Dynamics and Optimal Taxation Control in a Bioeconomic Model with Stage Structure and Gestation Delay

A prey-predator model with gestation delay, stage structure for predator, and selective harvesting effort on mature predator is proposed, where taxation is considered as a control instrument to protect the population resource in prey-predator biosystem from overexploitation. It shows that interior equilibrium is locally asymptotically stable when the gestation delay is zero, and there is no periodic orbit within the interior of the first quadrant of state space around the interior equilibrium. An optimal harvesting policy can be obtained by virtue of Pontryagin's Maximum Principle without considering gestation delay; on the other hand, the interior equilibrium of model system loses as gestation delay increases through critical certain threshold, a phenomenon of Hopf bifurcation occurs, and a stable limit cycle corresponding to the periodic solution of model system is also observed. Finally, numerical simulations are carried out to show consistency with theoretical analysis

Production of X

We investigate the production of Xb in the process Υ(5S,6S)→γXb, where Xb is assumed to be the counterpart of X(3872) in the bottomonium sector as BB¯⁎ molecular state. We use the effective Lagrangian based on the heavy quark symmetry to explore the rescattering mechanism and calculate their production ratios. Our results have shown that the production ratios for Υ(5S,6S)→γXb are orders of 10-5 with reasonable cutoff parameter range α≃2~3. The sizeable production ratios may be accessible at the future experiments like forthcoming BelleII, which will provide important clues to the inner structures of the exotic state Xb

Identification of special key genes for alcohol-related hepatocellular carcinoma through bioinformatic analysis

Background Alcohol-related hepatocellular carcinoma (HCC) was reported to be diagnosed at a later stage, but the mechanism was unknown. This study aimed to identify special key genes (SKGs) during alcohol-related HCC development and progression. Methods The mRNA data of 369 HCC patients and the clinical information were downloaded from the Cancer Genome Atlas project (TCGA). The 310 patients with certain HCC-related risk factors were included for analysis and divided into seven groups according to the risk factors. Survival analyses were applied for the HCC patients of different groups. The patients with hepatitis B virus or hepatitis C virus infection only were combined into the HCC-V group for further analysis. The differentially expressed genes (DEGs) between the HCCs with alcohol consumption only (HCC-A) and HCC-V tumors were identified through limma package in R with cutoff criteria│log2 fold change (logFC)|>1.0 and p 2.0 and adj.p < 0.05. The intersection of the two sets of DEGs was considered SKGs which were then investigated for their specificity through comparisons between HCC-A and other four HCC groups. The SKGs were analyzed for their correlations with HCC-A stage and grade and their prognostic power for HCC-A patients. The expressional differences of the SKGs in the HCCs in whole were also investigated through Gene Expression Profiling Interactive Analysis (GEPIA). The SKGs in HCC were validated through Oncomine database analysis. Results Pathological stage is an independent prognostic factor for HCC patients. HCC-A patients were diagnosed later than HCC patients with other risk factors. Ten SKGs were identified and nine of them were confirmed for their differences in paired samples of HCC-A patients. Three (SLC22A10, CD5L, and UROC1) and four (SLC22A10, UROC1, CSAG3, and CSMD1) confirmed genes were correlated with HCC-A stage and grade, respectively. SPP2 had a lower trend in HCC-A tumors and was negatively correlated with HCC-A stage and grade. The SKGs each was differentially expressed between HCC-A and at least one of other HCC groups. CD5L was identified to be favorable prognostic factor for overall survival while CSMD1 unfavorable prognostic factor for disease-free survival for HCC-A patients and HCC patients in whole. Through Oncomine database, the dysregulations of the SKGs in HCC and their clinical significance were confirmed. Conclusion The poor prognosis of HCC-A patients might be due to their later diagnosis. The SKGs, especially the four stage-correlated genes (CD5L, SLC22A10, UROC1, and SPP2) might play important roles in HCC development, especially alcohol-related HCC development and progression. CD5L might be useful for overall survival and CSMD1 for disease-free survival predication in HCC, especially alcohol-related HCC

BrLAS, a GRAS Transcription Factor From Brassica rapa, Is Involved in Drought Stress Tolerance in Transgenic Arabidopsis

GRAS proteins belong to a plant-specific transcription factor family and play roles in diverse physiological processes and environmental signals. In this study, we identified and characterized a GRAS transcription factor gene in Brassica rapa, BrLAS, an ortholog of Arabidopsis AtLAS. BrLAS was primarily expressed in the roots and axillary meristems, and localized exclusively in the nucleus of B. rapa protoplast cells. qRT-PCR analysis indicated that BrLAS was upregulated by exogenous abscisic acid (ABA) and abiotic stress treatment [polyethylene glycol (PEG), NaCl, and H2O2]. BrLAS-overexpressing Arabidopsis plants exhibited pleiotropic characteristics, including morphological changes, delayed bolting and flowering time, reduced fertility and delayed senescence. Transgenic plants also displayed significantly enhanced drought resistance with decreased accumulation of ROS and increased antioxidant enzyme activity under drought treatment compared with the wild-type. Increased sensitivity to exogenous ABA was also observed in the transgenic plants. qRT-PCR analysis further showed that expression of several genes involved in stress responses and associated with leaf senescence were also modified. These findings suggest that BrLAS encodes a stress-responsive GRASs transcription factor that positively regulates drought stress tolerance, suggesting a role in breeding programs aimed at improving drought tolerance in plants

BrRLP48, Encoding a Receptor-Like Protein, Involved in Downy Mildew Resistance in Brassica rapa

Downy mildew, caused by Hyaloperonospora parasitica, is a major disease of Brassica rapa that causes large economic losses in many B. rapa-growing regions of the world. The genotype used in this study was based on a double haploid population derived from a cross between the Chinese cabbage line BY and a European turnip line MM, susceptible and resistant to downy mildew, respectively. We initially located a locus Br-DM04 for downy mildew resistance in a region about 2.7 Mb on chromosome A04, which accounts for 22.3% of the phenotypic variation. Using a large F2 mapping population (1156 individuals) we further mapped Br-DM04 within a 160 kb region, containing 17 genes encoding proteins. Based on sequence annotations for these genes, four candidate genes related to disease resistance, BrLRR1, BrLRR2, BrRLP47, and BrRLP48 were identified. Overexpression of both BrRLP47 and BrRLP48 using a transient expression system significantly enhanced the downy mildew resistance of the susceptible line BY. But only the leaves infiltrated with RNAi construct of BrRLP48 could significantly reduce the disease resistance in resistant line MM. Furthermore, promoter sequence analysis showed that one salicylic acid (SA) and two jasmonic acid-responsive transcript elements were found in BrRLP48 from the resistant line, but not in the susceptible one. Real-time PCR analysis showed that the expression level of BrRLP48 was significantly induced by inoculation with downy mildew or SA treatment in the resistant line MM. Based on these findings, we concluded that BrRLP48 was involved in disease resistant response and the disease-inducible expression of BrRLP48 contributed to the downy mildew resistance. These findings led to a new understanding of the mechanisms of resistance and lay the foundation for marker-assisted selection to improve downy mildew resistance in Brassica rapa

Overexpressed transient receptor potential vanilloid 1 (TRPV1) in lung adenocarcinoma harbours a new opportunity for therapeutic targeting

The specific biological function of transient receptor potential vanilloid 1 (TRPV1) in pathogenesis of lung adenocarcinoma (LUAD) remains unclear. In this study, TRPV1 expression in tumor tissues, primary cells and cell lines of LUAD, as well as the mechanism mediating its hyperexpression were systematically studied. Multiple models and techniques were adopted to elucidate the relationship between TRPV1 hyperexpression and tumor recurrence and metastasis. Results showed that TRPV1 expression was increased in tumor tissues and primary tumor cells of LUAD patients. The increased expression was associated with worse overall survival outcome and raised HIF1α levels. TRPV1 expression in A549 and NCI-H292 cells was increased after pretreatment with cigarette smoke extract or spermine NONOate. Moreover, A549 cells with TRPV1 overexpression has enhanced tumor growth rates in subcutaneous grafted tumor models, and increased intrapulmonary metastasis after tail vein infusion in nude BALB/c nude mice. Mechanistically, TRPV1 overexpression in A549 cells promoted HIF1α expression and nuclear translocation by promoting CREB phosphorylation and activation of NOS1-NO pathway, ultimately leading to accelerated cell proliferation and stronger invasiveness. In addition, based on photothermal effects, CuS-TRPV1 mAb effectively targeted and induced apoptosis of TRPV1-A549 cells both in vivo and in vitro, thereby mitigating tumor growth and metastasis induced by xenotransplantation of TRPV1-A549 cells. In conclusion, TRPV1 hyperexpression in LUAD is a risk factor for tumor progression and is involved in proliferation and migration of tumor cells through activation of HIF1α. Our study also attempted a new strategy inhibiting the recurrence and metastasis of LUAD: by CuS-TRPV1 mAb precisely kill TRPV1 hyperexpression cells through photothermal effects

Gastrodin improves osteoblast function and adhesion to titanium surface in a high glucose environment

Objective: To investigate the effects of gastrodin on the biological behavior of osteoblasts and osseointegration on the surface of the titanium plate in a high glucose environment, and to explore the possible regulatory mechanisms involved. Methods: A high glucose-induced oxidative damage model of MC3T3-E1 cells was established in vitro to observe the effects of gastrodin on cellular oxidative stress, cell viability, osteogenic differentiation, mineralization, migration, and adhesion ability on the titanium surface. Results: High glucose environment can cause oxidative stress damage to MC3T3-E1 cells, leading to a decrease in cell viability, osteogenesis, migration, adhesion and other functions. Gastrodin can upregulate the expression of antioxidant enzymes (Nrf2 and HO-1) and osteogenic differentiation related proteins (RUNX2 and BMP2) in MC3T3-E1 cells in high glucose environment, thereby inhibiting the excessive production of intracellular reactive oxygen species (ROS), reversing the decrease in cell viability, and improving the osteogenic differentiation and mineralization ability of osteoblasts. And gastrodin alleviated the decline in cell migration ability, improved the morphology of the cytoskeleton and increased the adhesion ability of osteoblasts on the surface of titanium plates in high glucose environment. However, gastrodin itself did not affect the cell viability, osteogenic differentiation and mineralization ability of osteoblasts in normal environment. Conclusions: Gastrodin may protect MC3T3-E1 cells osteogenesis and osseointegration on the surface of the titanium plate in vitro by upregulating antioxidant enzymes expression, and attenuating high glucose-induced oxidative stress. Therefore, gastrodin may be a potential drug to address the problem of poor implant osseointegration in patients with diabetes