Improving maize growth and development simulation by integrating temperature compensatory effect under plastic film mulching into the AquaCrop model

Temperature compensatory effect, which quantifies the increase in cumulative air temperature from soil temperature increase caused by mulching, provides an effective method for incorporating soil temperature into crop models. In this study, compensated temperature was integrated into the AquaCrop model to investigate the capability of the compensatory effect to improve assessment of the promotion of maize growth and development by plastic film mulching(PM). A three-year experiment was conducted from2014 to 2016 with two maize varieties(spring and summer) and two mulching conditions(PM and non-mulching(NM)), and the AquaCrop model was employed to reproduce crop growth and yield responses to changes in NM, PM, and compensated PM. A marked difference in soil temperature between NM and PM was observed before 50 days after sowing(DAS) during three growing seasons. During sowing–emergence and emergence–tasseling, the increase in air temperature was proportional to the compensatory coefficient, with spring maize showing a higher compensatory temperature than summer maize. Simulation results for canopy cover(CC) were generally in good agreement with the measurements, whereas predictions of aboveground biomass and grain yield under PM indicated large underestimates from 60 DAS to the end of maturity. Simulations of spring maize biomass and yield showed general increase based on temperature compensation, accompanied by improvement in modeling accuracy, with RMSEs decreasing from 2.5 to 1.6 t ha^(-1)and from 4.1 t to 3.4 t ha^(-1). Improvement in biomass and yield simulation was less pronounced for summer than for spring maize, implying that crops grown during low-temperature periods would benefit more from the compensatory effect. This study demonstrated the effectiveness of the temperature compensatory effect to improve the performance of the AquaCrop model in simulating maize growth under PM practices.

Type XIX collagen: a promising biomarker from the basement membranes

Among collagen members in the collagen superfamily,type XIX collagen has raised increasing interest in relation to its structural and biological roles.Type XIX collagen is a Fibril-Associated Collagen with Interrupted Triple helices member,one main subclass of collagens in this superfamily.This collagen contains a triple helix composed of three polypeptide segments aligned in parallel and it is associated with the basement membrane zone in different tissues.The molecular structure of type XIX collagen consists of five collagenous domains,COL1 to COL5,interrupted by six non-collagenous domains,NCI to NC6.The most relevant domain by which this collagen exerts its biological roles is NCI domain that can be cleavage enzymatically to release matricryptins,exerting anti-tumor and anti-angiogenic effect in murine and human models of cancer.Under physiological conditions,type XIX collagen expression decreases after birth in different tissues although it is necessary to keep its basal levels,mainly in skeletal muscle and hippocampal and telencephalic interneurons in brain.Notwithstanding,in amyotrophic lateral sclerosis,altered transcript expression levels show a novel biological effect of this collagen beyond its structural role in basement membranes and its anti-tumor and anti-angiogenic properties.Type XIX collagen can exert a compensatory effect to ameliorate the disease progression under neurodegenerative conditions specific to amyotrophic lateral sclerosis in transgenic SOD1 G93 A mice and amyotrophic lateral sclerosis patients.This novel biological role highlights its nature as prognostic biomarker of disease progression in and as promising therapeutic target,paving the way to a more precise prognosis of amyotrophic lateral sclerosis.

Impaired Compensatory Vasodilatory Effect Mediated by Wolfram Syndrome 1 and Corticotropin-Releasing Hormone Family Peptides in 17α-Ethynylestradiol-Induced Intrahepatic Cholestasis Pregnant Rats When Under Additional Acute Hypoxia Stress

Objective:To investigate the possible regulatory mechanism of corticotropin-releasing hormone(CRH),urocortin(UCN),and Wolfram syndrome 1(WFS1)in 17α-ethynylestradiol(EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion(IR)model.Methods:Pregnant rats(n=60)were randomly divided into four experimental groups by random number table(Control,EE,IR,and EE-IR groups),and were studied on the 17^(th),19th,and 21st gestational days(GD)(n=5 in each group at the indicated time).Growth and development indicators of fetal rats among these four groups were recorded.Enzyme-linked immunosorbent assay was employed to detect CRH,UCN,and WFS1 levels in maternal sera.Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH,UCN,and WFS1.Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons.Results:A significant difference was found in placenta weight(F=8.10,P<0.05),fetal rat weight(F=40.86,P<0.05),fetal rat length(F=61.61,P<0.05),and fetal rat tail length(F=55.63,P<0.05)among four groups on the 17^(th),19th,and 21st GD.What’s more,the overall differences of maternal serum UCN levels among Control,EE,IR,and EE-IR groups were significant(F=2.48,P<0.05).Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control(0.46±0.15vs.0.24±0.09,P<0.05),EE(0.46±0.15vs.0.17±0.04,P>0.05),and IR(0.46±0.15vs.0.22±0.15,P>0.05)groups at 19th GD,indicating that endoplasmic reticulum stress may be activated.However,the expression of CRH(0.42±0.05vs.0.58±0.12,P<0.05),UCN(0.43±0.01vs.0.47±0.16,P>0.05),and WFS1(0.57±0.07vs.0.74±0.12,P>0.05)protein in the EE-IR group was subsided compared to the IR group at 17^(th) GD.Conclusion:Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model.This study revealed that significant changes in the maternal sera level of UCN,placental level of WFS1 mRNA and placental levels of CRH,UCN,and WFS1 protein in chronic versus acute stress in a rat model of pregnancy.This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels,following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.