Carbon storage through China's planted forest expansion.

China's extensive planted forests play a crucial role in carbon storage, vital for climate change mitigation. However, the complex spatiotemporal dynamics of China's planted forest area and its carbon storage remain uncaptured. Here we reveal such changes in China's planted forests from 1990 to 2020 using satellite and field data. Results show a doubling of planted forest area, a trend that intensified post-2000. These changes lead to China's planted forest carbon storage increasing from 675.6 ± 12.5 Tg C in 1990 to 1,873.1 ± 16.2 Tg C in 2020, with an average rate of ~ 40 Tg C yr-1. The area expansion of planted forests contributed ~ 53% (637.2 ± 5.4 Tg C) of the total above increased carbon storage in planted forests compared with planted forest growth. This proactive policy-driven expansion of planted forests has catalyzed a swift increase in carbon storage, aligning with China's Carbon Neutrality Target for 2060.

Comparison between the stem and leaf photosynthetic productivity in Eucalyptus urophylla plantations with different age.

MAIN CONCLUSION: We developed a more realistic modeling framework by integrating stem photosynthesis into the canopy carbon assimilation model to compare the photosynthetic productivity between the stem and leaf of Eucalyptus urophylla plantations. Stems of Eucalyptus species with smooth outer bark have photosynthetic green tissue that can recycle internal stem CO2. However, the potential contribution of stem photosynthesis to forest productivity has not previously been adequately quantified, and we also do not know how it compares to leaf photosynthetic productivity. To assist in addressing this knowledge gap, we conducted field surveys in Eucalyptus urophylla plantations of different ages and developed a more realistic modeling framework by integrating stem photosynthesis into the existing canopy carbon assimilation model. We calculated the proportion of tree stems shaded by neighboring tree trunks based on Poisson spatial point process. Under the stand density of 2000 trees per hectare, the light absorption area of tree trunks of 2-year-old and 7-year-old E. urophylla plantations were 0.11 (± 0.15) and 0.35 (± 0.12) m2 stem m-2 land, the stem photosynthetic productivity (GPPstem) was 0.72 (± 0.45) and 1.81 (± 1.12) mol C m-2 month-1, and the ratios of GPPstem to leaf photosynthetic productivity (GPPleaf) were 5.10 and 8.17% for 2- and 7-year-old plantations, respectively. Overall, this study presents the feasibility of incorporating stem photosynthesis into the productivity prediction of E. urophylla plantations by developing the stem light absorption model.

IL-6 inhibitors effectively reverse post-infarction cardiac injury and ischemic myocardial remodeling via the TGF-ß1/Smad3 signaling pathway.

Approximately one in four myocardial infarctions occur in older patients. The majority of therapeutic advances are either not appropriate or not tested in elderly patients. The main reasons for deviating from the guidelines are justified concerns regarding the effectiveness of the recommended forms of therapy, fear of adverse drug reactions and ethical concerns. Targeting interleukin 6 (IL-6) for ventricular remodeling after cardiovascular damage is a feasible alternative to standard polypharmaceutics, but the underlying molecular mechanisms are not well understood. Continuous activation of the IL-6-associated cytokine receptor gp130 leads to cardiomyopathic hypertrophy. TGFß1 is involved in forming fibrosis in various organs, and its overexpression can cause myocardial hypertrophy and fibrosis. Il-6 has been hypothesized to be indirectly involved in cardiac remodeling via the TGFß1/Smad signaling transduction pathway. In the present study, a rat model of acute myocardial ischemia, IL-6 and IL-6 receptor blockers were injected directly into the necrotic myocardium. Changes in cardiac function, myocardial infarction area, myocardial collagen, necrotic myocardial fibrosis and levels of TGFß1, IL-6 and MMP2/9 were quantified in myocardial tissue fibrosis by ELISA. The present study demonstrated that IL-6 stimulated myocardial fibrosis through the TGFß1-Smad-MM2/9 signaling transduction pathway. Overall, this provided a solid foundation for understanding the relationship between IL-6 and ventricular remodeling.

Impact of rising temperatures on the biomass of humid old-growth forests of the world.

BACKGROUND: Understanding how warming influence above-ground biomass in the world's forests is necessary for quantifying future global carbon budgets. A climate-driven decrease in future carbon stocks could dangerously strengthen climate change. Empirical methods for studying the temperature response of forests have important limitations, and modelling is needed to provide another perspective. Here we evaluate the impact of rising air temperature on the future above-ground biomass of old-growth forests using a model that explains well the observed current variation in the above-ground biomass over the humid lowland areas of the world based on monthly air temperature. RESULTS: Applying this model to the monthly air temperature data for 1970-2000 and monthly air temperature projections for 2081-2100, we found that the above-ground biomass of old-growth forests is expected to decrease everywhere in the humid lowland areas except boreal regions. The temperature-driven decrease is estimated at 41% in the tropics and at 29% globally. CONCLUSIONS: Our findings suggest that rising temperatures impact the above-ground biomass of old-growth forests dramatically. However, this impact could be mitigated by fertilization effects of increasing carbon dioxide concentration in the atmosphere and nitrogen deposition.

CXCR6 deficiency attenuates pressure overload-induced monocytes migration and cardiac fibrosis through downregulating TNF-α-dependent MMP9 pathway.

An immerging role of TNF-α in collagen synthesis and cardiac fibrosis implies the significance of TNF-α production in the development of myocardial remodeling. Our previous study showed a reduction of TNF-α and attenuated cardiac remodeling in CXCR6 knockout (KO) mice after ischemia/reperfusion injury. However, the potential mechanism of TNF-α-mediated cardiac fibrosis with pressure overload has not been well elucidated. In the present study, we aim to investigate the role of CXCR6 in TNF-α release and myocardial remodeling in response to pressure overload. Pressure overload was performed by constriction of transverse aorta (TAC) surgery on CXCR6 KO mice and C57 wild-type (WT) counterparts. At 6 weeks after TAC, cardiac remodeling was assessed by echocardiography, cardiac TNF-α release and its type I receptor (TNFRI), were detected by ELISA and western blot, collagen genes Col1a1 (type I) and Col3a1 (type III) were examined by real-time PCR. Compared with CXCR6 WT mice, CXCR6 KO mice exhibited less cardiac dysfunction, reduced expression of TNFRI, Col1a1 and Col3a. In vitro, we confirmed that CXCR6 deficiency led to reduced homing and infiltration of CD11b(+) monocytes, which contributed to attenuated TNF-α release in myocardium. Furthermore, TNFRI antagonist pretreatment blocked AT1 receptor signaling and NOX4 expression, reduced collagen synthesis, and blunted the activity of MMP9 in CXCR6 WT mice after TAC, but these were not observed in CXCR6 KO mice. In the present work, we propose a mechanism that CXCR6 is essential for pressure overload-mediated myocardial recruitment of monocytes, which contributes to cardiac fibrosis through TNF-α-dependent MMP9 activation and collagen synthesis.