A new empirical Chl-a algorithm has been developed and validated for the largest freshwater lake of China (Poyang Lake) using a normalized green-red difference index (NGRDI), where the uncertainty was estimated to be <45% for Chl-a ranging between 1.3 and 10.5 mg·m⁻³. The combined approach of using the NGRDI algorithm and atmospherically-corrected Medium Resolution Imaging Spectrometer (MERIS) data showed an advantage over other popular approaches. The algorithm was then applied to 325 carefully-selected MERIS full-resolution (300-m) scenes between 2003 and 2012, with pixels of extreme turbidity (NGRDI < 0.06, corresponding to >~25 mg·L⁻¹ total suspended sediments or TSS) masked. The long-term Chl-a distribution showed significant spatial gradient and temporal variability, with Chl-a ranging between 2.4 ± 0.2 mg·m⁻³ in April and 4.4 ± 1.0 mg·m⁻³ in July and no significant increasing or decreasing trend during the 10-year period. In waters where Chl-a was retrievable (i.e., where TSS is 10 mg·m⁻³) in summer. The study not only provides, for the first time, synoptic baseline information on the lake’s Chl-a distributions and potential eutrophic regions, but also demonstrates a practical approach that might be extended to assess eutrophication conditions in other inland waters.

Ferulic acid (FA) is a phenolic compound that has antioxidant, hepatoprotective, anticarcinogenic, anti-inflammatory, antiallergic, antimicrobial, antiviral, and vasodilatory effects. This study was conducted to explore the effects of dietary FA supplementation on antioxidant capacity and lipid metabolism in weaned piglets. Eighteen 21-day-old castrated male DLY (Duroc × Landrace × Yorkshire) weaned piglets were randomly divided into control, 0.05%, and 0.45% FA groups. The results showed that, in serum, CAT and T-SOD activities and content of HDL-C were increased, but the content of MDA and the activities of T-CHO and LDL-C were decreased, by FA supplementation. In liver, dietary FA supplementation increased CAT, T-SOD, and GSH-PX activities and upregulated the mRNA levels of SOD1, SOD2, CAT, GST, GPX1, GR, Nrf2, HSL, CPT1b, and PPARα but decreased the contents of MDA and TG. Furthermore, dietary FA supplementation increased the protein level of Nrf2, HO-1, and NQO-1. In longissimus dorsi muscle, dietary FA supplementation increased the activity of T-SOD and the mRNA abundance of SOD1, SOD2, CAT, GST, GPX1, GR, and Nrf2 but decreased the contents of MDA and T-CHO. Additionally, dietary FA supplementation increased the protein expressions of Nrf2, HO-1, and NQO1. Together, our data suggest that FA could improve antioxidant capacity and lipid metabolism in weaned piglets.

In flood-prone areas, the delineation of the spatial pattern of historical flood extents, damage assessment, and flood durations allow planners to anticipate potential threats from floods and to formulate strategies to mitigate or abate these events. The Chenab plain in the Punjab region of Pakistan is particularly prone to flooding but is understudied. It experienced its worst riverine flood in recorded history in September 2014. The present study applies Remote Sensing (RS) and Geographical Information System (GIS) techniques to estimate the riverine flood extent and duration and assess the resulting damage using Landsat-8 data. The Landsat-8 images were acquired for the pre-flooding, co-flooding, and post-flooding periods for the comprehensive analysis and delineation of flood extent, damage assessment, and duration. We used supervised classification to determine land use/cover changes, and the satellite-derived modified normalized difference water index (MNDWI) to detect flooded areas and duration. The analysis permitted us to calculate flood inundation, damages to built-up areas, and agriculture, as well as the flood duration and recession. The results also reveal that the floodwaters remained in the study area for almost two months, which further affected cultivation and increased the financial cost. Our study provides an empirical basis for flood response assessment and rehabilitation efforts in future events. Thus, the integrated RS and GIS techniques with supporting datasets make substantial contributions to flood monitoring and damage assessment in Pakistan.

The aim of this study was to investigate the effect of naringin on lipopolysaccharide (LPS)-induced jejunal barrier function in mice. Forty-five 3-week-old healthy male Balb/c mice with similar body weights were randomly divided into control group, LPS group, LPS + naringin group, with 15 mice in each treatment group. The mice were intraperitoneally injected with the same dose of saline or LPS (10 mg per kg BW) at 43 d. The blood samples, liver and jejunal tissues were collected after 3 h of injection. The results showed that LPS significantly increased the serum diamine oxidase (DAO) activity, D-lactate (D-LA) concentration, and malondialdehyde (MDA) content in liver and jejunum, while decreased the activities of superoxide dismutase (SOD), glutathione peroxidase (Gpx) and catalase (CAT) in liver and jejunum. The LPS treatment caused an increase in the crypt depth and a decrease in the villus height and the ratio of villus height to crypt depth (V/C) of the jejunum. In addition, the LPS treatment significantly increased the mRNA expressions of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, toll-like receptor 4 (TLR4), p38-mitogen-activated protein kinase (p38 MAPK), nuclear factor-κB (NF-κB) and kelch-like ECH-associated protein 1 (Keap1), while decreased mRNA expressions of zonula occludens 1 (ZO-1), occludin, claudin, mucin 2 (MUC2) and junctional adhesion molecule 2 (JAM2), Gpx, SOD1, GST, CAT and nuclear factor-erythroid 2-related factor 2 (Nrf2). However, the naringin treatment mitigated these effects induced by LPS. Taken together, our findings suggested that naringin attenuates LPS-induced intestinal barrier damage by inhibiting inflammatory factors and improving antioxidant function and intestinal tight junction, which might be mediated by activating the Nrf2 signaling and suppressing the TLR4/p38 MAPK/NF-κB signaling.