Search

To explore the effect of acacetin on myocardial mitochondrial dysfunction in spontaneously hypertensive rats (SHR) with insulin resistance (IR), and the possible mechanism. Rapid IR was first induced in fructose-fed SHR, and they were then treated with acacetin (25, 50 mg/kg). After 7 weeks, the rats were tested for hypertension, IR, cardiac function, and mitochondrial damage status. Potential mechanisms of action were explored in terms of oxidative stress, mitochondrial fission and division, apoptosis, and the insulin signaling pathway. Subsequently, the PI3K gene was silenced, after intervention with acacetin (5 μM) for 24 h, and H

Deep learning models have shown their great performances in natural language processing tasks. While much attention has been paid towards improvements in utility, privacy leakage and social bias are two major concerns arising in trained models. In this paper, we protect individual privacy and mitigate gender bias on classification models simultaneously. First, we propose a selective privacy-preserving method that only obscure individuals' sensitive information by adding noise on word embeddings. Then we propose a negative multi-task learning framework to mitigate the gender bias which contains a main task and a gender prediction task. The main task uses a positive loss constraint to ensure utility while the gender prediction task applies a negative loss constraint to remove gender-specific features. We analyze two existing word embeddings and evaluate them on sentiment analysis and medical text classification tasks. Our experimental results show that our negative multi-task learning framework can mitigate the gender bias while keeping models’ utility on both sentiment analysis and medical text classification.

Introduction: The spatiotemporal patterns of Corona Virus Disease 2019 (COVID-19) is detected in the United States, which shows temperature difference (TD) with cumulative hysteresis effect significantly changes the daily new confirmed cases after eliminating the interference of population density. Methodology: The nonlinear feature of updated cases is captured through Generalized Additive Mixed Model (GAMM) with threshold points; Exposure-response curve suggests that daily confirmed cases is changed at the different stages of TD according to the threshold points of piecewise function, which traces out the rule of updated cases under different meteorological condition. Results: Our results show that the confirmed cases decreased by 0.390% (95% CI: -0.478 ~ -0.302) for increasing each one degree of TD if TD is less than 11.5°C; It will increase by 0.302% (95% CI: 0.215 ~ 0.388) for every 1°C increase in the TD (lag0-4) at the interval [11.5, 16]; Meanwhile the number of newly confirmed COVID-19 cases will increase by 0.321% (95% CI: 0.142 ~ 0.499) for every 1°C increase in the TD (lag0-4) when the TD (lag0-4) is over 16°C, and the most fluctuation occurred on Sunday. The results of the sensitivity analysis confirmed our model robust. Conclusions: In US, this interval effect of TD reminds us that it is urgent to control the spread and infection of COVID-19 when TD becomes greater in autumn and the ongoing winter.

Yang Fu,1,2 Peipei Yuan,1,2 Yajuan Zheng,1 Yaxin Wei,1 Liyuan Gao,1 Yuan Ruan,1 Yi Chen,1 Panying Li,1 Weisheng Feng,1,2 Xiaoke Zheng1,2 1Department of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, People’s Republic of China; 2The Engineering and Technology Center for Chinese Medicine Development of Henan Province, Zhengzhou, 450046, People’s Republic of ChinaCorrespondence: Xiaoke Zheng; Weisheng Feng, Department of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, People’s Republic of China, Email zhengxk.2006@163.com; fwsh@hactcm.edu.cnPurpose: Pseudoephedrine (PSE) has rapid absorption and metabolism, which limits its pharmacologic actions. We postulated that pseudoephedrine nanoparticles (PSE-NPs) with high bioavailability could overcome this limitation. The defensive function of PSE-NPs nanoparticles against adriamycin-induced reproductive toxicity in mice was studied.Methods: We encapsulated PSE in polylactide-polyglycolide nanoparticles (PLGA-NPs) and verified their protective activity against testicular injury in vivo and in vitro.Results: We report a promising delivery system that loads PSE into PLGA-NPs and finally assembles it into a nanocomposite particle. In vitro, PSE-NPs reduced the adriamycin-induced apoptosis of GC-1 cells significantly, improved mitochondrial energy metabolism and promoted expression of the proteins related to the gonadotropin-releasing hormone (GnRh) receptor signaling pathway. In vivo, evaluation of sperm indices and histology showed that adriamycin could induce testicular toxicity. PSE-NPs significantly increased the sperm motility of mice, reduced the percent apoptosis and oxidative stress of testes, increased serum levels of GnRh, activated the GnRhR signaling pathway in testes and promoted expression of meiosis-related factors.Conclusion: In view of their safety and efficiency, these PSE-NPs have potential applications in alleviating adriamycin-induced reproductive toxicity.Graphical Abstract: Keywords: pseudoephedrine nanoparticles, adriamycin, reproductive toxicity, GnRhR signaling pathway, sperm meiosis

The aim of the work was to investigate the effects of acacetin on endothelial dysfunction and aortic fibrosis in insulin-resistant SHR rats and explore its mechanism. Seven-week-old male spontaneously hypertensive rats (SHR) were selected to establish a rat model of hypertension with insulin resistance induced by 10% fructose. The nuclear factor kappa B p65 (NF-κB p65) and Collagen I were observed by Immunohistochemistry. Immunofluorescence was used to observe estrogen receptor-alpha (ERα), estrogen receptor-beta (ERβ), and G protein-coupled receptor 30 (GPR30). Western blotting was used to detect interleukin (IL-1β), Arginase 2 (ARG2), Nostrin, endothelial nitric oxide synthase (eNOS), TGF-β, Smad3, ERK pathway proteins such as p-c-Raf, p-MEK1/2, p-ERK, ERK, p-P90RSK and p-MSK1. We found that acacetin did have an improvement on endothelial dysfunction and fibrosis. Meanwhile, it was also found to have a significant effect on the level of estrogen in this model by accident. Then, the experiment of uterine weight gain in mice confirmed that acacetin had a certain estrogen-like effect in vivo and played its role through the estrogen receptors pathway. In vitro experience HUVEC cells were stimulated with 30 mM/L glucose and 100 mM/L NaCl for 24 h to establish the endothelial cell injury model. HUVEC cells were treated with 1 μM/L estrogen receptors antagonist (ICI 182780) for 30 min before administration. Cell experiments showed that acacetin could reduce the apoptosis of HUVEC cells, the levels of inflammatory cytokines and the expression of TGF-β, Collagen I and Smad3 in endothelial cell injury model. After treatment with ICI 182780, the improvement of acacetin was significantly reversed. The results showed that acacetin relieved endothelial dysfunction and reduced the aortic fibrosis in insulin-resistant SHR rats by reducing the release of inflammatory factors and improving vasodilatory function through estrogen signaling pathway.

Context In the antihypertensive study of phenylacetamide (PA) on spontaneously hypertensive rats (SHR), it was occasionally found that PA prevents myocardial injury. Objective Clarify the protective mechanism of PA on myocardial injury in SHR rats. Materials and methods In vivo, SHR rats were treated with or without PA (15, 30, 45 mg/kg) for 3 weeks (12 per group). In vitro, H9c2 cells were treated with PA (1, 5, 10 μM) for 24 h, and then stimulated with H2O2 (300 μM) for 4 h. Molecular mechanisms were explored through cardiac pathology, cardiac function and biochemical markers. Results In vivo, PA (15, 30, 45 mg/kg) reduced CVF from 14.8 ± 1.62 to 9.94 ± 1.56, 8.6 ± 1.33, 8.14 ± 1.45%; increased the LVEF relative level from 0.8 ± 0.06 to 0.83 ± 0.04, 0.86 ± 0.05, 0.9 ± 0.04. All three doses can improve the cardiac pathological structure and function (LVEDD, LVESD, LVFS, heart index, NT-proBNP, CKMB, SBP); however, 45 mg/kg works best. But different doses show different molecular mechanisms. PA (15 mg/kg) improves RAAS system (REN, ACE), inflammation (ET-1, IL-1β) and MAPK pathway (p-ERK/ERK, p-JNK/JNK) better. PA (45 mg/kg) improves oxidative stress (SOD, NOX1) and TGF-β pathway (Smad3) better. In vitro, PA improved cell viability, oxidative stress (SOD, NOX1) and Smad3 protein expression. Discussion and conclusions: PA regulates different mechanisms at different concentrations to improve myocardial injury, and high dose is the best. This experiment provides a theoretical basis for the development of new clinical drugs for cardiovascular disease.

Pyroptosis is a novel form of programmed cell death (PCD), which is characterized by DNA fragmentation, chromatin condensation, cell swelling and leakage of cell contents. The process of pyroptosis is performed by certain inflammasome and executor gasdermin family member. Previous researches have manifested that pyroptosis is closely related to human diseases (such as inflammatory diseases) and malignant tumors, while the regulation mechanism of pyroptosis is not yet clear. Non-coding RNA (ncRNA) such as microRNA (miRNA), long non-coding RNA (lncRNA) and circular RNA (circRNA) have been widely identified in the genome of eukaryotes and played a paramount role in the development of cell function and fate after transcription. Accumulating evidences support the importance of ncRNA biology in the hallmarks of pyroptosis. However, the associations between ncRNA and pyroptosis are rarely reviewed. In this review, we are trying to summarize the regulation and function of ncRNA in cell pyroptosis, which provides a new research direction and ideas for the study of pyroptosis in different diseases.

Background β-Glucosidase is the rate-limiting enzyme of cellulose degradation. It has been stipulated and established that β-glucosidase-producing microbial communities differentially regulate the expression of glucose/non-glucose tolerant β-glucosidase genes. However, it is still unknown if this differential expression of functional microbial community happens accidentally or as a general regulatory mechanism, and of what biological significance it has. To investigate the composition and function of microbial communities and how they respond to different carbon metabolism pressures and the transcriptional regulation of functional genes, the different carbon metabolism pressure was constructed by setting up the static chamber during composting. Results The composition and function of functional microbial communities demonstrated different behaviors under the carbon metabolism pressure. Functional microbial community up-regulated glucose tolerant β-glucosidase genes expression to maintain the carbon metabolism rate by enhancing the transglycosylation activity of β-glucosidase to compensate for the decrease of hydrolysis activity under carbon catabolite repression (CCR). Micrococcales play a vital role in the resistance of functional microbial community under CCR. The transcription regulation of GH1 family β-glucosidase genes from Proteobacteria showed more obvious inhibition than other phyla under CCR. Conclusion Microbial functional communities differentially regulate the expression of glucose/non-glucose tolerant β-glucosidase genes under CCR, which is a general regulatory mechanism, not accidental. Furthermore, the differentially expressed β-glucosidase gene exhibited species characteristics at the phylogenetic level.

Lipid deposition in the kidney can cause serious damage to the kidney, and there is an obvious epithelial–mesenchymal transition (EMT) and fibrosis in the late stage. To investigate the interventional effects and mechanisms of phenolic compounds from Mori Cortex on the EMT and fibrosis induced by sodium oleate-induced lipid deposition in renal tubular epithelial cells (NRK-52e cells), and the role played by CD36 in the adjustment process, NRK-52e cells induced by 200 μmol/L sodium oleate were given 10 μmoL/L moracin-P-2″-O-β-d-glucopyranoside (Y-1), moracin-P-3′-O-β-d-glucopyranoside (Y-2), moracin-P-3′-O-α-l-arabinopyranoside (Y-3), and moracin-P-3′-O-[β-glucopyranoside-(1→2)arabinopyranoside] (Y-4), and Oil Red O staining was used to detect lipid deposition. A Western blot was used to detect lipid deposition-related protein CD36, inflammation-related protein (p-NF-κB-P65, NF-κB-P65, IL-1β), oxidative stress-related protein (NOX1, Nrf2, Keap1), EMT-related proteins (CD31, α-SMA), and fibrosis-related proteins (TGF-β, ZEB1, Snail1). A qRT-PCR test detected inflammation, EMT, and fibrosis-related gene mRNA levels. The TNF-α levels were detected by ELISA, and the colorimetric method was used to detects SOD and MDA levels. The ROS was measured by flow cytometry. A high-content imaging analysis system was applied to observe EMT and fibrosis-related proteins. At the same time, the experiment silenced CD36 and compared the difference between before and after drug treatment, then used molecular docking technology to predict the potential binding site of the active compounds with CD36. The research results show that sodium oleate can induce lipid deposition, inflammation, oxidative stress, and fibrosis in NRK-52e cells. Y-1 and Y-2 could significantly ameliorate the damage caused by sodium oleate, and Y-2 had a better ameliorating effect, while there was no significant change in Y-3 or Y-4. The amelioration effect of Y-1 and Y-2 disappeared after silencing CD36. Molecular docking technology showed that the Y-1 and Y-2 had hydrogen bonds to CD36 and that, compared with Y-1, Y-2 requires less binding energy. In summary, moracin-P-2″-O-β-d-glucopyranoside and moracin-P-3′-O-β-d-glucopyranoside from Mori Cortex ameliorated lipid deposition, EMT, and fibrosis induced by sodium oleate in NRK-52e cells through CD36.

Accurate forecasting of photovoltaic power output can provide technical guidance for smooth grid connection of photovoltaic power plants and avoid grid energy quality problems caused by large fluctuations in photovoltaic power. Therefore, it is very important to obtain more accurate photovoltaic energy forecast data. The traditional photovoltaic power forecasting model has the problems of low forecast accuracy and hysteresis.to further improve the prediction accuracy of pv power, this paper proposes a multi-layer fusion PV power prediction model based on dynamic modification of the weight parameters of each model. The model's benchmark algorithms include XGBoost, LigthGBM and ConvLSTM. In the case study, real photovoltaic station data were used to verify the simulation,The forecast results show that the model proposed in this paper has a better effect than any single model and has strong practicability.

Doxorubicin (DOX) is a highly effective chemotherapeutic that is effective for various tumours. However, the clinical application of DOX has been limited by adverse reactions such as cardiotoxicity and heart failure. Since DOX-induced cardiotoxicity is irreversible, drugs to prevent DOX-induced cardiotoxicity are needed.This study aimed to investigate the effect of total flavonoids of Selaginella tamariscina (P.Beauv.) Spring (TFST) on doxorubicin-induced cardiotoxicity.The present study established DOX-induced cardiotoxicity models in C57BL/6 mice treated with DOX (cumulative dose: 20 mg/kg body weight) and H9c2 cells incubated with DOX (1 μM/l) to explore the intervention effect and potential mechanism of TFST. Echocardiography was performed to evaluate left ventricular functions. Heart tissue samples were collected for histological evaluation. Myocardial injury markers and oxidative stress markers were examined. Mitochondrial energy metabolism pathway associated proteins PPARα/PGC-1α/Sirt3 were detected. We also explored the effects of TFST on endoplasmic reticulum (ER) stress and apoptosis. To further investigate the protective mechanism of TFST, we used the specific small interfering RNA MFN2 (siMFN2) to explore the effect of MFN2 on TFST against DOX-induced cardiotoxicity in vitro. Flow cytometry detected reactive oxygen species, mitochondrial membrane potential and apoptosis. Cell mitochondrial stress was measured by Seahorse XF analyser.Both in vivo and in vitro studies verified that TFST observably alleviated DOX-induced mitochondrial dysfunction and ER stress. However, these effects were reversed after transfected siMFN2.Our results indicated that TFST ameliorates DOX-induced cardiotoxicity by alleviating mitochondrial dysfunction and ER stress by activating MFN2/PERK. MFN2/PERK pathway activation may be a novel mechanism to protect against DOX-induced cardiotoxicity.

Aims This study was designated to illustrate the underlying mechanisms of emodin anti-liver fibrosis via network pharmacology and experiment. Methods The TSMCP and Genecards database were applied to screen the relevant targets of emodin or liver fibrosis. The essential target was selected by using Cytoscape to analyze the topological network of potential targets. Furthermore, we constructed a preliminary molecule docking study to explore the binding site by Surflex-Dock suite SYBYL X 2.0. The DAVID database was selected for gene functional annotations and KEGG enrichment analysis. Moreover, we demonstrated the ameliorating effect of emodin on carbon tetrachloride (CCl4 )-induced liver injury in mice. We also verified the network predictions in vitro via various techniques. Results The collected results showed that 35 targets were related to emodin, and 6,198 targets were associated with liver fibrosis. The Venn analysis revealed that 17 intersection targets were correlated with emodin anti-liver fibrosis. The topological network analysis suggested that the p53 was the remarkable crucial target. Besides, the molecule docking results showed that emodin could directly interact with p53 by binding the active site residues ASN345, GLN331 and TYR347. Finally, KEGG pathway enrichment results indicated that essential genes were mainly enriched in mitogen-activated protein kinase (MAPK) signaling pathways. Moreover, our study confirmed that emodin alleviated CCl4 -induced liver injury in mice，inducing hepatic stellate cells (HSCs) apoptosis via regulating the p53/ERK/p38 axis. Conclusions This study partially verified the network pharmacological prediction of emodin inducing HSCs cell apoptosis through the p53/ERK/p38 axis.

Ying Hou,1,* Peipei Yuan,1,* Yang Fu,1 Qi Zhang,1 Liyuan Gao,1 Yaxin Wei,1 Xiaoke Zheng,1,2 Weisheng Feng1,2 1College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, People’s Republic of China; 2Engineering and Technology Center for Chinese Medicine Development of Henan Province, Henan Science and Technology Department, Zhengzhou, 450046, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiaoke Zheng; Weisheng FengCollege of Pharmacy, Henan University of Chinese Medicine, No. 156, Jinshui East Road, Zhengzhou, 450046, People’s Republic of ChinaTel +86-371-6019-0296Email zhengxk.2006@163.com; fwsh@hactcm.edu.cnIntroduction: Hypertension is closely related to myocardial injury. Long-term hypertension can cause myocardial injury. Therefore, it is very important to find drugs to treat myocardial injury caused by hypertension. The aim of present study is to investigate the effects and mechanisms of geniposide on myocardial injuries in spontaneously hypertensive rats (SHR) and H9c2 cells induced by NaCl solution.Materials and Methods: Male Wistar–Kyoto (WKY) and SHR rats were given different doses of geniposide (25 mg/kg/d or 50 mg/kg/d) or distilled water for three consecutive weeks. Meanwhile, an H9c2 cell line-injury model was established using a solution of 150 μmol/L NaCl for 8 h. The cardiac function and related indexes of rats were detected.Results: The results showed that geniposide decreased the levels of COI and COIII, which promoted the phosphorylation of AMPK (p-AMPK) and enhanced the energy metabolism pathway. Geniposide improved myocardial apoptosis by regulating apoptotic proteins (p38, BAX and Bcl-2). Finally, heart function was regulated, and the markers of myocardial injury were decreased. Geniposide increased the viability of H9c2 cells treated with the NaCl solution and decreased the rate of apoptosis by regulating the levels of apoptotic proteins. Geniposide could activate energy metabolism signalling pathway (AMPK/SirT1/FOXO1) and reduce H9c2 cell apoptosis.Conclusion: Our results showed that the mechanisms by which geniposide improves myocardial injury in SHR may be through regulating the energy metabolism signalling pathway (AMPK/SirT1/FOXO1) and improving myocardial apoptosis by regulating apoptotic proteins.Keywords: geniposide, SHR, myocardial injury, apoptosis, energy metabolism

Aims Liver fibrosis is a difficult problem in the medical field. We previously reported that curcumol, a bioactive substance, may inhibit the pathological angiogenesis of liver sinusoidal endothelial cells (LSECs) and play a good anti-hepatic fibrosis effect. However, the mechanism of curcumol inhibiting angiogenesis in LSEC needs to be further clarified. Here, we focus on how curcumol inhibits LSEC angiogenesis in liver fibrosis. Materials and methods Primary rat LSECs were cultured in vitro, and various molecular experiments including real-time PCR, western blot, immunofluorescence, tube formation assay and transwell migration assay were used to clarify the potential mechanism of curcumol. Carbon tetrachloride (CCl4) was applied to create a mouse liver fibrosis model. Blood and livers were taken to elucidate the efficacy of curcumol in vivo. Key findings We found that curcumol could effectively inhibit LSEC angiogenesis in vitro. Interestingly, this process may depend on curcumol's inhibition of the expression of transcription factor KLF5. Mice experiment also showed that curcumol could alleviate chronic liver injury by reducing KLF5 expression. In addition, we suggested that curcumol could reduce the production of mitochondrial ROS and improve mitochondrial morphology in LSEC. More importantly, we proved that curcumol could suppress KLF5-mediated LSEC angiogenesis by inhibiting ROS/ERK signaling. Significance We suggested that transcription factor KLF5 could be considered as a new target molecule of curcumol in improving liver fibrosis, and pointed out that curcumol targeted ROS/ERK-mediated KLF5 expression could inhibit LSEC angiogenesis. This provided a new theoretical basis for curcumol to ameliorate liver fibrosis.

The novel coronavirus (COVID-19) that has been spreading worldwide since December 2019 has sickened millions of people, shut down major cities and some countries, prompted unprecedented global travel restrictions. Real data-driven modeling is an effort to help evaluate and curb the spread of the novel virus. Lockdowns and the effectiveness of reduction in the contacts in Italy has been measured via our modified model, with the addition of auxiliary and state variables that represent contacts, contacts with infected, conversion rate, latent propagation. Results show the decrease in infected people due to stay-at-home orders and tracing quarantine intervention. The effect of quarantine and centralized medical treatment was also measured through numerical modeling analysis.

Objective Early disease screening and diagnosis are important for improving patient survival. Thus, identifying early predictive features of disease is necessary. This paper presents a comprehensive comparative analysis of different Machine Learning (ML) systems and reports the standard deviation of the results obtained through sampling with replacement. The research emphasises on: (a) to analyze and compare ML strategies used to predict Breast Cancer (BC) and Cardiovascular Disease (CVD) and (b) to use feature importance ranking to identify early high-risk features. Results The Bayesian hyperparameter optimization method was more stable than the grid search and random search methods. In a BC diagnosis dataset, the Extreme Gradient Boosting (XGBoost) model had an accuracy of 94.74% and a sensitivity of 93.69%. The mean value of the cell nucleus in the Fine Needle Puncture (FNA) digital image of breast lump was identified as the most important predictive feature for BC. In a CVD dataset, the XGBoost model had an accuracy of 73.50% and a sensitivity of 69.54%. Systolic blood pressure was identified as the most important feature for CVD prediction.

Objectives Curcumol, a guaiane-type sesquiterpenoid hemiketal extracted from the herb Rhizoma Curcumae, exhibits multiple-pharmacological activities. We previously reported that curcumol ameliorated hepatic fibrosis by inhibiting hepatic stellate cell (HSC) activation. In this study, we aimed to investigate the effect of curcumol on HSC migration and adhesion, and reveal its regulation mechanisms. Materials and methods Cellular viability was determined by Cell Counting Kit-8. Cell migration was detected by boyden chamber and cell scratch experiment. Recombinant human periostin (rh POSTN) and adeno-associated viral (AAV)-GFP-periostin were used to achieve POSTN overexpression in vitro and in vivo, respectively. Nuclear factor kappa B (NF-κB)-p65 overexpression was achieved by using plasmid. ELISA was conducted to detect POSTN level. Immunohistochemistry, qRT-PCR, Western blotting, and immunofluorescence were performed to assess associated factor expression. Results Curcumol suppressed HSC migration and adhesion, and reduced the secretion and expression of POSTN. By gain of function POSTN in HSCs, using rh POSTN, we found that the inhibition of HSC migration and adhesion by curcumol depended on the decrease of POSTN. Besides, curcumol protection against chronic CCl4-caused hepatic fibrosis could be impaired by POSTN overexpression. Moreover, we showed that curcumol repressed NF-κB signaling and the production of pro-inflammatory factor. Importantly, curcumol down-regulation of POSTN was rescued by knock-in of NF-κB, as well as the inhibition of HSC migration and adhesion. Conclusion These findings reveal the molecular mechanism of curcumol-reduced HSC migration and adhesion, by which points to the possibility of using curcumol based on NF-κB dependent POSTN for the treatment of fibrogenesis.

Additional file 1: Table S1. Functional classification of glycosyl hydrolases and auxiliary used in this paper based on their characterized catalytic activities according to CAZy ( https://www.cazy.org/ ). Table S2. Primers for β-glucosidase genes used for qPCR. The primers were designed by Primer-BLAST in NCBI. Primer pairs are specific to amplified sequences as no other targets were found in selected database: RefSeq Representative Genome Database (Organism limited to Bacteria, Fungi, Cow, Zea mays).

Additional file 2: Figure S1. Phylogenetic analysis based on the partial amino acid sequences of GH1 family β-glucosidase genes selected from representative sequences used to design qPCR primers and their relationship with the reference sequences retrieved from Genbank. The tree was constructed using the neighbor-joining method. Figure S2. Transcription efficiency of GH1 family β-glucosidase genes from bacteria in the natural composting and the inoculated composting. Figure S3. Nucleotide sequence alignment of GH1 family BGL genes and primers used for this study.

Additional file 1. Information on feature selection, hyperparameter spaceand programing languages and libraries.The doc file contains two tables and one figure. The first table shows thecorrelation among the features of the breast cancer diagnosis dataset. Thefirst figure illustrates the feature selection process for the cardiovascular disease dataset. The second table shows the hyperparameter space.