Optimizing nitrogen removal is crucial for ensuring the efficient operation of wastewater treatment plants (WWTPs), but it is susceptible to variations in influent conditions and operational parameter constraints, and conflicts with the energy-saving and carbon emission reduction goals. To address these issues, this study proposes a hybrid framework integrating process simulation, machine learning, and multi-objective genetic algorithms for nitrogen removal diagnosis and optimization, aiming to predict the total nitrogen in effluent, diagnose nitrogen over-limit risks, and optimize the control strategies. Taking a full-scale WWTP as a case study, a process time-lag simulation-enhanced machine learning model (PTLS-ML) was developed, achieving R values of 0.
View Article and Find Full Text PDFAims: It has been reported that allopregnanolone (APα) promotes the neurogenesis of the neural progenitor cells (NPCs) in the subventricular zone (SVZ) and prevents the decrease of dopaminergic neurons in 6-hydroxydopamine (6-OHDA)-treated mice by binding to γ-aminobutyric acid A receptor (GABAAR) and then opening voltage-gated L-type Ca channel, but the underlying mechanisms remain elusive. The aim of this study was to explore the possible involvement of GABAAR and calcium/calmodulin-dependent protein kinase II delta 3 (CaMKIIδ3) in this process.
Methods: 6-OHDA-treated mice and primary cultured midbrain cells were administrated with APα and GABAAR antagonist bicuculline (Bic), and the proliferation and differentiation of NPCs, the tyrosine hydroxylase (TH)-positive neurons and their fibers, the expression levels of CaMKIIδ3 and brain-derived neurotrophic factor (BDNF), and motor functions were measured using ELISA, immunohistochemical staining, real-time RT-PCR, Western blot, and behavioral test.
Allopregnanolone (APα), as a functional neurosteroid, exhibits the neuroprotective effect on neurodegenerative diseases such as Parkinson's disease (PD) through γ-aminobutyric acid A receptor (GABAAR), but it has not been completely understood about its molecular mechanisms. In order to investigate the neuroprotective effect of APα, as well as to clarify its possible molecular mechanisms, SH-SY5Y neuronal cell lines were incubated with 6-hydroxydopamine (6-OHDA), which has been widely used as an model for PD, along with APα alone or in combination with GABAAR antagonist (bicuculline, Bic), intracellular Ca chelator (EGTA) and voltage-gated L-type Ca channel blocker (Nifedipine). The viability, proliferation, and differentiation of SH-SY5Y cells, the expression levels of calmodulin (CaM), Ca/calmodulin-dependent protein kinase II δ3 (CaMKIIδ3), cyclin-dependent kinase-1 (CDK1) and brain-derived neurotrophic factor (BDNF), as well as the interaction between CaMKIIδ3 and CDK1 or BDNF, were detected by morphological and molecular biological methodology.
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