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• A novel blended algorithm was proposed to remotely observe lake POC across China. • POC concentrations in 450 large lakes were first mapped using OLCI/Sentinel-3 data. • Lake POC concentration across China was low in the west and high in the east. Remote sensing monitoring of particulate organic carbon (POC) concentration is essential for understanding phytoplankton productivity, carbon storage, and water quality in global lakes. Some algorithms have been proposed, but only for regional eutrophic lakes. Based on in-situ data (N = 1269) in 49 lakes across China, we developed a blended POC algorithm by distinguishing Type-I and Type-II waters. Compared to Type-I, Type-II waters had higher reflectance peak around 560 nm (>0.0125 sr−1) and mean POC (4.65 ± 4.11 vs. 2.66 ± 3.37 mg/L). Furthermore, because POC was highly related to algal production (r = 0.85), a three-band index (R 2 = 0.65) and the phytoplankton fluorescence peak height (R 2 = 0.63) were adopted to estimate POC in Type-I and Type-II waters, respectively. The novel algorithm got a mean absolute percent difference (MAPD) of 35.93 % and outperformed three state-of-the-art formulas with MAPD values of 40.56–76.42 %. Then, the novel algorithm was applied to OLCI/Sentinel-3 imagery, and we first obtained a national map of POC in 450 Chinese lakes (> 20 km2), which presented an apparent spatial pattern of "low in the west and high in the east". In brief, water classification should be considered when remotely monitoring lake POC concentration over a large area. Moreover, a process-oriented method is required when calculating water column POC storage from satellite-derived POC concentrations in type-II waters. Our results contribute substantially to advancing the dynamic observation of the lake carbon cycle using satellite data. [Display omitted] [ABSTRACT FROM AUTHOR]

Sphingolipids (SPLs) represent a highly diverse and structurally complex lipid class. The discussion of SPL metabolism-related issues is of importance in understanding the neuropathological progression of Alzheimer's disease (AD). AD is characterized by the accumulation of extracellular deposits of the amyloid β-peptide (Aβ) and intraneuronal aggregates of the microtubule-associated protein tau. Critical roles of Aβ oligomer deposited and ganglioside GM1 could be formed as "seed" from insoluble GAβ polymer in initiating the pathogenic process, while tau might also mediate SPLs and their toxicity. The interaction between ceramide and α-Synuclein (α-Syn) accelerates the aggregation of ferroptosis and exacerbates the pathogenesis of AD. For instance, reducing the levels of SPLs can mitigate α-Syn accumulation and inhibit AD progression. Meanwhile, loss of SPLs may inhibit the expression of APOE4 and confer protection against AD, while the loss of APOE4 expression also disrupts SPLs homeostasis. Moreover, the heightened activation of sphingomyelinase promotes the ferroptosis signaling pathway, leading to exacerbated AD symptoms. Ferroptosis plays a vital role in the pathological progression of AD by influencing Aβ, tau, APOE, and α-Syn. Conversely, the development of AD also exacerbates the manifestation of ferroptosis and SPLs. We are compiling the emerging techniques (Derivatization and IM-MS) of sphingolipidomics, to overcome the challenges of AD diagnosis and treatment. In this review, we examined the intricate neuro-mechanistic interactions between SPLs and Aβ, tau, α-Syn, APOE, and ferroptosis, mediating the onset of AD. Furthermore, our findings highlight the potential of targeting SPLs as underexplored avenue for devising innovative therapeutic strategies against AD. [Display omitted] • The emerging technologies field of sphingolipidomic significantly improved the detectability to achieve more SPL biomarkers. • SPLs can affect AD development by regulating different pathogenesis (Aβ, tau, APOE, and α-Syn) of AD. • Ferroptosis may be a crucial potential pathway by which SPLs regulate AD. • Changes in SPLs might activate ferroptosis pathway consequently the pathogenesis of Aβ, tau, APOE, and α-Syn aggravated AD. [ABSTRACT FROM AUTHOR]