Shimane University

Coastal marine ecosystems face complex pressures from both anthropogenic activities and climate variability. However, due to the recent overwhelming signals of human-induced impacts, there is a paucity of evidence of paleoecological archives on the combined effects of anthropogenic and climatic impacts on coastal marine ecosystem. By analyzing ostracod(s) as an indicator of paleo benthic ecosystem at a unique, less urbanized marine site in Hong Kong, we discovered that moderate signal (i.e., not overly strong, like total defaunation) of gradual ostracod community shifts in response to mild human-induced stresses, and it gave us a chance to observe how the ecosystem change gradually in response to different types of human and climatic stressors. We found that pollutants shifted marine community from 1960s, aligning with Hong Kong's industrial development history. Local ecosystem has been affected by eutrophication gradually, starting rather late with major negative impacts from 1980s. We also found evidence of strong monsoons between ~1940s-1960s which aided the establishment of tropical species. Our integrated investigation on paleoecology, environmental human stresses (eutrophication, hypoxia, and pollution), climate change, and socioeconomics in the past century reveals complicated change of coastal marine ecosystem under various influences and provides a critical baseline for better optimized management and conservation in this rapidly developing subtropical region.

Light-dependent activation of ascorbate biosynthesis is essential for accumulating ascorbate to mitigate photooxidative stress. The VTC2 and VTC3 genes play key roles in this process: VTC2 encodes GDP-L-galactose phosphorylase (GGP), the rate-limiting enzyme in ascorbate biosynthesis, and VTC3 encodes a putative protein kinase/phosphatase with an unknown function. Here, we investigated their functional and genetic relationship. In vtc3 mutants, VTC2 transcription and GGP activity were slightly enhanced, suggesting that VTC3 is not required for VTC2 expression. Additionally, the vtc3 mutation had negligible effects on the transcriptome and the activity of enzymes involved in ascorbate redox cycle regulation, narrowing down the possible roles of VTC3 in ascorbate metabolism. Under low-light conditions, ascorbate concentrations were lower in vtc2 than in vtc3 mutants, but vtc2 retained the ability to increase ascorbate concentrations under high-light stress, unlike vtc3. The simultaneous knockout of VTC2 and VTC3 further reduced ascorbate concentrations compared with the single mutants and severely impaired light-stress-induced ascorbate accumulation, resulting in impaired non-photochemical quenching and enhanced photooxidative damage. These findings highlight the additive effects of VTC2 and VTC3 on ascorbate biosynthesis and stress tolerance. The vtc2 vtc3 double mutants provide a valuable model for further elucidating the physiological roles of ascorbate in plants.

Perirenal fat (PRF), an ectopic fat depot lying adjacent to kidneys, is a risk factor for cardiometabolic and renal dysfunctions in patients with obesity and type 2 diabetes. We aimed to investigate the involvement of PRF in the pathophysiology and treatment of primary aldosteronism (PA). To this end, we measured PRF volume by abdominal CT and evaluated the relationships among PRF volume, cardiometabolic and renin-angiotensin-aldosterone system (RAAS) parameters, and therapeutic response to mineralocorticoid receptor antagonist (MRA) treatment in well-phenotyped PA patients. In addition, we evaluated the effects of MRA treatment on inflammation and fibrosis, potential downstream targets of MR signaling, by analyzing PRF obtained from obese (db/db) mice. PRF volume (PRF%) and visceral fat volume (VFV) were associated with various cardiometabolic and renal risk markers and RAAS parameters, such as body mass index, creatinine, triglyceride, high-density lipoprotein cholesterol, uric acid, fasting glucose, C-reactive protein, 24-h urine aldosterone, and 24-h urine normetanephrine (all P < 0.05). PRF%, but not VFV, positively correlated with changes in systolic and diastolic blood pressure and initial estimated glomerular filtration rate (eGFR) fall following MRA treatment after adjusting for confounders (all P < 0.05). In addition, MRA treatment decreased PRF expression of markers of macrophage infiltration and fibrosis in db/db mice (all P < 0.05). In conclusion, our results suggest that PRF accumulation is involved in the mechanisms linking MR activation to cardiometabolic and renal dysfunctions in PA patients. Moreover, PRF could be not only a prognostic factor but also a new therapeutic target for MRA-resistant hypertension.