Response of the cultivation suitability of Pu'er tea (Camellia sinensis var. assamica) to climate conditions and change in China.

Crop cultivation suitability plays a vital role in determining the distribution, quality, and production of crop and can be greatly affected by climate change. Therefore, evaluating crop cultivation suitability under climate change and identifying the factors influencing it can optimize crop cultivation layout and improve production and quality. Based on comprehensive datasets including geographical distribution points, climate data, soil characteristics, and topography, our study employed the MaxEnt model to simulate the potential distribution of Pu'er tea (Camellia sinensis var. assamica) cultivation suitability in Yunnan Province from 1961 to 2020. Furthermore, we assessed the consistency between the simulated suitable areas and the actual production of Pu'er tea. The results showed that precipitation of the warmest quarter, precipitation of the driest month, and average temperature in January were the three dominant environmental variables affecting the cultivation distribution of Pu'er tea. The high suitable areas for Pu'er tea cultivation in Yunnan Province were mainly distributed in the western and southern regions, accounting for 13.89% of the total area of Yunnan Province. The medium suitable areas are mainly distributed in the central and western regions of Yunnan Province, accounting for 20.07% of the total area of Yunnan Province. Over the past 60 years, the unsuitable area for Pu'er tea has increased, while the suitable area has shown a trend of migration to the southwest. Changes in precipitation and temperature were found to be the main drivers of the changes in the distribution of suitable areas for Pu'er tea. We also found a mismatch between the cultivation suitability and the actual production of Pu'er tea. Our study provides an accurate assessment and zoning analysis of the suitability of Pu'er tea cultivation in Yunnan Province, which can help optimize the layout of Pu'er tea cultivation and reduce potential climate risks.

Improving the Properties of Gray Cast Iron by Laser Surface Modification.

Laser surface modification is a widely used technology to improve the properties of functional surfaces. In this study, the properties of gray cast iron are modified by laser surface modification, and the influence of laser quenching on the properties of cast iron in terms of frictional vibration and noise, friction and wear, internal structure, residual stress, hardness, and corrosion resistance is investigated. The experimental results show that, after high-power laser quenching, the frictional vibrations and noise of most gray cast iron specimens are decreased, but the coefficients of friction against a bearing steel counterface are increased and more stable. The surface and sub-surface hardness of all laser-quenched cast iron specimens is significantly increased. The residual stresses on the surface of the cast iron specimens are significantly increased and changed from tensile to compressive residual stresses. Experimental modal testing results show that the modal damping ratios of the laser-treated specimens are increased significantly, although their modal frequencies are not significantly changed. In addition, through the metallographic observation, XRD (X-ray diffraction) analysis, and TEM (transmission electron microscopy) observation, it is found that the microstructures of the cast iron specimen after high-power laser modification become fine-grained, and the pearlite and ferrite in the matrix become fine martensite, which leads to the improvement of the dynamical, tribological, and chemical properties of cast iron after laser modification.

Effect and mechanism of apelin on lipopolysaccharide induced acute pulmonary vascular endothelial barrier dysfunction.

Vascular endothelial barrier dysfunction is the most prominent manifestation and important cause of mortality in infectious acute lung injury (ALI). Exogenous apelin is effective in ameliorating lipopolysaccharide (LPS)-induced inflammatory response in ALI lungs, reducing exudation of lung tissue and decreasing mortality. This study set out to investigate the association between apelin and Friend leukemia integration-1 (Fli-1) in the prevention and treatment of ALI, and to elucidate the molecular mechanism by which apelin protects the permeability of the vascular endothelial barrier. At the vivo functional level, lung wet/dry weight ratio was used to detect whole lung permeability, evans blue assay and dual fluorescent protein tracking assay were used to detect lung vascular endothelial permeability, HE staining to observe the inflammatory status of lung tissue, and immunofluorescence staining for VE-cadherin expression levels in blood vessels. The changes in inflammatory factors in bronchoalveolar lavage fluid (BALF) were detected by ELASA. Western blot was used to detect the expression level of proteins. qRT-PCR was performed to detect changes in mRNA expression of Fli-1 and adherent junction-related proteins. The correlation analysis of Fli-1 with vascular endothelial permeability and SRC showed that Fli-1 participated in the process of ALI. After preventive and therapeutic treatment of ALI mice with exogenous apelin, Fli-1, APJ, VE-cadherin, phosphorylated-VE-cadherin (p-VE-cadherin) and ß-catenin were up-regulated, while SRC, phosphorylated-SRC (p-SRC), VEGF and VEGF-R were down-regulated, which indicated that the stability of vascular endothelial barrier was enhanced. With the use of Fli-1 inhibitor irinotecan, the protective effect of apelin was weakened in various functional indexes, genes and proteins. The lung was maintained at the level of the injury. Our research shows that Fli-1 is involved in the LPS-induced ALI process. The molecular mechanism for apelin in preventing endothelial barrier dysfunction in ALI is through up-regulating Fli-1, thus regulating adherens junction-related proteins, and finally recovering the endothelial barrier function.

EPAS1 (Endothelial PAS Domain Protein 1) Orchestrates Transactivation of Endothelial ICAM1 (Intercellular Adhesion Molecule 1) by Small Nucleolar RNA Host Gene 5 (SNHG5) to Promote Hypoxic Pulmonary Hypertension.

[Figure: see text].

[Effects of apolipoprotein E on proliferation of mouse pulmonary arterial smooth muscle cells induced by hypoxia].

OBJECTIVE: To investigate the effects of apolipoprotein E (apoE) on the proliferation of pulmonary arterial smooth muscle cells (PASMCs) induced by hypoxia. METHODS: Primary culture of mouse PASMCs was prepared from male C57BL/6 mouse pulmonary artery by the method of tissue block anchorage. PASMCs were divided into four groups: normoxia group, normoxia with apoE administration group, hypoxia group and hypoxia with apoE administration group. The proliferation of PASMCs was observed by EdU incorporation. The protein levels of apoE, proliferating cell nuclear antigen (PCNA), protein kinase C (PKC) and phosphorylated protein kinase C (p-PKC) were analyzed by Western blot. RESULTS: The percentage of PASMCs proliferation of hypoxia group was significantly higher than that of normoxia group by 64.7% (P＜0.05), and the protein expression levels of PCNA and p-PKC of hypoxia group were up-regulated than those of normoxia group by 69.0% and 120.0%, while the protein expression of apoE was down-regulated by 51.0% (P＜0.05), respectively. The percentage of PASMCs proliferation of hypoxia with apoE administration group was significantly lower than that of hypoxia group by 19.6% (P＜0.05), and the protein expression levels of PCNA and p-PKC of hypoxia with apoE administration group were down-regulated than those of hypoxia group by 19.8% and 103.2% (P＜0.05), respectively. There was no significant difference among each group in the protein expression of PKC, nor do there any significant difference between normoxia group and hypoxia group in the protein expression of p-PKC (P＞0.05). CONCLUSION: ApoE can inhibit the proliferation of PASMCs induced by hypoxia, and the mechanism of its effect may be attributed to blocking PKC pathway.

[Changes of apoE protein expression in lung of mice with hypoxic pulmonary arterial hypertension].

OBJECTIVE: To observe the changes of apolipoprotein E (apoE) protein expression of pulmonary tissue in mice with pulmonary hypertension induced by hypoxia. METHODS: The animal model of hypoxic pulmonary hypertension was established by exposing the mice to isobaric hypoxic chamber for 3 weeks (23 h/d, regular chow feed).Twenty male wild type (WT) C57BL/6 mice and twenty apoE gene knockout (apoE-KO) mice were randomly divided into normoxia group and hypoxia group. The plasma concentrations of low density lipoprotein (LDL), high density lipoprotein (HDL) and total cholesterol were detected by ELISA method. The protein expression of apoE in lung and liver, and peroxisome proliferators-activated receptor gamma (PPARγ) in lung were measured by Western blot. RESULTS: ①In WT mice, the right ventricular systolic pressure (RVSP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) of hypoxia group were significantly higher than those of normoxia group by 68% and 59% (P<0.05), respectively. The plasma concentration of HDL and HDL/LDL of hypoxia group were significantly lower than those of normoxia group by 17% and 40% (P<0.05), respectively.The protein expression of apoE in lung and in liver of hypoxia group were significantly down-regulated than those of normoxia group by 48% and 52% (P<0.05), respectively.The protein expression of PPARγ in lung was significantly down-regulated than that of normoxia group by 37%(P<0.05).RVSP were significantly negative correlated with the protein levels of apoE and PPARγ in lung (P<0.01).② In apoE-KO mice, RVSP and the weight ratio of RV to LV+S of hypoxia group were significantly higher than those of normoxia group by 96% and 86% (P<0.05), respectively.RVSP and RV to (LV+S) of hypoxia group in apoE-KO mice were significantly higher than those of hypoxia group in WT mice by 29% and 24% (P<0.05), respectively. CONCLUSIONS: Down-regulated expression of apoE in lung tissue participates in the pathological proceeding of pulmonary hypertension induced by hypoxia.