Potent Regulator Research Articles

Quercetin improves heart failure by inhibiting cardiomyocyte apoptosis via suppressing the MAPK signaling pathway.

To explore the mechanism that mediate the therapeutic effect of quercetin on heart failure. We searched the TCMSP and Swiss ADME databases for the therapeutic targets of quercetin and retrieved heart failure targets from the Genecards and OMIM databases. The intersecting targets were analyzed with GO and KEGG pathway analysis using DAVID database, and the key genes were identified via PPI analysis. Molecular docking between the core targets and quercetin was performed using PyMOL and AutoDock Tools. In a heart failure model established in H9C2 cardiomyocytes by treatment with isoproterenol, the effect of quercetin on the expressions of the MAPK signaling pathway was tested. A total of 60 intersecting targets were identified. Enrichment analysis revealed that quercetin may inhibit heart failure through the MAPK signaling pathway. The core genes, including AMPK3 and BCL-2, were identified as potential key regulators in quercetin-mediated improvement of heart failure. Cellular experiments demonstrated that quercetin significantly reduced isoproterenol-induced apoptosis of cardiomyocytes in a dose-dependent manner and obviously decreased the Bax/Bcl-2 ratio and the expression levels of caspase-3, ERK and p38 in the cells. Quercetin improves heart failure possibly by inhibiting cardiomyocyte apoptosis through the MAPK signaling pathway.

Unveiling the Role of GhP5CS1 in Cotton Salt Stress Tolerance: A Comprehensive Genomic and Functional Analysis of P5CS Genes

Proline, a critical osmoregulatory compound, is integral to various plant stress responses. The P5CS gene, which encodes the rate-limiting enzyme in proline biosynthesis, known as ∆1-pyrroline-5-carboxylate synthetase, is fundamental to these stress response pathways. While the functions of P5CS genes in plants have been extensively documented, their specific roles in cotton remain inadequately characterized. In this study, we identified 40 P5CS genes across four cotton species with diverse sequence lengths and molecular weights. Phylogenetic analysis of 100 P5CS genes from nine species revealed three subgroups, with Gossypium hirsutum closely related to Gossypium barbadense. Collinearity analysis highlighted significant differences in collinear gene pairs, indicating evolutionary divergence among P5CS genes in tetraploid and diploid cotton. Exon–intron structures and conserved motifs correlated with phylogenetic relationships, suggesting functional differentiation. Stress-responsive elements in P5CS promoters suggest involvement in abiotic stress. Expression analysis under salt stress revealed differential expressions of GhP5CS genes, with GhP5CS1 emerging as a potential key regulator. Virus-induced gene silencing confirmed the pivotal role of GhP5CS1 in cotton’s salt stress response, as evidenced by increased salt sensitivity in the silenced plants. This study enhances our understanding of the functional diversity and roles of P5CS genes in cotton under stress conditions.

Characterization and molecular targeting of CFIm25 (NUDT21/CPSF5) mRNA using miRNAs.

Changes in protein levels of the mammalian cleavage factor, CFIm25, play a role in regulating pathological processes including neural dysfunction, fibrosis, and tumorigenesis. However, despite these effects, little is known about how CFIm25 (NUDT21) expression is regulated at the RNA level. A potential regulator of NUDT21 mRNA are small non-coding microRNAs (miRNAs). In general, miRNAs bind to the 3'untranslated regions (3'UTRs) and can target the bound mRNA for degradation or inhibit translation thus affecting the levels of protein in cells. Interestingly, a mechanism known as alternative polyadenylation (APA) enables mRNAs to escape miRNA regulation by generating mRNAs with 3'UTRs of different sizes. As many miRNA target sites are located within the 3'UTR, shortening the 3'UTR allows mRNAs to evade miRNAs targeting this region. The differences in the lengths and the sequence composition of the 3'UTRs may also impact the mRNA's translatability and subcellular localization. APA has been reported to regulate over 70% of protein coding genes, thus increasing the transcript repertoire. Several proteins, including mammalian cleavage factor, CFIm25 (NUDT21), have been shown to regulate APA. In this study we wanted to determine whether CFIm25 (NUDT21), itself a regulator of APA, undergoes APA to evade miRNA regulation. We used the blood cancer mantle cell lymphoma (MCL) cells as a model and showed that in these cells, NUDT21 is relatively stable with a long half-life. In addition, the NUDT21 pre-mRNA undergoes alternative APA within the same terminal exon. The three different sized NUDT21 mRNAs have different 3'UTR lengths and they each use a different canonical polyadenylation signal, AAUAAA, for 3'end cleavage and polyadenylation. Use of miRNA mimics and inhibitors showed that miR-23a, miR-222, and miR-323a play a significant role in regulating NUDT21 expression. Hence, these results suggest that NUDT21 mRNA is stable and the different 3'UTRs generated through APA of NUDT21 play an important role in evading miRNA regulation and offers insights into how levels of CFIm25 (NUDT21) may be fine-tuned as needed under different physiological and pathological conditions.

Karnozin EXTRA® causes changes in mitochondrial bioenergetics response in MCF-7 and MRC-5 cell lines.

Numerous studies reported about potential effects of L-carnosine in regulation of tumor growth and metabolism. We evaluated the effects of different concentrations of L-carnosine from Karnozin EXTRA® supplement on mitochondrial respiratory chain complexes of human embryo lung fibroblasts (MRC-5) and human breast cancer cells (MCF-7), with different energy pathways. Also, we analyzed the proliferation index and expression of various markers of oxidative stress. Treatment with Karnozin EXTRA® (concentration of L-carnosine were 2, 5 and 10mM) for 24hours gradually decreased the number of cells and changed their morphological features. In both cell lines, a dose-dependent reduction of cell viability was recorded compared to the control group. Also, experimental groups showed a concentration-dependent decrease in fluorescence intensity of SOD2 expressions in MCF-7, while in MRC-5 we noticed higher fluorescence intensity in Carnosine 2mM group. Treated cells, in both cell lines, showed different intensity of iNOS cytoplasmic immunopositivity in a concentration-dependent manner. In all experimental groups, we noticed an increased expression of marker of oxidative stress-cytochrome P450 2E1 (CYP2E1). The effects of Karnozin EXTRA® capsule on mitochondrial respiration, assessed with the Clark-type electrode, were manifested as a reduction of: basal cell respiration, maximum capacity of electron transport chain and mitochondrial ATP-linked respiration. Also, significant decrease in the activity of complex I (NADH-ubiquinone oxidoreductase), complex II (succinate dehydrogenase) and complex IV (cytochrome c oxidase) was observed in both cell lines. Bearing in mind that Karnozin EXTRA® is a potential regulator of energy metabolism of MCF-7 and MRC-5, these results provide a good basis for further preclinical and clinical research.

Single-cell transcriptome analysis reveals cellular reprogramming and changes of immune cell subsets following tetramethylpyrazine treatment in LPS-induced acute lung injury.

Acute lung injury (ALI) is a disordered pulmonary disease characterized by acute respiratory insufficiency with tachypnea, cyanosis refractory to oxygen and diffuse alveolar infiltrates. Despite increased research into ALI, current clinical treatments lack effectiveness. Tetramethylpyrazine (TMP) has shown potential in ALI treatment, and understanding its effects on the pulmonary microenvironment and its underlying mechanisms is imperative. We established a mouse model of lipopolysaccharide (LPS)-induced ALI and performed single cell RNA sequencing (scRNA-seq). Bioinformatic analyses of the immune, epithelial and endothelial cells were then performed to explore the dynamic changes of the lung tissue microenvironment. We also analyzed the effects of TMP on the cell subtypes, differential gene expression and potential regulation of transcriptional factors involved. Immunohistochemistry and enzyme-linked immunosorbent assay were performed to identify the effects of TMP on immune inflammatory response. We found that TMP efficiently protected against LPS-induced acute lung injury. Results of scRNA-seq showed that the cells were divided into seven major cell clusters, including immune cells, fibroblasts, endothelial cells and epithelial cells. Neither dexamethasone (Dex) nor TMP treatment showed any significant protective effects in these clusters. However, TMP treatment in the LPS-induced ALI model significantly increased follicular helper T cells and reduced CD8+ naive T cells, Vcan-positive monocytes and Siva-positive NK cells. In addition, TMP treatment increased the number of basal epithelial cells and lymphatic endothelial cells (LECs), indicating its protective effects on these cell types. Scenic analysis suggested that TMP likely mitigates LPS-induced injury in epithelial and endothelial cells by promoting FOSL1 in basal epithelial cells and JunB in LECs. Our findings suggest that TMP appears to alleviate LPS-induced lung injury by regulating the immune response, promoting epithelial cell survival and boosting the antioxidant potential of endothelial cells. This study highlights the potential therapeutic use of TMP in the management of ALI.

FGF21 Exhibits Neuroprotective Effects by Promoting 5-HT1AR-FGFR1 Heteroreceptor Complexes and Triggering MEK1/2-ERK1/2 Signaling Pathway.

Approaches of promoting a neural milieu permissive for plasticity and resilience against neuronal injury are important strategies for the treatment of a range of neurological disorders. Fibroblast growth factor 21 (FGF21) which is known for its role as a potent regulator of glucose and energy metabolism has also proved to be neuroprotective against various mental diseases. However, the underlying molecular mechanisms remain elusive. Here, we report a study of the neuroprotective effects of FGF21 by promoting 5-HT1AR-FGFR1 heteroreceptor formation and triggering MEK1/2-ERK1/2 signaling pathway in normal or abnormal neurological conditions. First, the in vitro cellular experiments demonstrated that FGF21 exerted a protective effect against glutamate-induced cytotoxicity and promoted cell differentiation and growth. Then, in wild-type and FGF21-/- mice, exogenous FGF21 promoted FGFR1-5-HT1AR heteromers formation in the CA3 and dentate gyrus region of the hippocampus and activated MEK1/2-ERK1/2 signaling. Coordinately, FGF21 exerted similar influences in the hippocampi of IBA-induced neurological injury mice or combined stress-exposed mice. Besides, FGF21 treatment activated the phosphorylation of FGFR1 and elevated the expression of synaptophysin in these mice with neurological injury or combined stress exposure. These results illustrated that FGF21 alleviated neurological impairment through FGFR1-5-HT1AR heteromer and ERK1/2 signal activation and suggested that the regulation of FGFR1-5-HT1AR heteromers and MEK1/2/ERK1/2 pathway may play a key role in mediating the neuroprotective effects of FGF21 against various neurodegeneration conditions.

Functional Characteristics of the Crosstalk Between Vocal Fold Fibroblasts and Macrophages-The Role of Vibration in Vocal Fold Inflammation.

This in vitro study investigated the interaction between human vocal fold fibroblasts (hVFF) and macrophages under the influence of cigarette smoke extract (CSE) and vibration as potential regulators of vocal fold (VF) inflammation. Experimental in vitro pilot study. Immortalized hVFF were cultured in flexible-bottomed cell culture plates, treated with CSE, and subjected to static or dynamic conditions in a phonomimetic bioreactor. For coculture, unstimulated orlipopolysaccharide/IFNγ-stimulated THP-1 (human leukemia monocytic cell line) macrophages were added in inserts for a final 24hours of vibration period. We measured messenger ribonucleic acid (mRNA) (quantitative polymerase chain reaction [qPCR]) and protein levels (Western Blot, ELISA, and LUMINEX®) of hVFF and analyzed the results using two- and three-way ANOVA with post hoc tests. Under inflammatory stimulation, we observed a reduction of collagen (COL) type 1A1, 1A2, and 3A1, and increased gene expression of COL4A1, matrix metallopeptidase 2, and vascular endothelial growth factor A in hVFF. Additionally, the pro-inflammatory markers cyclooxygenase (COX) 1 and 2, interleukin (IL) 1β, IL-6, and IL-8 were upregulated. CSE increased COX1 and COX2 levels, whereas vibration reduced CSE-induced increases of COL4A1 and COX2 in pro-inflammatory stimulated hVFF. This study indicates that vibration may mitigate CSE-induced inflammatory damage in the hVFF, thereby offering new insights into the cellular crosstalk that underlies the pathophysiology of VF inflammation in smoking-related voice disorders.

HCAR2 Modulates the Crosstalk between Mammary Epithelial Cells and Macrophages to Mitigate Staphylococcus aureus Infection in the Mouse Mammary Gland.

Staphylococcus aureus (S. aureus) is a major zoonotic pathogen, with mammary gland infections contributing to mastitis, a condition that poses significant health risks to lactating women and adversely affects the dairy industry. Therefore, understanding the immune mechanisms underlying mammary infections caused by S. aureus is essential for developing targeted therapeutic strategies against mastitis. This study identified hydroxycarboxylic acid receptor 2 (HCAR2) as a potential regulator of S. aureus infection in mammary glands. It is demonstrated that HCAR2 deficiency exacerbates the inflammatory response and disrupts the blood-milk barrier in the mammary gland during S. aureus infection, with NLRP3 inflammasome-mediated pyroptosis playing a central role. Activation of HCAR2, on the other hand, suppressed CMPK2 expression, thereby mitigating mitochondrial damage and pyroptosis in mouse mammary epithelial cells (mMECs) induced by S. aureus. Additionally, mitochondrial DNA (mtDNA) released from S. aureus-infected mMECs activates the cGAS/STING signaling pathway in macrophages, impairing their bactericidal activity. In conclusion, this study highlights the critical role of HCAR2 in S. aureus infection of the mammary gland and provides a theoretical basis for identifying potential therapeutic targets for such infections.

Design, synthesis of N-thianyl indole acetamide derivatives as potential plant growth regulator

Design, synthesis of N-thianyl indole acetamide derivatives as potential plant growth regulator

SRPKs Homolog Dsk1 Regulates Homologous Recombination Repair in Schizosaccharomyces pombe

ABSTRACTSerine‐arginine protein kinases (SRPKs) play important roles in diverse biological processes such as alternative splicing and cell cycle. However, the functions of SRPKs in DNA damage response remain unclear. Here we characterized the function of SRPKs homolog Dsk1 in regulating DNA repair in the fission yeast Schizosaccharomyces pombe. We demonstrated that Dsk1 defective mutants of loss of the gene, spacer domain, and kinase activity as well as its overexpression mutant exhibited sensitivities of replication stress. Genetic analysis revealed that the loss of dsk1+ compromised the efficiency of homologous recombination (HR) repair, and Dsk1 was probably involved in the Rad52‐ and Rad51‐dependent HR repair pathways. Interestingly, Dsk1 translocated into the nucleus upon replication stress and directly interacted with Rad51‐mediator Rad52 and phosphorylated Rad52‐Ser365 residue. The Rad52‐Ser365 phosphorylation‐defective mutant was slightly sensitive to replication stress, and the phosphorylation‐mimicking mutants exhibited more sensitivities, which were partially correlated with phenotypes of the loss‐ and gain‐of‐function of dsk1+. This study uncovers a potential HR repair regulator Dsk1 in response to replication stress and implies that its homolog SRPKs may have the conserved targets and functions in higher eukaryotes.

Mammalian Mitochondrial Inorganic Polyphosphate (polyP) and Cell Signaling: Crosstalk Between PolyP and the Activity of AMPK.

Inorganic polyphosphate (polyP) is an evolutionary ancient polymer composed by orthophosphate units linked by phosphoanhydride bonds. In mammalian cells, polyP shows a high localization in mammalian mitochondria, and its regulatory role in various aspects of bioenergetics has already been demonstrated, via molecular mechanism(s) yet to be fully elucidated. In recent years, a role for polyP in signal transduction, from brain physiology to bloodstream, has also emerged. The intriguing possibility is that the effects of polyP on signal transduction could be mechanistically linked to those exerted on bioenergetics. Here, using a combination of cellular and animal models, we demonstrate for the first time the intimate crosstalk between the levels of polyP and the activation status of the AMPK signaling pathway, via a mechanism involving free phosphate homeostasis. AMPK is a key player in mammalian cell signaling, and a crucial regulator of cellular and mitochondrial homeostasis. Our results show that the depletion of mitochondrial polyP in mammalian cells downregulates the activity of AMPK. Moreover, increased levels of polyP activate AMPK. Accordingly, the genetic downregulation of AMPKα1 impairs polyP levels in both SH-SY5Y cells and in the brains of female mice. Our findings shed new light on the regulation of AMPK and position polyP as a potent regulator of mammalian cell physiology beyond mere bioenergetics, paving the road for using its metabolism as an innovative pharmacological target in pathologies characterized by dysregulated bioenergetics.

Lactate modulates microglial inflammatory responses through HIF-1α-mediated CCL7 signaling after cerebral ischemia in mice.

Lactate is a potent regulator of neuroinflammation. We recently demonstrated that lactate alleviated neuronal injury via HIF-1α-regulated microglial inflammation after oxygen-glucose deprivation (OGD). However, the underlying mechanisms and the effect of lactate on microglial responses after ischemic stroke remained unknown. Mouse acute cerebral ischemia-reperfusion injury was induced by middle cerebral artery occlusion (MCAO). L-lactate (100mM, 2μl) was intracerebroventricularly administrated 30min after the reperfusion. Microglia responses were evidenced by the expression of multiple markers such as CD86, iNOS, arginase-1, CD206 and Ym1 in the peri-infarction 24h after MCAO using western blot analysis and quantitative real-time PCR. Inflammatory factors IL-6, TNF-α, TGF-β and IL-10, as well as NF-κB signaling were also detected. Infarct size and neuronal apoptosis in the peri-infarction at 24h, mice survival within 7days and long-term neurobehavioral function were evaluated. The involvement of HIF-1α in lactate-mediated microglial inflammation after MCAO was assessed using a HIF-1α inhibitor. Additionally, transcriptome analysis was used to identify the potential lactate targets in BV2 cells after OGD. The recombinant product of the identified CCL7 gene was used to verify its effect on cerebral ischemia-reperfusion injury in vivo. Lactate supplementation reduced infarction volume, neuronal apoptosis and neurological deficits. Lactate reduced the expression of CD86, iNOS, IL-6, TNF-α and elevated the expression of arginase-1, CD206, Ym1, TGF-β and IL-10 in the peri-infarction at 24h after reperfusion. Consistently, lactate inhibited the NF-κB signaling. Additionally, lactate upregulated HIF-1α in microglia 24h after reperfusion, while inhibition of HIF-1α reversed the effects of lactate on brain damage and neuroinflammation after cerebral ischemia. Furthermore, CCL7 was identified as the top down-regulated inflammatory gene induced by lactate in OGD-treated BV2 cells. It was also found high expression of CCL7 in the peri-infarction at 24h after reperfusion and lactate treatment inhibited CCL7 expression. However, HIF-1α inhibitor reversed the effect of lactate treatment on CCL7 expression. Finally, supplementation of recombinant CCL7 reversed the mitigated neuroinflammation and neuroprotective effect rendered by lactate treatment after MCAO. We concluded that treatment with lactate modulated the microglia inflammatory responses and alleviated cerebral ischemia injury. The inhibition of CCL7/NF-κB signaling by HIF-1α might be involved in the beneficial effect of lactate treatment.

Spermidine synthase promotes liver cancer progression in a paracrine manner by altering the macrophage immunometabolic state.

Understanding the molecular mechanisms of adaptive regulation in the tumor microenvironment is crucial for precision therapy in hepatocellular carcinoma (HCC). We hypothesized that cargo proteins carried by extracellular vesicles (EVs) released in a hypoxic microenvironment might promote HCC progression by remodeling tumor-associated macrophages (TAMs). EV protein analysis by label-free proteomics mass spectrometry of HCC cell lines of different tumor grades was performed. The promotional effect if spermidine synthase（SRM） on M2 polarized TAMs was further investigated using various biological approaches. SRM expression was positively correlated with liver cancer progression in HCC cell lines, liver cancer samples, and nude mouse models. In a mouse model, SRM expression was positively correlated with TAM infiltration and liver cancer progression. Pan-cancer dataset analysis confirmed that SRM overexpression in HCC tumors is correlated with poor patient prognosis. However, a hypoxic microenvironment is an internal driving factor for exosomal SRM that participates in microenvironmental modifications. Moreover, we defined a hitherto unknown pattern of microenvironmental crosstalk involving SRM in EVs, whereby macrophages complete the phenotypic fate of M2 tumor-associated macrophages through SRM uptake. SRM regulation within the immune microenvironment is metabolically driven. By upregulating spermidine, which serves as a substrate for eIF5A hypusination, excessive oxidative phosphorylation (OXPHOS) assembly is achieved. This, in turn, leads to the expression of immunosuppressive marker molecules and ultimately promotes liver cancer progression. SRM, which is enriched in the EVs of HCC cells under hypoxic conditions, acts as a potent regulator linking polyamine and energy metabolism in TAMs, thereby promoting liver cancer progression.

Kisspeptin participates in the positive reward state induced by paced mating and modulates sexual receptivity and paced mating behavior in female rats

Kisspeptin (Kp), a potent regulator of the hypothalamic-pituitary-gonad axis, was recently shown to be involved in partner preference and sexual receptivity in females. Interestingly, Kp and its receptor (Kiss1r) are expressed in brain regions involved in the reward and motivation of reinforcing behaviors. Therefore, in the present study, we designed 3 experiments to determine the participation of Kp in female sexual behavior and the positive affective (PA) reward state induced by paced mating (PM). In all experiments, we used sexually naïve ovariectomized Wistar female rats primed with estradiol benzoate (EB, 2.5 μg/rat) 48 h before behavioral tests. In experiment 1 (n = 9), we tested the effect of Kp on PM. We demonstrated that Kp-10 (14 nmol) induced similar levels of receptivity to treatment with EB + progesterone and facilitated PM by reducing the return latency after intromissions. In experiment 2 (n = 8), we evaluated the effect of p234 penetratin, a Kiss1r antagonist, on PM. The administration of p234 in doses of 7.5 nmol and 15 nmol reduced the mean lordosis intensity and increased mount and intromission return latencies. Finally, in Experiment 3, we tested the capacity of Kp to induce a PA state or the antagonist to block the reward state induced by PM. Kp-10 (7 and 14 nmol) induced a clear conditioned place preference. This reward state and that produced by PM were blocked by p234 (15 nmol). Our findings underscore the critical role of Kp in modulating female sexual behavior and the PA state associated with PM, highlighting its potential to enhance sexual motivation.

Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the H2S/AKT/GSK3β signaling axis.

Pyridoxal-5-phosphate (PLP) enhances the synthesis of endogenous hydrogen sulfide, a potent regulator of cell metabolism. We used 24-month-old rats to investigate the PLP mitoprotective function in the aging heart. We demonstrated improvement of mitochondrial bioenergetic functions, inhibition of mPTP opening after PLP administration. Moreover, PLP treatment increased glucose consumption and utilization, decreased lipid transport into the cells, but increased fatty acid β-oxidation, providing sufficient energy. An ECG study showed a significant improvement in cardiac function in PLP-treated old rats. Our data suggest that PLP may exert its effect through the H2S/AKT/GSK3β axis with further targeting of the Sirt1/PGC-1α signaling pathway.

Potential Regulation of ARID1A by miR-129-5p and miR-3613-3p and Their Prognostic Value in Gastric Cancer.

Gastric cancer (GC) remains the most common malignant tumor of the gastrointestinal tract and one of the leading causes of cancer-related deaths worldwide. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), are involved in the pathogenesis and progression of GC and, therefore, may be potential diagnostic and prognostic biomarkers. Our work was aimed at investigating the predicted regulation of ARID1A by miR-129-5p and miR-3613-3p and the clinical value of their aberrant expression in GC. The study included tumor and adjacent non-tumor tissues from 110 GC patients, 38 sectional normal gastric tissue samples, as well as 65 plasma samples of GC patients and 49 plasma samples of healthy donors. Expression levels of ARID1A and both miRNAs were quantified by reverse transcription-polymerase chain reaction (RT-PCR). We have identified significant associations of their expression with the clinical and pathological characteristics of GC patients both in tissues and plasma. To validate predicted target pairs miR-129-5p/ARID1A and miR-3613-3p/ARID1A, in vitro experiments on cancer cell lines were conducted. The obtained results suggest a complex role of ARID1A, miR-129-5p and miR-3613-3p in GC and potential regulation of ARID1A expression by both miRNAs.

Optimizing carrier transport properties in the intrinsic layer of a-Si single and double junction solar cells through numerical design

This research aims to improve the performance of a-Si: H solar cells, particularly in terms of carrier transport properties, through a numerical design approach utilizing AFORS-HET simulation software. By performing a series of rigorous computer simulations, we explore the potential regulation of the intrinsic layer thickness, carrier mobility, loading factor, and density of states (DoS) distribution in the solar cell's intrinsic layer. Recombination losses are reduced, and light absorption efficiency is significantly increased when the intrinsic layer thickness is adjusted, as shown by simulation findings. Moreover, reduction of transit times and enhancement of the total efficiency of the solar cells depend on increased carrier mobility. Parameters can be adjusted to attain optimal performance under various operating situations by adjusting the DoS and load factors. Furthermore, the simulations provide insightful information about the interactions between the junctions in solar cells with double junctions. Our results of this research provide an important contribution to efforts to develop more efficient and sustainable a-Si: H solar cells and emphasize the importance of numerical design approaches in photovoltaic technology.

Modelling and experimental validation of DSTATCOM using a deep belief learning network with an anti-wind-up regulator

This article proposes the shunt compensation capability improvement using a deep belief learning network approach (DBLN) with anti-wind-up regulator-supported distributed static compensator (DSTATCOM). Six subnets make up this proposed DBLN controller. Three subnets for each active and reactive mass part are employed to isolate the basic component of the output current. Numerous issues such as past and normalising weight and learning rates are engaged in the DBLN-based weight-updating formula to have a superior dynamic presence, reduce the computational load and achievesfaster estimation, etc. This proposed DBLN is suggested for both proportional-integral (PI) and anti-wind-up regulator to showcase the better DC link voltage which further leads to providing better PQ improvement. This method offers excellent dynamics and resilience to outside disturbances. The suggested study is examined by simulation and experimental development using MATLAB/Simulink by a real-time interface based on a dSPACE 1104 for healthier potential regulation, potential balancing, input current harmonic distortion and PF correction under different load scenarios.

Unravelling the photosynthetic dynamics and fluorescence parameters under ameliorative effects of 24-epibrassinolide in wheat (Triticum aestivum L.) grown under heat stress regime

An experiment was performed at the Banaras Hindu University, India to study the effect of terminal heat stress on photosynthetic dynamics and fluorescence parameters of wheat genotypes and ameliorative effects of epibrassinolide by taking two genotypes with four concentrations as foliar spray at two growth stages of wheat. The highest values were observed in plots foliar sprayed with 1.0 µM 24-epibrassinolide (T1) under normal conditions (D1) where the genotype Sonalika (V1) performed significantly well w.r.t. the parameters viz. steady-state fluorescence (Fs) 116.22, quantum efficiency of PSII 0.59, maximum fluorescence (Fm) 776.5, normalized stress detection ratio (Fv/Fo) 4.47, maximum potential quantum efficiency of PSII (Fv/Fm) 0.82.Whereas under heat stress condition (late sown D2), there was significant reduction in these parameters in both the genotypes which was improved by the application of epibrassinolide suggesting its potential role in improving the photoinhibition process by raising the efficiency of PSII. Overall, the calibrated application of 24-epibrassinolide was found to be a potent growth regulator involved in the positive modulation of heat stress tolerance in wheat, coupled with improved photosynthetic efficiency in treated plots as compared to control.

Correlation analysis of the impact of Clonorchis sinensis juvenile on gut microbiota and transcriptome in mice.

This study highlighted the impact of C. sinensis juvenile infection on the gut microbiota and transcriptome of BALB/c mice. It induced liver inflammation, promoted intestinal villi growth, and altered goblet cell numbers. The infection also disrupted the diversity and structure of gut microbiota, particularly affecting beneficial bacteria. Transcriptome analysis revealed increased expression of genes related to immune response and detoxification processes. Important pathways affected included circadian rhythm, glutathione metabolism, and glycolysis/gluconeogenesis. Notable genes implicated included Igkv12-41, Mcpt2, Arntl, Npas2, Cry1, and Gsta1. Bacteroides_sartorii emerged as a potential key regulator in this interaction.