The storm runoff management strategy based on agricultural ditch nutrient loss characteristics in Erhai Lake, China.

Initial flush management is an effective measure to control non-point source pollution (NPSP) in storm runoff. However, determining the parameter of the initial flush in different areas may pose challenges in storm runoff management strategies. To address this issue, Erhai Lake in China, Yunnan-Guizhou Plateau, was selected as an example for the study. Erhai Lake is a typical mesotrophic lake with the profound influence of NPSP. The NPSP control strategy in this area will provide a valuable reference for other lakes. In 2021, 289 storm events and 190 ditchwater samples were detected around Erhai Lake. The average flow in the ditches ranged from 0.004 to 0.147 m3/s, the instant total nitrogen (TN) concentration ranged from 0.28 to 91.43 mg/L, and the instant total phosphorus (TP) concentration ranged from 0.26 to 7.35 mg/L in the storm events. It was found that the concentration of pollutants was lower than expected in the initial flush period. Instead, the event mean concentrations of TN and TP were 9.3 and 2.1 times higher than in the wet seasons, showing high nutrient concentration levels throughout the entire rainfall period. To manage storm runoff effectively, a flow-processes-division method was proposed to analyze the inflow condition and pollutant removal rate in different runoff periods. The peak flow interception strategy was recommended as the optimal stormwater management plan, as it showed the highest inflow conditions and 50% pollutant removal rate. Considering the need to reduce the constant flush of stormwater runoff, it is essential to establish a healthy water cycle system to alleviate NPSP and raise the Erhai water level. The storm runoff management method can serve as a practical tool for lake areas that do not exhibit initial flush characteristics.

Modified Magnetic Resonance Imaging Burden of Cerebral Small Vessel Disease and Related Risk Factors in Patients With Thalassemia.

OBJECTIVE: This study aimed to explore the burden of magnetic resonance imaging (MRI) of cerebral small vessel disease (CSVD) in patients with thalassemia and related risk factors. METHODS: The clinical data and MRI of patients with thalassemia were retrospectively analyzed, and non-thalassemia controls with matched sex and age were selected. The modified MRI burden of CSVD included recent small subcortical infarct, presumed vasogenic white matter hyperintensity, presumed vasogenic lacunae, perivascular space (PVS), and brain atrophy. RESULTS: This study included 110 patients in each of the thalassemia and control groups. There was no significant difference in sex, age, and common cerebrovascular disease risk factors between the 2 groups. The patients with thalassemia had a higher red blood cell count and lower content of hemoglobin. The PVS and modified MRI burden scores in the thalassemia group were higher than in the control group. With the increase in age, patients with thalassemia have a more severe CSVD burden. CONCLUSION: Patients with thalassemia have a heavier modified MRI burden of CSVD than non-thalassemia patients, particularly PVS, and aging is an important risk factor for CSVD changes.

MicroRNA-152 inhibits ovarian cancer cell proliferation and migration and may infer improved outcomes in ovarian cancer through targeting FOXP1.

microRNA (miR) are a class of endogenous small non-coding RNA that are aberrantly expressed and are critical in tumorigenesis. Amongst them, miR-152 was reported to be dysregulated in epithelial ovarian cancer (EOC). However, the function and mechanism of miR-152 is not well understood. In the present study, total RNA was extracted from 58 ovarian epithelial carcinoma tissue samples and adjacent non-tumor tissues and measured by reverse transcription-quantitative polymerase chain reaction. The observations of the present study revealed that the expression of miR-152 was significantly downregulated in EOC specimens, as well as three ovarian cancer (OC) cell lines. The higher expression of miR-152 indicated a better overall survival rate in patients with EOC. Following miR-152 mimic transfection into SKOV3 or OVCAR3 cells, MTT assay revealed that cell proliferation was significantly inhibited (P<0.05). Although miR-152 had no effect on SKOV3 cell migration, miR-152 inhibited OVCAR3 cell migration. Bioinformatics analyses and luciferase reporter assays demonstrated that miR-152 targeted the 3'-untranslated region (3'-UTR) of the forkhead box protein 1 (FOXP1). Furthermore, introducing FOXP1 without the 3'-UTR abrogated the effect of miR-152-induced proliferation and migration alteration, respectively. In addition, the expression level of FOXP1 was higher in the EOC tumor tissues and cell lines. Additionally, the level of miR-152 and FOXP1 was inversely correlated in grade 3 and 4 ovarian tumor tissues. Altogether, these observations indicated that miR-152 may be involved in the inhibition of OC through repression of FOXP1. In the future, miR-152 and FOXP1 may act as novel biomarkers for early detection of EOC or therapeutic targets.

Inhibiting microRNA-449 Attenuates Cisplatin-Induced Injury in NRK-52E Cells Possibly via Regulating the SIRT1/P53/BAX Pathway.

BACKGROUND: Acute kidney injury (AKI) is quite common in the patients who frequently use the anticancer drug cisplatin. microRNAs (miRNAs) are powerful tools in modulating the expression of key factors in disease progression, but little is known about roles of miRNAs in AKI. This study explored the expression and function of miR-449 in cisplatin-induced AKI. MATERIAL/METHODS: Rat renal proximal tubular cell line NRK-52E was used for cisplatin treatment and miR-449 sponge transfection. MTT assay and flow cytometry were performed to detect cell viability and apoptosis in different cell groups. Protein expression of sirtuin 1 (SIRT1), acetylated p53, and BCL-associated X protein (BAX) was detected to deduce the possible regulatory mechanism of miR-449. RESULTS: Results showed that cisplatin treatment in NRK-52E cells significantly up-regulated miR-449 levels (P<0.05), inhibited cell viability (P<0.05), accelerated cell apoptosis (P<0.05), and changed SIRT1, acetylated p53, and BAX protein levels (P<0.01). However, inhibiting miR-449 by its sponge transfection in cisplatin-treated cells significantly promoted cell viability (P<0.05), suppressed cell apoptosis (P<0.05), elevated SIRT1 expression (P<0.01), and inhibited acetylated p53 and BAX protein levels (P<0.001). CONCLUSIONS: These results indicate that inhibiting miR-449 allows the attenuation of cisplatin-induced injury in NRK-52E cells, suggesting that miR-449 is a potential target for treating AKI. miR-449 regulates the SIRT1/p53/BAX pathway, which may be its possible mechanism in modulating cell apoptosis of cisplatin-induced AKI. Further verification and a thorough understanding are necessary for targeting miR-449 in AKI treatment.