, the data revealed a previously unrecognized mechanism, in which spermidine controls antibiotic production through controlling both the biosynthetic genes and the substrate-production genes

HiPSC-derived cardiac tissue for disease modeling and drug discovery

Li, J.; Hua, Y.; Miyagawa, S.; Zhang, J.; Li, L.; Liu, L.; Sawa, Y. hiPSC-Derived Cardiac Tissue for Disease Modeling and Drug Discovery. Int. J. Mol. Sci. 2020, 21, 8893

Isolation of mouse mesenchymal stem cells with normal ploidy from bone marrows by reducing oxidative stress in combination with extracellular matrix

<p>Abstract</p> <p>Background</p> <p>Isolation of mouse MSCs (mMSCs) with normal ploidy from bone marrow remains challenging. mMSCs isolated under 20% O₂are frequently contaminated by overgrown hematopoietic cells, and could also be especially vulnerable to oxidative damage, resulting in chromosomal instability. Culture under low oxygen or extracellular matrix (ECM) improves proliferation of MSCs in several species. We tested the hypothesis that culture under low oxygen in combination with ECM prepared from mouse embryonic fibroblast (MEF-ECM) could be used to purify proliferative mMSCs, and to reduce oxidative damage and maintain their chromosomal stability.</p> <p>Results</p> <p>Optimization of culture conditions under 20% O₂resulted in immortalization of mMSCs, showing extensive chromosome abnormalities, consistent with previous studies. In contrast, culture under low oxygen (2% O₂) improved proliferation of mMSCs and reduced oxidative damage, such that mMSCs were purified simply by plating at low density under 2% O₂. MEF-ECM reduced oxidative damage and enhanced proliferation of mMSCs. However, these isolated mMSCs still exhibited high frequency of chromosome abnormalities, suggesting that low oxygen or in combination with MEF-ECM was insufficient to fully protect mMSCs from oxidative damage. Notably, antioxidants (alpha -phenyl-t-butyl nitrone (PBN) and N-acetylcysteine (NAC)) further reduced DNA damage and chromosomal abnormalities, and increased proliferation of mMSCs. mMSCs isolated by the combination method were successfully used to generate induced pluripotent stem (iPS) cells by ectopic expression of Oct4, Sox2, Klf4 and c-Myc.</p> <p>Conclusions</p> <p>We have developed a technique that allows to reduce the number of karyotypic abnormalities for isolation of primary mMSCs and for limited culture period by combination of low oxygen, MEF-ECM, antioxidants and low density plating strategy. The effectiveness of the new combination method is demonstrated by successful generation of iPS cells from the isolated mMSCs. However, a culture system for mMSCs still is needed to prevent all the anomalies, especially after a long-term culture period.</p

Angiotensin II upregulates the expression of placental growth factor in human vascular endothelial cells and smooth muscle cells

<p>Abstract</p> <p>Background</p> <p>Atherosclerosis is now recognized as a chronic inflammatory disease. Angiotensin II (Ang II) is a critical factor in inflammatory responses, which promotes the pathogenesis of atherosclerosis. Placental growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family cytokines and is associated with inflammatory progress of atherosclerosis. However, the potential link between PlGF and Ang II has not been investigated. In the current study, whether Ang II could regulate PlGF expression, and the effect of PlGF on cell proliferation, was investigated in human vascular endothelial cells (VECs) and smooth muscle cells (VSMCs).</p> <p>Results</p> <p>In growth-arrested human VECs and VSMCs, Ang II induced PlGF mRNA expression after 4 hour treatment, and peaked at 24 hours. 10^-6mol/L Ang II increased PlGF protein production after 8 hour treatment, and peaked at 24 hours. Stimulation with Ang II also induced mRNA expression of VEGF receptor-1 and -2(VEGFR-1 and -2) in these cells. The Ang II type I receptor (AT₁R) antagonist blocked Ang II-induced PlGF gene expression and protein production. Several intracellular signals elicited by Ang II were involved in PlGF synthesis, including activation of protein kinase C, extracellular signal-regulated kinase 1/2 (ERK1/2) and PI3-kinase. A neutralizing antibody against PlGF partially inhibited the Ang II-induced proliferation of VECs and VSMCs. However, this antibody showed little effect on the basal proliferation in these cells, whereas blocking antibody of VEGF could suppress both basal and Ang II-induced proliferation in VECs and VSMCs.</p> <p>Conclusion</p> <p>Our results showed for the first time that Ang II could induce the gene expression and protein production of PlGF in VECs and VSMCs, which might play an important role in the pathogenesis of vascular inflammation and atherosclerosis.</p