Ecological network construction and optimization in Guangzhou from the perspective of biodiversity conservation.

Rapid urbanization has resulted in fragmentation and decreased connectivity in urban landscapes, endangering regional biodiversity conservation and high-quality, sustainable development. networks (ENs) construction and optimization is a critical technique to enhance landscape connectivity effectively, promote species interaction and dispersal, and thereby hence urban biodiversity., most existing studies on ENs construction have been undertaken from the perspective of ecosystem service functions or the value of landscape structure, with regional species still being overlooked. on the distribution data of critical species in this study, the maximum entropy model (MaxEnt), wilderness mapping model, and granularity reverse method were integrated to identify ecological sources. the habitat quality (HQ) index was utilized to construct a resistance surface modified by landscape connectivity and ecological sensitivity. findings indicate that: (1) a grid scale of 1700 m is the relatively optimal minimum threshold for ecological source sites in Guangzhou; (2) 35 crucial ecological sources in Guangzhou are identified, with a total area of 1100.42 km2, mainly woodlands, distributed in mountain systems in the northern and central parts of the city; and (3) 59 ecological corridors are identified, with a total length of 817.4 km, with a relatively high density in the central part of the city. some extent, this study offers fresh ideas for constructing urban ENs from the standpoint of biodiversity conservation. contributes to the city achieving a win-win economic development and ecological protection situation.

Effect of Oyster Meat Preload on Postmeal Glycemic Control in Healthy Young Adults.

Objective: Evidence suggests that food preload improves postmeal glycemic profiles, but the effects of marine food are poorly understood. Our study aims to verify the regulating effects of premeal oyster meat (OM) on postprandial blood glucose.Method: Edible parts of the flesh of oyster were prepared for a randomized crossover experiment. After overnight fasting, 20 healthy young men consumed 300 mL of preload drinks with 0 g/kg body weight (BW) (control), 0.1 g/kg BW, and 0.2 g/kg BW. Peripheral blood concentrations of glucose and gastrointestinal hormones were measured before preloading at baseline (0 minutes) and at intervals after the preload and after a preset rice meal. The nutrient composition of OM was analyzed.Results: Compared with other doses, 0.2 g/kg BW OM preload induced higher plasma premeal insulin (p < 0.05), C-peptide (p < 0.05), and glucagon-like peptide-1 (GLP-1; p < 0.05) without altering the glucose concentrations during premeal times. By contrast, 0.2 g/kg BW OM induced less secretion of glucose (p < 0.05) and gastric inhibitory peptide (GIP; p < 0.05), but higher secretion of GLP-1 (p < 0.05) than 0.1 g/kg BW of OM after a meal. During the entire experiment (0-170 minutes), OM reduced the blood glucose (p < 0.05) and GIP (p < 0.05), but increased GLP-1 (p < 0.05). OM was rich in protein (78.4%) and low in fat (6%). Glutamic acid, aspartic acids, glycine, and taurine are the amino acids with high content found in OM.Conclusions: OM preload reduces postmeal glycemia in healthy young people with associated changes in gastrointestinal hormone responses. This effect may be attributed to the rich contents of protein and amino acids of OM.

Oyster (Ostrea plicatula Gmelin) polysaccharides intervention ameliorates cyclophosphamide-Induced genotoxicity and hepatotoxicity in mice via the Nrf2-ARE pathway.

In this study, we explored the protective effects of oyster (Ostrea plicatula Gmelin) polysaccharides (OPS) against genotoxicity and liver injury induced by cyclophosphamide (CP) in BALB/c mice. OPS was administered to mice at doses of 100 and 200mg/kg for 7 consecutive days, then 50mg/kg CP was injected via abdomen. Then mice were sacrificed and samples were collected. Bone marrow micronuclei (MN) and polychromatic erythrocytes (PCE): normochromatic erythrocytes (NCE) ratio were calculated to evaluate CP induced genetic toxicity. Activites of transaminase and antioxidants in serum as well as liver histopathology were examined to assess the severity of liver damage. We further investigate the molecular mechanism by Western blot analysis. When CP induced group pretreated with OPS, the generation of MN was obviously reduced accompanying by the restoration of PCE: NCE ratio. We also found that pretreatment of mice with OPS markedly reduced the release of serum alanine transaminase (ALT) and aspartate transferase (AST). Histological examination and grading evaluation also showed that OPS could significantly attenuated CP-induced liver damage. At the same time, OPS supplementation attenuated CP-induced oxidative stress as evident by the alternation of malondialdehyde (MDA) and superoxide dismutase (SOD) activity. Furthermore, CP induced mice showed the downregulation of Nrf2 (nuclear factor E2 - related factor 2) - ARE (antioxidant response element) and the downstream genes i.e. NAD(P)H: quinine oxidoreductase-1 (NQO - 1) and Hemoxygenase-1 (HO - 1), which were obviously reversed by OPS pretreatment. In conclusion, OPS protects against the genotoxicity and hepatotoxicity induced by CP in vivo. The beneficial effect may depend on activation of Nrf2 - ARE pathway and subsequent suppression of oxidative stress and genetic toxicity.