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We investigated the impact and predictive value of bladder function in patients with benign prostatic hyperplasia (BPH) on the efficacy of transurethral prostatectomy. Symptomatic, imaging, and urodynamic data of patients who underwent transurethral prostatectomy at West China Hospital of Sichuan University (Chengdu, China) from July 2019 to December 2021 were collected. Follow-up data included the quality of life (QoL), International Prostate Symptom Score (IPSS), and IPSS storage and voiding (IPSS-s and IPSS-v). Moreover, urinary creatinine (Cr), nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and prostaglandin estradiol (PGE2) were measured in 30 patients with BPH and 30 healthy participants. Perioperative indicators were determined by subgroup analyses and receiver operating characteristic (ROC) curve analysis. Among the 313 patients with BPH included, patients with severe micturition problems had more improvements but higher micturition grades postoperatively than those with moderate symptoms. Similarly, good bladder sensation, compliance, and detrusor contractility (DC) were predictors of low postoperative IPSS and QoL. The urinary concentrations of BDNF/Cr, NGF/Cr, and PGE2/Cr in patients were significantly higher than those in healthy participants (all P < 0.001). After evaluation, only DC was significantly related to both urinary indicators and postoperative recovery of patients. Patients with good DC, as predicted by urinary indicators, had lower IPSS and IPSS-v than those with reduced DC at the 1st month postoperatively (both P < 0.05). In summary, patients with impaired bladder function had poor recovery. The combined levels of urinary BDNF/Cr, NGF/Cr, and PGE2/Cr in patients with BPH may be valid predictors of preoperative bladder function and postoperative recovery.

Both eutrophication and salinization are growing global environmental problems in freshwater ecosystems, threatening the water quality and various aquatic organisms. However, little is known about their interactive effects on theses stressors and the role of lake depth on these interactions. We used field surveys to compared zooplankton assemblages over four seasons in eight Yunnan Plateau lakes with different trophic states, salinization levels, and water depths. The results showed that: 1) the species number (S), density (DZoop), and biomass (BZoop) of zooplankton exhibited strong seasonal dynamics, being overall higher in the warm seasons. 2) Data collected over four seasons and summer data both revealed highly significant positive relationships of S, DZoop, and BZoop with total nitrogen (TN), total phosphorus (TP), and phytoplankton chlorophyll a (Chl a). 3) S, DZoop, and BZoop displayed a unimodal relationship with salinity, peaking at 400–1000 μS/cm (conductivity, to reflect salinity). 4) The two large-sized taxa (cladocerans and copepods) generally increased at low-moderate levels of TN, TP, Chl a, and Cond and was constant or decreased at high levels. The average body mass (biomass/density) of crustaceans decreased with increasing TN, TP, Chl a, and conductivity. Our findings indicate that zooplankton may be more vulnerable in deep lakes than in shallow lakes when exposed to conductivity stress even under mesotrophic conditions, and the overall decrease in size in zooplankton assemblages under the combined stress of eutrophication and salinization may result in a lowered grazing effect on phytoplankton.

Eutrophication and salinization are serious global environmental problems in freshwater ecosystems, occasionally acting jointly to exert harmful effects on aquatic ecosystems. To elucidate the interactive effects of nutrients and salinity on phytoplankton assemblages, we conducted a four-season study during 2020–2021 of eight lakes from Yunnan Plateau (Southwest China) with a wide range of conductivities (Cond, reflecting degree of salinization), eutrophic states, and water depths and used General Additive Modeling (GAM) of the data. We found that: (1) species number (SN), density (DPhyt), and biomass (BPhyt) of phytoplankton showed stronger seasonal dynamics in shallow lakes than in deep lakes, all being, as expected, higher in the warm season; (2) annual and summer data revealed highly significant positive relationships between SN, DPhyt, and BPhyt with total nitrogen (TN) and total phosphorus (TP), which became weaker at high TP occurring when the N:P ratio was low, indicating N limitation; (3) SN, DPhyt, and BPhyt showed a unimodal relationship with salinity, peaking at 400–1000 μS/cm (Cond); (4) the two dominant taxa (cyanobacteria and chlorophyta) showed different patterns, with chlorophyta generally dominating at low TN and cyanobacteria at high TN and Cond, suggesting the synergistic effect of nitrogen and Cond on cyanobacterial dominance.

Eutrophication and salinization are serious global environmental problems in freshwater ecosystems, occasionally acting jointly to exert harmful effects on aquatic ecosystems. To elucidate the interactive effects of nutrients and salinity on phytoplankton assemblages, we conducted a four-season study during 2020–2021 of eight lakes from Yunnan Plateau (Southwest China) with a wide range of conductivities (Cond, reflecting degree of salinization), eutrophic states, and water depths and used General Additive Modeling (GAM) of the data. We found that: (1) species number (SN), density (DPhyt), and biomass (BPhyt) of phytoplankton showed stronger seasonal dynamics in shallow lakes than in deep lakes, all being, as expected, higher in the warm season; (2) annual and summer data revealed highly significant positive relationships between SN, DPhyt, and BPhyt with total nitrogen (TN) and total phosphorus (TP), which became weaker at high TP occurring when the N:P ratio was low, indicating N limitation; (3) SN, DPhyt, and BPhyt showed a unimodal relationship with salinity, peaking at 400–1000 μS/cm (Cond); (4) the two dominant taxa (cyanobacteria and chlorophyta) showed different patterns, with chlorophyta generally dominating at low TN and cyanobacteria at high TN and Cond, suggesting the synergistic effect of nitrogen and Cond on cyanobacterial dominance. [ABSTRACT FROM AUTHOR]

Adenosine can exhibit cytotoxic activity in vivo and in vitro, though its mechanisms are still uncertain. In this study, we investigated the adenosine-mediated apoptotic signaling pathway and the role of NF-κB in human hepatocellular carcinoma HepG2 cells. HepG2 cells were treated with different concentrations of adenosine for 12-48 h, and the effect of adenosine on cell proliferation was evaluated by MTT assay. The cytotoxicity of adenosine alone or in combination with an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), was also evaluated by MTT assay and the mode of cell death was detected by Hoechst 33342 staining. Cell cycle progress was performed by flow cytometry with PI staining. The protein expressions of Bcl-2, p53, NF-κB subunit p65, and caspase-3 were assayed by Western blot. Caspase-3 activity was measured by spectrophotomteric assay. The results showed that adenosine significantly reduced the viability of HepG2 cells in a dose- and time-dependent manner, with [IC.sub.50] (24 and 48 h) of 2.52 and 1.89 mmol x [L.sup.-1], respectively. The apoptotic index (percentage of sub-[G.sub.1] phase) of HepG2 cells in adenosine treatment alone for 12 and 24 h or in combination with PDTC were 8.30%, 22.32% and 20.18%, 30.89%, respectively. All of them were higher than that in the control group (0.81%, p < 0.01). The characteristic changes of cell apoptosis (chromatin condensation and sub-G1 peak) were observed under fluorescent microscopy and flow cytometry. We also found that the apoptotic process triggered by adenosine was involved in [G.sub.0]-[G.sub.1] cell-cycle arrest, enhanced the activity of caspase-3, upregulated p53 and NF-κB p65 expression, and downregulated Bcl-2 expression. Inhibition of NF-κB by PDTC decreased NF-κB p65 expression, enhanced cell apoptosis ratio, and increased caspase-3 activity. NF-κB may play an anti-apoptosis role in adenosine-induced HepG2 cytotoxicity. Key words: adenosine, apoptosis, HepG2 cells, NF-κB. L'adenosine peut exercer une activite cytotoxique in vivo et in vitro mais son mecanisme d'action demeure incertain. Dans cette etude, nous avons examine la voie de signalisation de l'apoptose causee par l'adenosine ainsi que le role du facteur NF-κB dans les cellules de carcinome hepatocellulaire HepG2. Les cellules HepG2 ont ete traitees avec differentes concentrations d'adenosine pendant 12-18 h, et l'effet de l'adenosine sur la proliferation cellulaire a ete; evalue par un dosage au MTT. La cytotoxicite de l'adenosine seule ou combinee a un inhibiteur du NF-κB, le pyrrolidine dithiocarbamate (PDTC) a aussi ete evaluee par un dosage MTT, et le mode de mort cellulaire a ete detecte par coloration au Hoechst 33342. La progression du cycle cellulaire a etee suivie par cytometrie de flux apres coloration a l'iodure de propidium. L'expression de Bcl-2, p53, de la sous-unite p65 du NF-κB et de la caspase-3 a ete detectee par buvardage Western. L'activite de la caspase-3 a ete mesuree a l'aide d'une mesure spectrophotometrique. Les resultats ont montre que l'adenosine reduisait de facjon significative la viabilite des cellules HepG2 de maniere dependante de la concentration et du temps, avec des [CI.sub.50] (24 et 48 h) de 2.52 et 1.89 mmol x [L.sup.-1], respectivement. Les indices d'apoptose (pourcentage de cellules en phase sub-G1) des cellules HepG2 traitees a l'adenosine seule pendant 12 ou 24 h, ou combinee au PDTC etaient de 8.30% et 22.32%, et 20.18% et 30.89%, respectivement. Ils etaient tous superieurs a l'indice du groupe controle (0.81%, p < 0.01). Les changements caracteristiques de l'apoptose (condensation de la chromatine et pic en sub- [G.sub.1]) ont ete observees par microscopie en fluorescence et par cytometrie de flux. Nous avons aussi trouve que le processus d'apoptose enclenche par l'adenosine etait implique; dans l'arret du cycle cellulaire en [G.sub.0]-[G.sub.1], augmentait l'activite; de la caspase-3, augmentait l'expression de p53 et de la sous-unite p65 du NF-κB, et diminuait l'expression de Bcl-2. L'inhibition du NF-κB par le PDTC augmentait la cytotoxicite;, l'indice d'apoptose et l'activite; de la caspase-3, et diminuait l'expression de p65. L'inhibition du NF-κB pourrait augmenter l'apoptose a travers la voie de la caspase-3 et de Bcl-2. NF-κB peut jouer un role anti-apoptose dans la cytotoxicite; induite par l'adenosine dans les cellules HepG2. Mots-cles: adenosine, apoptose, HepG2, NF-κB. [Traduit par la Redaction], Introduction Apoptosis (programmed cell death), which plays a critical role during normal development, homeostasis, and pathology of a wide variety of diseases including cancer, occurs in response to various intracellular [...]

Abstract: Nuclear receptor subfamily 4 group A member 1 (NR4A1) is an orphan nuclear receptor with diverse functions. It has been reported that NR4A1, as a transcriptional activator, is implicated in glucose and lipid metabolism. The aim of this study was to investigate the regulatory role of NR4A1 in adipogenesis and explore the underlying mechanisms. Quantitative real‐time PCR and Western blotting were used to analyse the expression of genes involved in synthesis and mobilization of fats in vivo and in vitro. Dual‐luciferase reporter assay was conducted to study the regulatory mechanisms of NR4A1. Our data from in vivo study confirmed that NR4A1 knockout (KO) mice fed with high‐fat diet were more prone to obesity, and gene expression levels of PPARγ and FAS were increased in KO mice compared to controls; our data from in vitro study showed that NR4A1 overexpression in 3T3‐L1 pre‐adipocytes inhibited adipogenesis. Moreover, NR4A1 enhanced GATA binding protein 2 (GATA2) expression, which in turn inhibited peroxisome proliferator‐activated receptor γ (PPARγ); NR4A1 inhibited sterol regulatory element binding transcription factor 1 (SREBP1) and its downstream gene fatty acid synthase (FAS) by up‐regulating p53. NR4A1 inhibits the differentiation and lipid accumulation of adipocytes by enhancing the expression of GATA2 and p53. [ABSTRACT FROM AUTHOR]