Multi-Omics Analysis of the Effects of Soil Amendment on Rapeseed (Brassica napus L.) Photosynthesis under Drip Irrigation with Brackish Water.

Drip irrigation with brackish water increases the risk of soil salinization while alleviating water shortage in arid areas. In order to alleviate soil salinity stress on crops, polymer soil amendments are increasingly used. But the regulation mechanism of a polymer soil amendment composed of polyacrylamide polyvinyl alcohol, and manganese sulfate (PPM) on rapeseed photosynthesis under drip irrigation with different types of brackish water is still unclear. In this field study, PPM was applied to study the responses of the rapeseed (Brassica napus L.) phenotype, photosynthetic physiology, transcriptomics, and metabolomics at the peak flowering stage under drip irrigation with water containing 6 g·L-1 NaCl (S) and Na2CO3 (A). The results showed that the inhibitory effect of the A treatment on rapeseed photosynthesis was greater than that of the S treatment, which was reflected in the higher Na+ content (73.30%) and lower photosynthetic-fluorescence parameters (6.30-61.54%) and antioxidant enzyme activity (53.13-77.10%) of the A-treated plants. The application of PPM increased the biomass (63.03-75.91%), photosynthetic parameters (10.55-34.06%), chlorophyll fluorescence parameters (33.83-62.52%), leaf pigment content (10.30-187.73%), and antioxidant enzyme activity (28.37-198.57%) under S and A treatments. However, the difference is that under the S treatment, PPM regulated the sulfur metabolism, carbon fixation and carbon metabolism pathways in rapeseed leaves. And it also regulated the photosynthesis-, oxidative phosphorylation-, and TCA cycle-related metabolic pathways in rapeseed leaves under A treatment. This study will provide new insights for the application of polymer materials to tackle the salinity stress on crops caused by drip irrigation with brackish water, and solve the difficulty in brackish water utilization.

G-/C-rich ssDNA-based Fe and Cu/Fe nanoclusters with peroxidase-like activity for intracellular ROS production and cytotoxicity applications.

Five G-/C-rich single-stranded DNA (ssDNA) with different sequences and lengths were templated to prepare the DNA-Cu, DNA-Fe, and bimetallic DNA-Cu/M nanoclusters (NCs). The peroxidase-like activities of these nanomaterials were studied using H2O2 and 3,3',5,5''-tetramethylbenzidine (TMB) as the reaction substrates in HAc-NaAc buffer. It was found that T30-G2-Fe NCs and T30-G2-Cu/Fe NCs, with a size of about 2 nm, exhibit similar and the strongest enzyme-like activity under optimal conditions. Both NCs possess a similarly high affinity to substrates, and the Michaelis-Menten constant (Km) values to TMB and H2O2 are about 11 and 2-3 times lower than those of natural horseradish peroxidase (HRP), respectively. The activity of both nanozymes decreases to about 70% after being kept for one week in pH 4.0 buffer at 4 °C, which is comparable with HRP. Hydroxyl radicals (•OH) are the main reactive oxygen species (ROS) produced in the catalytic reaction. Moreover, both NCs can facilitate in situ generation of ROS in HeLa cells using endogenous H2O2. MTT assays indicate that the T30-G2-Cu/Fe NCs exhibit the strong selective cytotoxicity to HeLa cells over HL-7702 cells. The cellular viability is about 70% and 50% after incubating with 0.6 M NCs for 24 h without or with 2 mM H2O2, respectively. The current study shows that the T30-G2-Cu/Fe NCs have the potential for chemical dynamic treatment (CDT).

Crescent-Shaped Carbazole Derivatives as Light-Up Fluorescence Probes for G-Quadruplex DNA and Live Cell Imaging.

In recent years, studies on the organic small molecule fluorescent probes targeting G-quadruplexes have attracted a wide attention, because G-quadruplexes play an important role in various biological functions. Herein, we reported three crescent-shaped carbazole derivatives (4a-4c) and studied their interactions with the single-stranded, duplex, G-quadruplex and i-motif DNA. Both 4b and 4c have an above 100 nm Stokes shift and low fluorescence intensity, moreover, they exhibit the stronger affinity to G-quadruplex than to the other DNA structures. 4b with a cyanovinyl pyridine salt group displays a specific light-up fluorescence response to G-quadruplexes. FRET and CD results suggest that both 4b and 4c are able to improve the stability of G-quadruplexes and maintain their topology, moreover, they induce G-rich sequences (bcl-2, HTG, and KSS) to fold into G-quadruplexes in Na+ /K+ free buffer. In addition, CLSM images suggest that 4b and 4c are mainly distributed in the mitochondrion of living HepG2 cells, and a weak fluorescence signal is also observed in the nucleus for 4c. Given that the two compounds have the larger association constants to G-quadruplexes over to duplex and single-stranded DNA, we speculate that the fluorescence signals in cells may mainly be attributed to the compound/G-quadruplex DNA complexes.

The sensitive detection of ATP and ADA based on turn-on fluorescent copper/silver nanoclusters.

A simple turn-on fluorescence strategy is proposed for the detection of ATP based on DNA-stabilized copper/silver nanoclusters (DNA-Cu/Ag NCs). The fluorescence intensity of DNA-Cu/Ag NCs increases significantly in the presence of ATP, because the specific interaction between ATP and its aptamer causes two darkish Cu/Ag NCs to be situated at the 5' and 3' termini close to each other. A limit of detection (LOD) of 7.0 µM is found, in a linear range of 2-18 mM, and the proposed sensor is simple, sensitive, and selective. Additionally, the DNA-Cu/Ag NCs/ATP system is further developed into a sensor for ADA detection and demonstrates a linear response to ADA from 5 to 50 U/L with a LOD of 5 U/L. The proposed method is also shown to be successful in detecting ATP and ADA in a solution of fetal bovine serum.

Cytosine-rich ssDNA-templated fluorescent silver and copper/silver nanoclusters: optical properties and sensitive detection for mercury(II).

DNA-templated silver nanoclusters (DNA-Ag NCs) with cytosine (C)-rich sequences (four or more segments of consecutive (2-5) C-bases) were synthesized. They display green and/or orange/red emissions under different excitation wavelengths. There is indication that more consecutive C-bases lead to longer emission wavelengths. The ratio of the red and green emissions of the DNA-Ag NCs depends on whether the NCs were synthesized under acidic or basic conditions. We also prepared the DNA copper/silver nanoclusters (DNA-Cu/Ag NCs) which can be synthesized in shorter time and display higher stability. The DNA-Cu/Ag NCs, under 470 nm photoexcitation, always display green emission, with a peak at 550 nm, irrespective of whether being prepared under acidic or basic conditions. The fluorescence of the Cu/Ag NCs is selectively quenched by Hg(II) ions which can be quantified by this nanoprobe with a detection limit as low as 2.4 nM. The quenching mechanism was studied by Stern-Volmer plots and lifetime studies which revealed that both static and dynamic quenching are operative. Graphical abstract Schematic presentation of fluorescent DNA-Ag nanoclusters (NCs) exhibiting red and green emission under different pH values, and green emissive DNA-Cu/Ag NCs for sensitive and rapid detection of Hg2+.

Vaspin Prevents Tumor Necrosis Factor-α-Induced Apoptosis in Cardiomyocytes by Promoting Autophagy.

Visceral adipose tissue-derived serine protease inhibitor (Vaspin) is an adipocytokine that has been shown to exert anti-inflammatory effects and inhibits apoptosis under diabetic conditions. This study was designed to investigate the impact of vaspin on autophagy in tumor necrosis factor (TNF)-α-induced injury in cardiomyocytes and its cardioprotective effects in the pathogenesis of diabetic cardiomyopathy (DCM). H9C2 cells were treated with TNF-α with or without vaspin in vitro. Tumor necrosis factor-α treatment inhibited autophagy and promoted apoptosis in H9C2 cells after stimulating for 24 hours. Pretreatment with vaspin significantly mitigated apoptosis induced by TNF-α partly because of augment effects of vaspin on autophagy as demonstrated by a higher ratio of LC3-II/LC3-I, higher expression of Beclin-1, and increased autophagosomes formation. Furthermore, the AKT agonist IGF-1 significantly reversed the effect of vaspin on autophagy. In vivo DCM model was also developed by treating rats with streptozotocin followed by intraperitoneal injection with vaspin. In DCM rats, upregulation of vaspin reversed cardiac dysfunction, as identified by increased left ventricular ejection fractions and fractional shortening levels, a higher Em/Am ratio, and lower levels of TNF-α, lactate dehydrogenase, creatine kinase, and creatine kinase-myocardial isoenzyme. In conclusion, vaspin attenuated the TNF-α-induced apoptosis by promoting autophagy probably through inhibiting the PI3K/AKT/mTOR pathway and further ameliorated the cardiac dysfunction in DCM rats.

Studies on interactions of carbazole derivatives with DNA, cell image, and cytotoxicity.

DNA-binding agents have been considered as an established opportunity for the development of anticancer drugs and DNA fluorescence probes. This work reported the synthesis of two novel carbazole derivatives (1 and 2) and investigated their DNA binding properties, living cell image, and cytotoxicity. The results demonstrated that both compounds presented the higher binding affinity to G-quadruplex than to duplex DNA by means of UV-Vis absorption titration and fluorescent intercalator displacement. Continuous variation analysis indicated that their binding stoichiometries of the compound/G-quadruplex were near 2 except the compound/bcl-2. Circular dichroism spectra showed that both compounds had no influence on the conformation of G-quadruplexes. Fluorescence titrations indicated that 2 had the potential to be a G-quadruplex selective fluorescent probe, while 1 could be used as a fluorescent probe for duplex DNA. Confocal fluorescence images indicated that both compounds could enter the living HepG2 cells, and 1 mainly located in nucleus whereas 2 mainly distributed in cytoplasm. DNase and RNase digest tests indicated that both compounds could enter into the nucleus and interact with duplex DNA, especially, 2 could interact with RNA and/or G-quadruplex DNA. They also exhibited an obvious antiproliferative activity to HepG2 by using MTT assays, with IC50 values of 2.7 and 9.5 µM for 1 and 2, respectively.

Mechanism studies on anti-HepG2 cell proliferation of phenanthroline derivatives as G-quadruplex DNA stabilizers.

In our previous study, two similar phenanthroline derivatives (1 and 2) were confirmed to be potent and selective stabilizers of the G-quadruplex DNAs of c-myc promoter and human telomere in vitro. In this study, we investigated the anti-proliferative mechanism of both ligands to HepG2 cells. MTT assay indicated that IC50 values are 1.26 and 0.5 µM for 1 and 2, respectively. Flow cytometric assays showed that both ligands could induce cell apoptosis, and 1 could arrest cell cycle in S and G2/M phases whereas the cell cycle was arrested in G0/G1 phase for 2, which are attributed to the expression decreases of the key regulating proteins cyclin B1/Cdk1 and cyclin D1/Cdk4 in the G2/M and G0/G1 phases, respectively. Both ligands could inhibit the transcription of c-myc gene and down-regulate the expression of c-myc, Sp1, and hTERT protein but up-regulate the p53 protein expression. 2 performed higher inhibitory activity than 1. Furthermore, both 1 and 2 had no effect on the elongation of telomeric DNA. The current results suggested that the decreases of c-myc, Sp1, and hTERT expressions and the increase of p53 expression, together with the reduction of cyclins/Cdks proteins in the regulation of the cell cycle, and/or the telomeric chromatin alteration led to cell cycle arrest, apoptosis, and growth inhibition induced by both ligands.

DNA-based FeCuAg nanoclusters with peroxidase-like and GSH depletion activities for toxicity of in vitro cancer cells.

Developing the efficient nanozymes for reactive oxygen species (ROS)-mediated highly potent tumor catalytic therapy has become a great challenge. In this study, we prepared the DNA-Fe, -FeAg, and -FeCuAg nanocluster (NCs) using the G-/C-rich single-stranded DNA (ssDNA) templates. The steady-state kinetic and the catalytic performances and mechanisms of DNA-metal NCs were first systematically investigated. The results indicated that c-kit-TBA-Fe, c-kit-TBA-FeAg, and c-kit-TBA-FeCuAg NCs exhibited the high peroxidase-like activity. All of three types of NCs presented the higher affinity to the substrate TMB and better storage stability at 4 °C than horseradish peroxidase (HRP). Moreover, c-kit-TBA-FeAg and c-kit-TBA-FeCuAg NCs presented the 6.7- and 4.7-fold stronger affinity to TMB than c-kit-TBA-Fe, respectively. However, the maximum reaction rate (Vmax) of c-kit-TBA-FeCuAg NCs with H2O2 was the largest, which promoted the generation of much more •OH in the reaction system. More importantly, c-kit-TBA-FeCuAg NCs were able to deplete largely the intracellular GSH and thus generate lots of endogenous ROS in HeLa cells, thereby exhibiting the significant and specific in vitro cancer cells toxicity. Therefore, c-kit-TBA-FeCuAg NCs, with peroxidase-like activity and glutathione (GSH) consumption ability, hold the ROS-based promising therapeutic effects for cancer.

Migration Inhibition Factor Secreted by Peripheral Blood Memory B Cells Binding to CD74-CD44 Receptor Complex Drives Macrophage Behavior in Alzheimer's Disease.

Dysregulation of the peripheral immune system is be involved in the neuroinflammation in Alzheimer disease (AD) and accelerate the disease progression. The contribution of immune cells, particularly B cells, to AD pathogenesis has gained attention in recent research. In this study, we investigated the role of Peripheral Blood Memory B cells (PBMBs) and their secreted Migration Inhibition Factor (MIF) in driving macrophage behavior in AD based on the scRNA-seq technique, immunofluorescence and flow cytometry. We discovered that MIF binds to the CD74-CD44 receptor complex on macrophages, influencing their behavior. The dysregulated macrophage response hampers the clearance of amyloid-beta (Aß) plaques, exacerbating AD pathology. Targeting the MIF-CD74-CD44 signal pathway may hold therapeutic potential in modulating macrophage activity and mitigating neuroinflammation in AD. This study provides a further understanding of peripheral immune cells dysregulated in AD.

Synthesis and binding studies of novel di-substituted phenanthroline compounds with genomic promoter and human telomeric DNA G-quadruplexes.

Six novel di-substituted phenanthroline derivatives 5a-7a and 3b-5b have been prepared, and their binding interactions with human telomeric (h-telo) and promoter (c-kit2 and c-myc) G-quadruplex DNAs were investigated. All the compounds are potent stabilisers of the G-quadruplex structures and compounds 3b, 4b, and 5b exhibit high G-quadruplex DNA selectivity over duplex DNA. The binding affinities of these compounds to G-quadruplex DNA are higher than to duplex DNA. CD spectra show that the compound can induce the formation of an anti-parallel structure of the h-telo G-quadruplex. Each h-telo quadruplex binds two compound molecules by the end-stacking mode. Six new compounds are able to inhibit significantly the telomerase activity at low µM concentration.

4-(1H-imidazo[4,5-f]-1,10-phenanthrolin-2-yl)phenol-based G-quadruplex DNA binding agents: telomerase inhibition, cytotoxicity and DNA-binding studies.

Four novel 4-(1H-imidazo[4,5-f]-1,10-phenanthrolin-2-yl)phenol derivatives 1-4 have been synthesized, and their G-quadruplex DNA-binding interactions, telomerase inhibition, antiproliferative activity, cell cycle arrest, and apoptotic induction were studied. All compounds show the preferential h-telo, c-myc, and c-kit2 G-quadruplex binding affinity and the G-quadruplex versus duplex selectivity. In the case of the same G-quadruplex target, the compound 1 exhibits better stabilization effect (ΔT(m)) than the other three compounds and also gives 80.2% inhibition of telomerase activity at 7.5 µM. All compounds can promote selectively the formation of parallel G-quadruplex structure of both c-myc and c-kit2 without addition of any cations. Four compounds display the cytotoxicity activities against HeLa and HepG2 cells by MTT assay with IC50 values of about 10(-6) and 10(-5) M, respectively, and cause a substantial decrease in the G2/M-phase cell population and a significant increase in the number of apoptotic cells.

Spectroscopic and biological studies of phenanthroline compounds: selective recognition of gene-promoter G-quadruplex DNAs preferred over duplex DNA.

G-Quadruplex DNA formed in the promoter regions of proto-oncogenes would block the transcription process and eventually suppress the development of tumors, so compounds that stabilize G-quadruplex DNA are potential antitumor drugs. This article describes the interactions of three phenanthroline compounds, a-c, with proto-oncogene c-kit2 and c-myc G-quadruplex DNAs by means of polymerase chain reaction (PCR) stop assay, fluorescence resonance energy transfer melting (FRET melting) assay, fluorescence indicator displacement (FID) assay, UV/VIS absorption, fluorescence, and circular dichroism (CD) spectroscopies. All three compounds displayed selectivity for the G-quadruplex over duplex, with binding constants (Ka) for the both quadruplexes varying from 0.49×106 to 3.32×106 M⁻¹ (4.1- to 33.2-fold specificity). Compounds a, b, and c were potential stabilizers for the c-kit2 G-quadruplex with the melting-temperature increase (ΔTm) values of 12-15°. CD Spectra indicated that a-c disrupted the structure of c-kit2 G-quadruplex, whereas no significant change was observed for c-myc G-quadruplex.

A stilbene derivative as dual-channel fluorescent probe for mitochondrial G-quadruplex DNA in living cells.

G-quadruplex DNA has attracted the widespread attention as a novel target of anticancer strategy. Herein, two novel stilbene derivatives 2a and 2b were designed and synthesized under mild reaction conditions, and their interactions with G-quadruplex DNA, cytotoxicity, and distribution in living cells were investigated in detail. Both compounds display a low cytotoxicity and the higher affinity to G-quadruplex DNA than to the other secondary structures, including duplex, single-stranded and i-motif DNA, moreover, the affinity of 2b with m-allyl pyridine salt group to G-quadruplex DNA is about 10-fold stronger than that of 2a with p-allyl pyridine salt group. The interactions of the compounds with the promoter G-quadruplexes are enthalpy-driven by an ITC assay. 2a and 2b not only stabilize the G-quadruplex structure but also induce the G-rich sequences (bcl-2, HRCC and KSS) to fold into the mixed-type G-quadruplex in Na+/K+ free Tris-HCl buffer at pH 7.0, and 2b presents the higher stabilization to G-quadruplex than 2a by a FRET-melting assay. 2b presents a dual-emission at 508 and 600 nm and gives a turn-on and stronger and more sensitive fluorescence response over 2a to the promoter (bcl-2, c-kit 2 and c-myc) and mitochondrial (HRCC and KSS) G-quadruplex DNA at both emission wavelengths, moreover, the peak at 508 nm is blue-shifted to 466 nm after binding to DNA. The blue and red dual-channel CLSM images indicate that 2b is mainly distributed in the mitochondrion of living HepG2 cells. The results show that 2b is a potential dual-channel fluorescent probe for mitochondrial G-quadruplex DNA in living cells.

Highly selective turn-on red fluorescence probes for visualization of the G-quadruplexes DNA in living cells.

Studies on small molecule fluorescent probes for detecting G-quadruplexes DNA have bring about an extensive attention in recent years. In this paper, we designed and synthesized three benzothiazole derivatives named 2a-2c under moderate reaction conditions and investigated their interactions with DNA (single-stranded, duplex, i-motif and G-quadruplex) and distribution in living cell. Three compounds present a large Stokes shift (∼90 nm) and a weak red fluorescence emission, and they exhibit a good selectivity and sensitive turn-on fluorescence response for the promoter G-quadruplex DNA (bcl-2, c-myc and c-kit 2) and mitochondria G-quadruplex (KSS). The affinity of 2a and 2b with N-alkyl side chain group to DNA is stronger than that of 2c with an anion group, therefore, they also increase the stability of the G-quadruplex structure. 2b induces the conformational change of both bcl-2 and KSS G-quadruplexes, while all compounds induce the folding of bcl-2 from the coiled structure to the hybrid G-qrudruplex. Three compounds interact with the G-quadruplex DNA mainly by end-stacking mode. Furthermore, MTT assays and confocal fluorescence images show that these compounds can enter the living HepG2 cells with low cytotoxicity. 2a-2c are mainly located in the mitochondrion and interacted with mitochondria G-quadruplex DNA, while only weak fluorescence can be found in cell nucleus. In a word, 2a-2c can be implied in image of G-quadruplex DNA in living cells.

Single-Cell Sequencing Revealed Pivotal Genes Related to Prognosis of Myocardial Infarction Patients.

Objectives: Myocardial infarction (MI) is a common cardiovascular disease. Histopathology is a main molecular characteristic of MI, but often, differences between various cell subsets have been neglected. Under this premise, MI-related molecular biomarkers were screened using single-cell sequencing. Methods: This work examined immune cell abundance in normal and MI samples from GSE109048 and determined differences in the activated mast cells and activated CD4 memory T cells, resting mast cells. Weighted gene coexpression network analysis (WGCNA) demonstrated that activated CD4 memory T cells were the most closely related to the turquoise module, and 10 hub genes were screened. Single-cell sequencing data (scRNA-seq) of MI were examined. We used t-distributed stochastic neighbor embedding (t-SNE) for cell clustering. Results: We obtained 8 cell subpopulations, each of which had different marker genes. 7 out of the 10 hub genes were detected by single-cell sequencing analysis. The expression quantity and proportion of the 7 genes were different in 8 cell clusters. Conclusion: In general, our study revealed the immune characteristics and determined 7 prognostic markers for MI at the single-cell level, providing a new understanding of the molecular characteristics and mechanism of MI.

Promoting the formation and stabilization of human telomeric G-quadruplex DNA, inhibition of telomerase and cytotoxicity by phenanthroline derivatives.

Four new di-substituted phenanthroline-based compounds a-d have been designed and prepared, and they have been shown to induce the formation of anti-parallel structure of human telomeric G-quadruplex DNA by CD spectra. FRET assay indicates that the melting temperature increases (ΔT(m) values) of G-quadruplex in buffer (pH 7.4) containing 100 mM NaCl are 31.6, 34.6, 17.8 and 32.6 °C for the compounds (1.0 µM) a, b, c and d, respectively. Competitive FRET assay shows that the four compounds exhibit a high G-quadruplex DNA selectivity over duplex DNA. Three of the compounds are the potent telomerase inhibitors and HeLa cell proliferation inhibitors.

An aptasensor for the label-free detection of thrombin based on turn-on fluorescent DNA-templated Cu/Ag nanoclusters.

A highly sensitive thrombin aptasensor was constructed based on the alteration of the aptamer conformation induced by the target recognition and the turn-on fluorescence due to the proximity of two darkish DNA-templated copper/silver nanoclusters (DNA-Cu/Ag NCs). Two DNA templates were designed as the functional structures consisting of the Cu/Ag NC-nucleation segment located at two termini or one terminus and the aptamer segment in the middle of a DNA template. Two darkish DNA-Cu/Ag NCs came close to each other when the aptamer combined with the target due to the conformational alteration of the aptamer structure, resulting in an increased fluorescence signal readout. Thrombin was sensitively determined as low as 1.6 nM in the range of 1.6-8.0 nM with a high selectivity. Finally, this sensor succeeded in detecting thrombin in a real fetal bovine serum.

Weighted correlation network bioinformatics uncovers a key molecular biosignature driving the left-sided heart failure.

BACKGROUND: Left-sided heart failure (HF) is documented as a key prognostic factor in HF. However, the relative molecular mechanisms underlying left-sided HF is unknown. The purpose of this study is to unearth significant modules, pivotal genes and candidate regulatory components governing the progression of left-sided HF by bioinformatical analysis. METHODS: A total of 319 samples in GSE57345 dataset were used for weighted gene correlation network analysis (WGCNA). ClusterProfiler package in R was used to conduct functional enrichment for genes uncovered from the modules of interest. Regulatory networks of genes were built using Cytoscape while Enrichr database was used for identification of transcription factors (TFs). The MCODE plugin was used for identifying hub genes in the modules of interest and their validation was performed based on GSE1869 dataset. RESULTS: A total of six significant modules were identified. Notably, the blue module was confirmed as the most crucially associated with left-sided HF, ischemic heart disease (ISCH) and dilated cardiomyopathy (CMP). Functional enrichment conveyed that genes belonging to this module were mainly those driving the extracellular matrix-associated processes such as extracellular matrix structural constituent and collagen binding. A total of seven transcriptional factors, including Suppressor of Zeste 12 Protein Homolog (SUZ12) and nuclear factor erythroid 2 like 2 (NFE2L2), adrenergic receptor (AR), were identified as possible regulators of coexpression genes identified in the blue module. A total of three key genes (OGN, HTRA1 and MXRA5) were retained after validation of their prognostic value in left-sided HF. The results of functional enrichment confirmed that these key genes were primarily involved in response to transforming growth factor beta and extracellular matrix. CONCLUSION: We uncovered a candidate gene signature correlated with HF, ISCH and CMP in the left ventricle, which may help provide better prognosis and therapeutic decisions and in HF, ISCH and CMP patients.

Meta-analysis of related factors of impulse control disorders in patients with Parkinson's disease.

BACKGROUND: To explore the related factors of impulse control disorders (ICDs) in patients with Parkinson's disease (PD). METHODS: We conducted a comprehensive search to identify studies on impulse control disorders in patients with Parkinson's disease. The related factors were compared to discriminate between PD patients with ICDs (PD-ICDs+)and PD patients without ICDs(PD-ICDs-)by a meta-analysis. RESULTS: 96 full-texts were assessed, and 15 were included (PD-ICDs+: 999; PD-ICDs-: 3507). The results showed that PD-ICDs + were significantly associated with younger age (SMD =-0.39, 95% CI: -0.50 - -0.28, P < 0.01), male sex(OR = 1.64, 95% CI: 1.34-2.02, P < 0.01), smoking habit(OR = 2.28, 95% CI: 1.16-4.47,P = 0.02), dopamine receptor agonist use(DA use) (OR = 3.41, 95% CI: 1.86-6.26,P < 0.01), dopamine receptor agonist equivalent daily dose(DA LEDD) (SMD = 0.42, 95% CI: 0.14 - 0.70,P = 0.003), levodopa equivalent daily dose(total LEDD) (SMD = 0.32, 95% CI: 0.14 - 0.49,P < 0.01), and amantadine use(OR = 2.26, 95% CI: 1.67-3.06,P < 0.01). While levodopa dose (SMD = 0.05, 95% CI: -0.09 -0.19,P = 0.48), Hoehn and Yahr stage(H & Y stage) (SMD =-0.05, 95% CI: -0.14 - 0.04,P = 0.27), MDS-UPDRS Part III score(UPDRS III score) (SMD =-0.05, 95% CI: -0.13 - 0.03,P = 0.24), PD duration (SMD =-0.23, 95% CI: 0.10 - 0.37,P < 0.01)and Mini-Mental Status Examination score (MMSE score) (SMD = 0.10, 95% CI: -0.11 - 0.31,P = 0.33)were not related with PD-ICDs+. CONCLUSION: Our study confirmed the previous results that younger age, male gender, smoking habit, longer PD duration, DA use, DA LEDD, total LEDD were high risk factors of PD-ICDs+.