Publications by authors named "Haifeng Zhang"

662 Publications

Effects and Mechanism of Oxymatrine Combined with Compound Yinchen Granules on the Apoptosis of Hepatocytes through the Akt/FoxO3a/Bim Pathway.

Biomed Res Int 2022 6;2022:8644356. Epub 2022 Jan 6.

Affiliated Hospital of Nantong University, China.

The aim of the present study was to investigate the effects and mechanism of oxymatrine (OMT) combined with compound yinchen granules (CYG) on the apoptosis of hepatocytes through the Akt/FoxO3a/Bim pathway in rats with acute liver failure. The rat model of acute liver failure was established using lipopolysaccharide/D-galactosamine (LPS/D-GalN). The expression of proteins in rat liver tissues was detected by western blot analysis. The mRNA expression of FoxO3a, Bim, Bax, Bcl-2, and caspase-3 in rat liver tissues was detected by RT-qPCR. The apoptosis rate of rat hepatocytes was determined by flow cytometry. Western blots showed that when compared with the normal group, the expression of p-Akt and p-FoxO3a in the model group was decreased ( < 0.05), while the expression of Bim was increased ( < 0.01). Compared with the model group, the expression of p-Akt and p-FoxO3a in the OMT group and the OMT combined with CYG groups was increased ( < 0.05 or < 0.01), while the expression of Bim was decreased ( < 0.05). The Bax/Bcl-2 ratio and caspase-3 protein expression in the model group were significantly higher than those in the normal group ( < 0.01). The Bax/Bcl-2 ratio and the expression of caspase-3 protein in the OMT group and the OMT combined with CYG groups were significantly lower than those in the model group ( < 0.01). The results of RT-qPCR were consistent with those of western blot. The results of flow cytometry showed that the apoptosis rate of hepatocytes in the OMT group and the OMT combined with CYG groups was significantly lower than that in the model group ( < 0.05 or < 0.01). We concluded that LPS/D-GalN can induce apoptosis of hepatocytes in rats with acute liver failure through the Akt/FoxO3a/Bim pathway. OMT combined with CYG inhibits apoptosis of hepatocytes in rats with acute liver failure via the Akt/FoxO3a/Bim pathway.
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http://dx.doi.org/10.1155/2022/8644356DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8758272PMC
January 2022

Rosiglitazone Ameliorates Spinal Cord Injury Inhibiting Mitophagy and Inflammation of Neural Stem Cells.

Oxid Med Cell Longev 2022 4;2022:5583512. Epub 2022 Jan 4.

Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China.

Background: Neurodegenerative diseases, such as Alzheimer's disease, and traumatic brain and spinal cord injury (SCI) are prevalent in clinical practice. Inhibition of hyperactive inflammation and proliferation of endogenous neural stem cells (NSCs) is a promising treatment strategy for SCI. Our previous studies demonstrated the beneficial effects of rosiglitazone (Rosi) on SCI, but its roles in inflammation inhibition and proliferation of NSCs are unknown.

Methods: SCI in a rat model was established, and the effects of Rosi on motor functions were assessed. The effects of Rosi on NSC proliferation and the underlying mechanisms were explored in details.

Results: We showed that Rosi ameliorated impairment of moto functions in SCI rats, inhibited inflammation, and promoted proliferation of NSCs . Rosi increased ATP production through enhancing glycolysis but not oxidative phosphorylation. Rosi reduced mitophagy by downregulating PTEN-induced putative kinase 1 (PINK1) transcription to promote NSC proliferation, which was effectively reversed by an overexpression of PINK1 . Through KEGG analysis and experimental validations, we discovered that Rosi reduced the expression of forkhead box protein O1 (FOXO1) which was a critical transcription factor of PINK1. Three FOXO1 consensus sequences (FCSs) were found in the first intron of the PINK1 gene, which could be potentially binding to FOXO1. The proximal FCS (chr 5: 156680169-156680185) from the translation start site exerted a more significant influence on PINK1 transcription than the other two FCSs. The overexpression of FOXO1 entirely relieved the inhibition of PINK1 transcription in the presence of Rosi.

Conclusions: Besides inflammation inhibition, Rosi suppressed mitophagy by reducing FOXO1 to decrease the transcription of PINK1, which played a pivotal role in accelerating the NSC proliferation.
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http://dx.doi.org/10.1155/2022/5583512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8752267PMC
January 2022

Apathy as a Risky Neuropsychiatric Syndrome of Progression From Normal Aging to Mild Cognitive Impairment and Dementia: A Systematic Review and Meta-Analysis.

Front Psychiatry 2021 20;12:792168. Epub 2021 Dec 20.

Beijing Dementia Key Lab, Dementia Care and Research Center, Peking University Institute of Mental Health (Sixth Hospital), Beijing, China.

Apathy has been suggested as a potential predictor of mild cognitive impairment (MCI) progression to dementia. Whether it might predict the transition from normal cognitive function to cognitive impairment has been less studied. The current study aimed to provide a comprehensive summary of the evidence on the association between apathy and the transition from normal cognitive function to cognitive impairment. We searched the PubMed, Embase, and Web of Science databases for longitudinal prospective cohort studies that evaluated apathy at baseline in the cognitively normal population and had cognitive impairment as the outcome. Random effects models were used, and heterogeneity was explored with stratification. The stability of the synthesized result was indicated using sensitivity analysis by excluding one study each time and recalculating the overall effect. Ten studies comprising 26,195 participants were included. Apathy status was available for 22,101 participants. Apathy was present in 1,803 of 22,101 participants (8.16%). Follow-up ranged from 1 to 13 years. The combined odds ratio (OR) of cognitive impairment for patients with apathy was 2.07 (95% CI: 1.43-2.99; I = 86%), and the combined hazard ratio was 2.70 (95% CI: 1.38-5.27; I = 94%). The OR meta-analyses for different conversion outcomes were MCI (OR = 3.38, 95% CI: 1.57-7.28; I =71%), cognitive decline (OR = 1.27, 95% CI: 0.81-2.00; I = 64%) and dementia (OR = 2.12, 95% CI: 1.32-3.41; I = 86%). Subgroup analysis suggested that the association between apathy and cognitive impairment changed with age, depression adjustments, apathy measurement, and follow-up time. Apathy was associated with a greater than 2-fold increased risk of progression to cognitive impairment in the cognitively normal population. Future interventions targeting apathy management in the general population may reduce the risk of cognitive impairment.
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http://dx.doi.org/10.3389/fpsyt.2021.792168DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8721876PMC
December 2021

Identification of unknown disinfection byproducts in drinking water produced from Taihu Lake source water.

J Environ Sci (China) 2022 Mar 13;113:1-11. Epub 2021 Jun 13.

Key Laboratory of Drinking Water Science and Technology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:

Although disinfection byproducts (DBPs) in drinking water have been suggested as a cancer causing factor, the causative compounds have not yet been clarified. In this study, we used liquid chromatography quadrupole-time-of-flight spectrometry (LC-QTOF MS) to identify the unknown disinfection byproducts (DBPs) in drinking water produced from Taihu Lake source water, which is known as a convergence point for the anthropogenic pollutants discharged from intensive industrial activities in the surrounding regions. In total, 91 formulas of DBPs were discovered through LC-QTOF MS nontarget screen, 81 of which have not yet been reported. Among the 91 molecules, 56 only contain bromine, 15 only contain chlorine and 20 DBPs have both bromine and chlorine atoms. Finally, five DBPs including 2,4,6-tribromophenol, 2,6-dibromo-4-chlorophenol, 2,6-dichloro-4-bromophenol, 4-bromo-2,6-di-tert-butylphenol and 3,6-dibromocarbazole were confirmed using standards. The former three compounds mainly formed in the predisinfection step (maximum concentration, 0.2-2.6 µg/L), while the latter two formed in the disinfection step (maximum concentration, 18.2-33.6 ng/L). In addition, 19 possible precursors of the discovered DBPs were detected, with the aromatic compounds being a major group. 2,6-di-tert-butylphenol as the precursor of 4-bromo-2,6-di-tert-butylphenol was confirmed with standard, with a concentration of 20.3 µg/L in raw water. The results of this study show that brominated DBPs which are possibly formed from industrial pollutants are relevant DBP species in drinking water produced form Taihu source water, suggesting protection of Taihu Lake source water is important to control the DBP risks.
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http://dx.doi.org/10.1016/j.jes.2021.05.040DOI Listing
March 2022

Terahertz exposure enhances neuronal synaptic transmission and oligodendrocyte differentiation .

iScience 2021 Dec 22;24(12):103485. Epub 2021 Nov 22.

Department of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

Terahertz (THz) frequency occupies a large portion of the electromagnetic spectrum that is between the infrared and microwave regions. Recent advances in THz application have stimulated interests regarding the biological effects within this frequency range. In the current study, we report that irradiation with a single-frequency THz laser on mice cortical neuron cultures increases excitatory synaptic transmission and neuronal firing activities. Microarray assay reveals gene expression dynamics after THz exposure, which is consistent with morphology and electrophysiology results. Besides, certain schedule of THz irradiation inhibits the proliferation of oligodendrocyte precursor cells (OPCs) and promotes OPC differentiation. Of note, the myelination process is enhanced after THz exposure. In summary, our observations suggest that THz irradiation can modulate the functions of different neuronal cells, with different sensitivity to THz. These results provide important understanding of the mechanisms that govern THz interactions with nervous systems and suggest THz wave as a new strategy for neuromodulation.
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http://dx.doi.org/10.1016/j.isci.2021.103485DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8649796PMC
December 2021

Exercise Training Increases Serum Cardiac Troponin T Independent of Left Ventricular Mass.

Int J Sports Med 2021 Dec 6. Epub 2021 Dec 6.

Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom of Great Britain and Northern Ireland.

The purpose of this study was to determine whether exercise training mediated cardiac troponin T (cTnT) and whether this was associated with increases in left ventricular mass (LVM). Fifty-four sedentary obese women were randomised to high-intensity interval training (HIIT, repeated 4-min cycling at 90% V̇O interspersed with 3-min rest), work-equivalent continuous aerobic training (CAT, continuous cycling at 60% V̇O) or a control group (CON). Resting serum cTnT was assessed using a high-sensitivity assay before and after 12 weeks of training. LVM was determined from 2D echocardiography at the same timepoints. Both HIIT and CAT induced a similar elevation (median 3.07 to 3.76 ng.l, 0.05) in resting cTnT compared with pre-training and the CON (3.49 to 3.45 ng.l, 0.05). LVM index in HIIT increased (62.2±7.8 to 73.1±14.1 g.m, 0.05), but not in CAT (66.1±9.7 to 67.6±9.6 g.m, 0.05) and CON (67.9±9.5 to 70.2±9.1 g.m, 0.05). Training-induced changes in resting cTnT did not correlate with changes in LVM index (=-0.025, =0.857). These findings suggest that twelve weeks of either HIIT or CAT increased resting cTnT, but the effects were independent of any changes in LVM in sedentary obese women.
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http://dx.doi.org/10.1055/a-1670-7707DOI Listing
December 2021

Effects of Semiconduction on Thickness-extensional Modes of Piezoelectric Resonators.

IEEE Trans Ultrason Ferroelectr Freq Control 2021 Nov 23;PP. Epub 2021 Nov 23.

We study thickness-extensional vibrations of a piezoelectric semiconductor plate for resonator application. A perturbation integral for the semiconduction-induced frequency shift is obtained, which shows that the first-order frequency shift represents a damping effect due to semiconduction. Numerical results for ZnO and AlN plates are presented.
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http://dx.doi.org/10.1109/TUFFC.2021.3130542DOI Listing
November 2021

MoErv29 promotes apoplastic effector secretion contributing to virulence of the rice blast fungus Magnaporthe oryzae.

New Phytol 2022 Feb 26;233(3):1289-1302. Epub 2021 Nov 26.

Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095, China.

During plant-pathogenic fungi and host plants interactions, numerous pathogen-derived proteins are secreted resulting in the activation of the unfolded protein response (UPR) pathway. For efficient trafficking of secretory proteins, including those important in disease progression, the cytoplasmic coat protein complex II (COPII) exhibits a multifunctional role whose elucidation remains limited. Here, we discovered that the COPII cargo receptor MoErv29 functions as a target of MoHac1, a previously identified transcription factor of the UPR pathway. In Magnaporthe oryzae, deletion of MoERV29 severely affected the vegetative growth, conidiation and biotrophic invasion of the fungus in susceptible rice hosts. We demonstrated that MoErv29 is required for the delivery of secreted proteins through recognition and binding of the amino-terminal tripeptide motifs following the signal peptide. By using bioinformatics analysis, we predicted a cargo spectrum of MoErv29 and found that MoErv29 is required for the secretion of many proteins, including extracellular laccases and apoplastic effectors. This secretion is mediated through the conventional endoplasmic reticulum-Golgi secretion pathway and is important for conferring host recognition and disease resistance. Taken together, our results revealed how MoErv29 operates on effector secretion, and our findings provided a critical link between COPII vesicle trafficking and the UPR pathway.
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http://dx.doi.org/10.1111/nph.17851DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8738142PMC
February 2022

Correction to: Vitamin D mediates the association between acrylamide hemoglobin biomarkers and obesity.

Environ Sci Pollut Res Int 2021 Nov 8. Epub 2021 Nov 8.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China.

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http://dx.doi.org/10.1007/s11356-021-17332-6DOI Listing
November 2021

Urolithin A suppresses RANKL-induced osteoclastogenesis and postmenopausal osteoporosis by, suppresses inflammation and downstream NF-κB activated pyroptosis pathways.

Pharmacol Res 2021 Dec 3;174:105967. Epub 2021 Nov 3.

Department of Orthopedics, The First Affiliated Hospital of Soochow University, No. 188 Shizi Street, Suzhou, Jiangsu 215006, China. Electronic address:

Osteoporosis (OP) is characterized by decreased trabecular bone volume and microarchitectural deterioration in the medullary cavity. Urolithin A (UA) is a biologically active metabolite generated by the gut microbiota. UA is the measurable product considered the most relevant urolithin as the final metabolic product of polyphenolic compounds. Considering that catabolic effects mediated by the intestinal microbiota are highly involved in pathological bone disorders, exploring the biological influence and molecular mechanisms by which UA alleviates OP is crucial. Our study aimed to investigate the effect of UA administration on OP progression in the context of estrogen deficiency-induced bone loss. The in vivo results indicated that UA effectively reduced ovariectomy-induced systemic bone loss. In vitro, UA suppressed Receptor Activator for Nuclear Factor-κB Ligand (RANKL)-triggered osteoclastogenesis in a concentration-dependent manner. Signal transduction studies and sequencing analysis showed that UA significantly decreased the expression of inflammatory cytokines (e.g., IL-6 and TNF-α) in osteoclasts. Additionally, attenuation of inflammatory signaling cascades inhibited the NF-κB-activated NOD-like receptor signaling pathway, which eventually led to decreased cytoplasmic secretion of IL-1β and IL-18 and reduced expression of pyroptosis markers (NLRP3, GSDMD, and caspase-1). Consistent with this finding, an NLRP3 inflammasome inhibitor (MCC950) was employed to treat OP, and modulation of pyroptosis was found to ameliorate osteoclastogenesis and bone loss in ovariectomized (OVX) mice, suggesting that UA suppressed osteoclast formation by regulating the inflammatory signal-dependent pyroptosis pathway. Conceivably, UA administration may be a safe and promising therapeutic strategy for osteoclast-related bone diseases such as OP.
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http://dx.doi.org/10.1016/j.phrs.2021.105967DOI Listing
December 2021

CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling.

Arterioscler Thromb Vasc Biol 2021 12 21;41(12):2943-2960. Epub 2021 Oct 21.

Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology (L.Q., H.Z., B.L., Q.L., W.M., J.H.Z.), Yale University School of Medicine, New Haven, CT.

Objective: Cerebral cavernous malformations (CCMs) can happen anywhere in the body, although they most commonly produce symptoms in the brain. The role of CCM genes in other vascular beds outside the brain and retina is not well-examined, although the 3 CCM-associated genes (, , and ) are ubiquitously expressed in all tissues. We aimed to determine the role of gene in lymphatics. Approach and Results: Mice with an inducible pan-endothelial cell (EC) or lymphatic EC deletion of ( or ) exhibit dilated lymphatic capillaries and collecting vessels with abnormal valve structure. Morphological alterations were correlated with lymphatic dysfunction in mice as determined by Evans blue dye and fluorescein isothiocyanate(FITC)-dextran transport assays. lymphatics had increased VEGFR3 (vascular endothelial growth factor receptor-3)-ERK1/2 (extracellular signal-regulated kinase 1/2) signaling with lymphatic hyperplasia. Mechanistic studies suggested that VEGFR3 is primarily regulated at a transcriptional level in Ccm3-deficient lymphatic ECs, in an NF-κB (nuclear factor κB)-dependent manner. CCM3 binds to importin alpha 2/KPNA2 (karyopherin subunit alpha 2), and a CCM3 deletion releases KPNA2 to activate NF-κB P65 by facilitating its nuclear translocation and P65-dependent VEGFR3 transcription. Moreover, increased VEGFR3 in lymphatic EC preferentially activates ERK1/2 signaling, which is critical for lymphatic EC proliferation. Importantly, inhibition of VEGFR3 or ERK1/2 rescued the lymphatic defects in structure and function.

Conclusions: Our data demonstrate that CCM3 deletion augments the VEGFR3-ERK1/2 signaling in lymphatic EC that drives lymphatic hyperplasia and malformation and warrant further investigation on the potential clinical relevance of lymphatic dysfunction in patients with CCM.
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http://dx.doi.org/10.1161/ATVBAHA.121.316707DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8613000PMC
December 2021

Vitamin D mediates the association between acrylamide hemoglobin biomarkers and obesity.

Environ Sci Pollut Res Int 2021 Oct 18. Epub 2021 Oct 18.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China.

Mediation analysis aims to discover the role of intermediate variables from exposure to disease. The current study was performed to evaluate how vitamin D mediates the association between acrylamide hemoglobin biomarkers and obesity. Data were collected on 10,377 adults participating in the National Health and Nutrition Examination Survey (NHANES) 2003-2006 and 2013-2014 aged ≥ 18 years. Obesity was assessed through body mass index and abdominal circumference measurements. Generalized linear and restricted cubic spline (RCS) regression were used to estimate the association between vitamin D and acrylamide hemoglobin biomarkers, and the mediation effect of vitamin D was also discussed. After adjusting for potentially confounding factors, vitamin D had strong negative associations with serum concentrations of acrylamide hemoglobin adducts (HbAA, HbGA, and HbAA + HbGA). The RCS plots demonstrated that vitamin D was inversely and nonlinearly associated with HbAA and HbAA + HbGA while inversely and linearly associated with HbGA, and also a striking difference when vitamin D was lower than 60 nmol/L. Mediation analysis suggested that a negative correlation between acrylamide and obesity was mediated by vitamin D. The current study is expected to offer a fresh perspective on reducing the toxicity of acrylamide.
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http://dx.doi.org/10.1007/s11356-021-16798-8DOI Listing
October 2021

A Heterogeneous RISC-V Processor for Efficient DNN Application in Smart Sensing System.

Sensors (Basel) 2021 Sep 28;21(19). Epub 2021 Sep 28.

Engineering and Research Center of Embedded Systems Integration (Ministry of Education), Xi'an 710129, China.

Extracting features from sensing data on edge devices is a challenging application for which deep neural networks (DNN) have shown promising results. Unfortunately, the general micro-controller-class processors which are widely used in sensing system fail to achieve real-time inference. Accelerating the compute-intensive DNN inference is, therefore, of utmost importance. As the physical limitation of sensing devices, the design of processor needs to meet the balanced performance metrics, including low power consumption, low latency, and flexible configuration. In this paper, we proposed a lightweight pipeline integrated deep learning architecture, which is compatible with open-source RISC-V instructions. The dataflow of DNN is organized by the very long instruction word (VLIW) pipeline. It combines with the proposed special intelligent enhanced instructions and the single instruction multiple data (SIMD) parallel processing unit. Experimental results show that total power consumption is about 411 mw and the power efficiency is about 320.7 GOPS/W.
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http://dx.doi.org/10.3390/s21196491DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8511981PMC
September 2021

Design of ultra-broadband absorption enhancement in plasmonic absorber by interaction resonance of multi-plasmon modes and Fabry-Perot mode.

Opt Express 2021 Aug;29(18):29228-29241

This paper shows a strategy to realize ultra-broadband absorption of multi-spectral coverage. A vertical cascaded plasmonic absorber constructed by multilayer helical metallic nanostructure wrapped in a pyramid-shaped dielectric jacket is presented and investigated by numerical simulations. By premeditated planning of the scale proportions of the spirals and the dimension size of the pyramid-shaped dielectric, more than 90% of absorption is realized in 189-3896 nm, an ultra-wide spectral range that basically covers the bands of near-ultraviolet, visible light, and near-infrared. The excitation mechanism of electromagnetic resonance and the formation process of light trapping are both included in the investigation through the analysis of electromagnetic field distribution. The localized surface plasmon mode in the metallic nano-spiral and the Fabry-Perot cavity mode with the gap plasmon resonance in the dielectric gap cooperatively make a significant contribution to reduce the reflection and form the ultra-broadband absorption. The simulation results show that the proposed absorber is basically insensitive to the incident angle and polarization angle, which basically keeps more than 90% absorption within the incident angle of ± 80 °. Such a specific implementation idea can also be applied to the terahertz region by modifying the geometrical size of the structure. This presented design implies new viability to develop the broadband photodetectors, solar cells, and thermal emitters.
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http://dx.doi.org/10.1364/OE.440172DOI Listing
August 2021

Impact of high-intensity interval and moderate-intensity continuous exercise on heart rate variability and cardiac troponin.

J Sports Med Phys Fitness 2021 Sep;61(9):1301-1308

Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.

Background: It remains uncertain whether exercise modality (high-intensity interval [HIE]; moderate-intensity continuous [MCE]) mediates exercise-induced changes in markers of pro-arrhythmogenic state and/or cardiac damage. This study examines heart rate variability (HRV) and cardiac troponin T (cTnT) kinetic responses to HIE and MCE.

Methods: Fourteen sedentary, overweight/obese females completed two trials including HIE (2-min running at 90% V̇O2max followed by 2-min running at 50% V̇O2max, repeated for 60 min) and MCE (70% V̇O2max steady-state running for 60 min) in a randomized, counterbalanced fashion. Supine HRV was evaluated as root mean square of successive differences (RMSSD), normalized low-frequency (LF) and high-frequency (HF) spectral power, as well as the LF/HF ratio before (PRE), immediately (0 HR), 3 (3 HR) and 24 (24 HR) hours after exercise. Serum cTnT was assessed using a high-sensitivity assay at the same time-points and the values were corrected for plasma volume changes.

Results: Exercise temporarily altered all HRV indices (i.e. RMSSD and HF decreased; LF and LF/HF ratio increased at 0 HR, all P<0.05) but a rebound increase of RMSSD was observed at 24 HR, and the kinetic responses of HRV were similar between exercise modalities. The cTnT was significantly elevated (P<0.05) after exercise at 3 HR (by 688%) and 24 HR (by 374%) with no between-modality differences. There was no significant correlation between delta change in cTnT and HRV metrics.

Conclusions: Exercise modality (workload-equivalent HIE vs. MCE) did not mediate exercise-induced alteration in autonomic activity and cTnT elevation, and it seems these are largely separate exercise-induced phenomena.
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http://dx.doi.org/10.23736/S0022-4707.20.11657-8DOI Listing
September 2021

Disinfection by-product (DBP) research in China: Are we on the track?

J Environ Sci (China) 2021 Dec 2;110:99-110. Epub 2021 Apr 2.

Key Laboratory of Drinking Water Science and Technology, Research Center for Eco-Environmental Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100085, China. Electronic address:

Disinfection by-products (DBPs) formed during water disinfection has drawn significant public concern due to its toxicity. Since the first discovery of the trihalomethanes in 1974, continued effort has been devoted on DBPs worldwide to investigate the formation mechanism, levels, toxicity and control measures in drinking water. This review summarizes the main achievements on DBP research in China, which included: (1) the investigation of known DBP occurrence in drinking water of China; (2) the enhanced removal of DBP precursor by water treatment process; (3) the disinfection optimization to minimize DBP formation; and (4) the identification of unknown DBPs in drinking water. Although the research of DBPs in China cover the whole formation process of DBPs, there is still a challenge in effectively controlling the drinking water quality risk induced by DBPs, an integrated research framework including chemistry, toxicology, engineering, and epidemiology is especially crucial.
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http://dx.doi.org/10.1016/j.jes.2021.03.023DOI Listing
December 2021

Porous g-CN with defects for the efficient dye photodegradation under visible light.

Water Sci Technol 2021 Sep;84(6):1354-1365

School of Chemistry and Chemical Engineering, Henan University of Technology, Zhengzhou 450001, China E-mail:

Porous graphitic carbon nitride (p-CN) was fabricated via simple pyrolyzing treatment of graphitic carbon nitride (g-CN). The defects could be introduced into the structure of g-CN by breakage of some bonds, which was beneficial for the generation of electron-hole pairs and inhibiting their recombination. Compared with g-CN, p-CN showed a narrow band gap to promote the utilization of visible light. Furthermore, the porous structure also increased the specific surface area to maximize the exposure of active sites and promote mass transfer during photodegradation. As a result, the as-reported p-CN exhibited considerably higher degradation efficiency for Rhodamine B (RhB) and Methyl Orange (MO) than that of the original g-CN. Moreover, the photocatalyst showed high durability and stability in recycling experiments.
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http://dx.doi.org/10.2166/wst.2021.313DOI Listing
September 2021

β-Hydroxybutyrate Mitigated Heart Failure with Preserved Ejection Fraction by Increasing Treg Cells via Nox2/GSK-3β.

J Inflamm Res 2021 16;14:4697-4706. Epub 2021 Sep 16.

Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215002, People's Republic of China.

Background: This study was designed to investigate the cardioprotective role of β-hydroxybutyrate (BHB) in heart failure with preserved ejection fraction (HFpEF) and the underlying mechanism.

Methods: A two-hit model with a high-fat diet (HFD) and N-nitrol-arginine methyl ester (L-NAME) was used as an HFpEF model. The treatment group received a weekly intraperitoneal injection of β-hydroxybutyrate (BHB). Cardiac function, inflammation, and fibrosis were evaluated. CD3CD4Foxp3 positive cells within the myocardium were quantified by flow cytometry. The NADPH oxidase 2 (NOX2)/glycogen synthase kinase-3β (GSK3β) pathway was examined by immunoblot analysis.

Results: BHB improved diastolic function, fibrosis and cardiac remodeling in HFpEF. Additionally, BHB inhibited cardiac inflammation and increased cardiac Treg cells, which could be due to the downregulation of the NOX2/GSK-3β pathway.

Conclusion: BHB protected against the progression of HFpEF by increasing cardiac Treg cells by modulating the NOX2/GSK-3β pathway.
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http://dx.doi.org/10.2147/JIR.S331320DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8453303PMC
September 2021

Bioinformatic analysis for potential biological processes and key targets of heart failure-related stroke.

J Zhejiang Univ Sci B 2021 Sept 15;22(9):718-732

Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China.

This study aimed to uncover underlying mechanisms and promising intervention targets of heart failure (HF)-related stroke. HF-related dataset GSE42955 and stroke-related dataset GSE58294 were obtained from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was conducted to identify key modules and hub genes. Gene Ontology (GO) and pathway enrichment analyses were performed on genes in the key modules. Genes in HF- and stroke-related key modules were intersected to obtain common genes for HF-related stroke, which were further intersected with hub genes of stroke-related key modules to obtain key genes in HF-related stroke. Key genes were functionally annotated through GO in the Reactome and Cytoscape databases. Finally, key genes were validated in these two datasets and other datasets. HF- and stroke-related datasets each identified two key modules. Functional enrichment analysis indicated that protein ubiquitination, Wnt signaling, and exosomes were involved in both HF- and stroke-related key modules. Additionally, ten hub genes were identified in stroke-related key modules and 155 genes were identified as common genes in HF-related stroke. OTU deubiquitinase with linear linkage specificity() and nuclear factor interleukin 3-regulated() were determined to be the key genes in HF-related stroke. Through functional annotation, was involved in protein ubiquitination and Wnt signaling, and was involved in DNA binding and transcription. Importantly, and were also validated to be differentially expressed in all HF and stroke groups. Protein ubiquitination, Wnt signaling, and exosomes were involved in HF-related stroke. and may play a key role in HF-related stroke through regulating these processes, and thus serve as promising intervention targets.
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http://dx.doi.org/10.1631/jzus.B2000544DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435344PMC
September 2021

The J-Curve Association Between Blood Pressure and Mortality in Stroke Survivors.

Int J Gen Med 2021 29;14:5039-5049. Epub 2021 Aug 29.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, People's Republic of China.

Purpose: The optimal blood pressure (BP) targets in terms of mortality risk after stroke remain unclear. This study aimed to assess the relationship between BP and mortality in stroke survivors.

Patients And Methods: We included 1696 participants with self-reported history of stroke aged 18 years and older from the National Health and Nutrition Examination Survey (NHANES) 1999-2014 and NHANES III with public-use linked mortality files from 2015. Baseline systolic BP (SBP) and diastolic BP (DBP) levels were obtained by taking the average of 3 measures. Cox proportional hazard models and restricted cubic splines were conducted to explore the relationship between BP and all-cause mortality.

Results: During a median follow-up period of 5.6 years, 888 deaths occurred. After fully adjusting for confounding factors, SBP displayed a J-curve relationship (nadir 135 mm Hg), while DBP exhibited a reverse J-curve relationship (nadir 73 mm Hg) with the risk of all-cause mortality. However, the J-curve or reverse J-curve pattern between blood pressure and mortality appeared to be limited to individuals with an age >65 years, identifying a nadir of SBP/DBP of 142/73 mm Hg. The risk of mortality followed a linear relationship for SBP and DBP in stroke survivors aged ≤65 years, with risks increasing with higher SBP and lower DBP.

Conclusion: In this cross-sectional study that used national survey data, these data suggest a strong J-curve or reverse J-curve relationship between blood pressure and risk of all-cause mortality, whereas the pattern appears to be limited to individuals with an age >65 years, with a nadir at 142/73 mmHg. However, missing data on stroke type and stroke treatment limits the generalizability. Future prospective studies are needed to determine preferential blood pressure target in patients after stroke.
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http://dx.doi.org/10.2147/IJGM.S326301DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8412835PMC
August 2021

ASPM promotes hepatocellular carcinoma progression by activating Wnt/β-catenin signaling through antagonizing autophagy-mediated Dvl2 degradation.

FEBS Open Bio 2021 10 14;11(10):2784-2799. Epub 2021 Sep 14.

College of Public Health, Zhengzhou University, China.

Hepatocellular carcinoma (HCC) is one of the most fatal cancers worldwide. In this article, we show that expression of abnormal spindle-like microcephaly-associated protein (ASPM) is up-regulated in liver cancer samples, and this up-regulation is significantly associated with tumor aggressiveness and reduced survival times of patients. Down-regulation of ASPM expression inhibits the proliferation, invasion, migration and epithelial-to-mesenchymal transition of HCC cells in vitro and inhibits tumor formation in nude mice. ASPM interacts with disheveled-2 (Dvl2) and antagonizes autophagy-mediated Dvl2 degradation by weakening the functional interaction between Dvl2 and the lipidated form of microtubule-associated proteins 1A/1B light chain 3A (LC3II), thereby increasing Dvl2 protein abundance and leading to Wnt/β-catenin signaling activation in HCC cells. Thus, our results define ASPM as a novel oncoprotein in HCC and indicate that disruption of the Wnt-ASPM-Dvl2-β-catenin signaling axis might have potential clinical value.
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http://dx.doi.org/10.1002/2211-5463.13278DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8487047PMC
October 2021

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPAR and PGC1.

PPAR Res 2021 6;2021:9947656. Epub 2021 Aug 6.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

Materials And Methods: C57BL/6 mice were treated with coronary artery ligation to generate an MI model, followed by treatment for 3 weeks with NOB (50 mg/kg/d) or vehicle (50 mg/kg/d), with or without the peroxisome proliferator-activated receptor gamma (PPAR) inhibitor T0070907 (1 mg/kg/d). Cardiac function (echocardiography, survival rate, Evans blue, and triphenyl tetrazolium chloride staining), fibrosis (Masson's trichrome staining, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB)), hypertrophy (haematoxylin-eosin staining, wheat germ agglutinin staining, and qRT-PCR), and apoptosis (WB and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining) were evaluated. Hypoxia-induced apoptosis (TUNEL, WB) and phenylephrine- (PE-) induced pathological hypertrophy (immunofluorescence staining, qRT-PCR) models were established in primary neonatal rat ventricular myocytes (NRVMs). The effects of NOB with or without T0070907 were examined for the expression of PPAR and PPAR coactivator 1 (PGC1) by WB in mice and NRVMs. The potential downstream effectors of PPAR were further analyzed by WB in mice.

Results: Following MI in mice, NOB intervention enhanced cardiac function across three predominant dimensions of pathological cardiac remodeling, which reflected in decreasing cardiac fibrosis, apoptosis, and hypertrophy decompensation. NOB intervention also alleviated apoptosis and hypertrophy in NRVMs. NOB intervention upregulated PPAR and PGC1 and . Furthermore, the PPAR inhibitor abolished the protective effects of NOB against pathological cardiac remodeling during the progression from MI to CHF. The potential downstream effectors of PPAR were nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1).

Conclusions: Our findings suggested that NOB alleviates pathological cardiac remodeling after MI via PPAR and PGC1 upregulation.
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http://dx.doi.org/10.1155/2021/9947656DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8373512PMC
August 2021

Inhibition of LOXL1-AS1 alleviates oxidative low-density lipoprotein induced angiogenesis via downregulation of miR-590-5p mediated KLF6/VEGF signaling pathway.

Cell Cycle 2021 Aug 12:1-18. Epub 2021 Aug 12.

Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou Henan, China.

Increasing evidences have confirmed that long non-coding RNA LOXL1-AS1 functions in multiple human diseases. Here, we aim to explore the function and mechanism of LOXL1-AS1 in modulating oxidized low-density lipoprotein (ox-LDL)-induced angiogenesis of endothelial cells (ECs). Presently, we found that LOXL1-AS1 and KLF6 were upregulated in ECs treated by Ox-LDL in a dose- and time-dependent manner while miR-590-5p was downregulated. Overexpression of LOXL1-AS1 aggravated Ox-LDL mediated ECs proliferation and migration, and promoted angiogenesis both and . On the contrary, enhancing miR-590-5p or inhibiting LOXL1-AS1 level led to suppressive effects on the proliferation, migration and angiogenesis of ECs. Moreover, LOXL1-AS1 upregulation promoted the expression of vascular endothelial growth factor (VEGF), MMPs (including MMP2, MMP9, and MMP14) and also activated VEGF/VEGFR2/PI3K/Akt/eNOS pathway. Mechanistically, LOXL1-AS1 works as a competitive endogenous RNA (ceRNA) by sponging miR-590-5p, which targeted at the 3'-untranslated region (3'UTR) of KLF6. Additionally, the proliferation, migration, and angiogenesis of ECs were elevated following KLF6 upregulation. By detecting the expression of LOXL1-AS1 and miR-590-5p in the serum of healthy donors and atherosclerosis patients, it was found that LOXL1-AS1 was upregulated in atherosclerosis patients (compared with healthy donors) and had a negative relationship with miR-590-5p. Taken together, LOXL1-AS1 promoted Ox-LDL induced angiogenesis via regulating miR-590-5p-modulated KLF6/VEGF signaling pathway. The LOXL1-AS1-miR-590-5p axis exerts a novel role in the progression of atherosclerosis.
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http://dx.doi.org/10.1080/15384101.2021.1958501DOI Listing
August 2021

Feedback regulation of Notch signaling and myogenesis connected by MyoD-Dll1 axis.

PLoS Genet 2021 08 9;17(8):e1009729. Epub 2021 Aug 9.

Center for Molecular Medicine, University of Georgia, Athens, Georgia, United States of America.

Muscle precursor cells known as myoblasts are essential for muscle development and regeneration. Notch signaling is an ancient intercellular communication mechanism that plays prominent roles in controlling the myogenic program of myoblasts. Currently whether and how the myogenic cues feedback to refine Notch activities in these cells are largely unknown. Here, by mouse and human gene gain/loss-of-function studies, we report that MyoD directly turns on the expression of Notch-ligand gene Dll1 which activates Notch pathway to prevent precautious differentiation in neighboring myoblasts, while autonomously inhibits Notch to facilitate a myogenic program in Dll1 expressing cells. Mechanistically, we studied cis-regulatory DNA motifs underlying the MyoD-Dll1-Notch axis in vivo by characterizing myogenesis of a novel E-box deficient mouse model, as well as in human cells through CRISPR-mediated interference. These results uncovered the crucial transcriptional mechanism that mediates the reciprocal controls of Notch and myogenesis.
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http://dx.doi.org/10.1371/journal.pgen.1009729DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8376015PMC
August 2021

Effects of an Enhanced Training on Primary Care Providers Knowledge, Attitudes, Service and Skills of Dementia Detection: A Cluster Randomized Trial.

Front Neurol 2021 23;12:651826. Epub 2021 Jul 23.

Beijing Dementia Key Lab, Dementia Care & Research Center, Peking University Institute of Mental Health (Sixth Hospital), Beijing, China.

Effective training programs for primary care providers (PCPs) to support dementia detection are needed, especially in developing countries. This study aimed to investigate the effect of an enhanced training on the competency and service of PCPs for dementia detection. We conducted a cluster randomized trial in Beijing, China. Community healthcare centers (CHCs) located in Fengtai or Fangshan District were eligible. The enrolled CHCs in each district were randomly assigned to the standard or the enhanced training group at a 1:1 ratio. PCPs serving older adults in enrolled CHCs were eligible to participate. The standard training group received three-hour didactic lectures, three monthly supervisions, 3 months of online support and dementia screening packages. The enhanced training group additionally received three monthly face-to-face supervisions and 3 months of online support. The participants became aware of their group membership at the end of the standard training. The knowledge, attitudes, service, and skills regarding dementia detection were assessed using questionnaires and submitted dementia detection records, respectively. A total of 23 and 21 CHCs were randomly assigned to the standard and the enhanced training group, respectively, and 58 participants from 20 CHCs assigned to the standard training group and 48 from 16 CHCs assigned to the enhanced training group were included in the final analysis (mean age 37.5 years, and 67.0% women). A significant increase in the knowledge score was found in both groups, but the increase was similar in the two groups ( = 0.262). The attitude score remained stable in both groups, and no between-group difference was found. Compared with the baseline, both groups reported an increase in dementia detection service, especially the enhanced training group (24.1% to 31.0% in the standard training group and 14.6% to 45.8% in the enhanced training group). The completion rate and accuracy of submitted dementia detection records in the enhanced training group were both significantly higher than those in the standard training group (both < 0.001). The enhanced training had similar effect on the knowledge of PCPs comparing with the standard training, but was better on continuous service and skills of PCPs related to dementia detection. www.ClinicalTrials.gov, identifier: NCT02782000. Registration date: May 2016. The trial was completed in July 2017.
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http://dx.doi.org/10.3389/fneur.2021.651826DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8342805PMC
July 2021

Commercialization-Driven Electrodes Design for Lithium Batteries: Basic Guidance, Opportunities, and Perspectives.

Small 2021 Oct 5;17(43):e2102233. Epub 2021 Aug 5.

College of Chemical Engineering, Fuzhou University, Fuzhou, 350116, P. R. China.

Current lithium-ion battery technology is approaching the theoretical energy density limitation, which is challenged by the increasing requirements of ever-growing energy storage market of electric vehicles, hybrid electric vehicles, and portable electronic devices. Although great progresses are made on tailoring the electrode materials from methodology to mechanism to meet the practical demands, sluggish mass transport, and charge transfer dynamics are the main bottlenecks when increasing the areal/volumetric loading multiple times to commercial level. Thus, this review presents the state-of-the-art developments on rational design of the commercialization-driven electrodes for lithium batteries. First, the basic guidance and challenges (such as electrode mechanical instability, sluggish charge diffusion, deteriorated performance, and safety concerns) on constructing the industry-required high mass loading electrodes toward commercialization are discussed. Second, the corresponding design strategies on cathode/anode electrode materials with high mass loading are proposed to overcome these challenges without compromising energy density and cycling durability, including electrode architecture, integrated configuration, interface engineering, mechanical compression, and Li metal protection. Finally, the future trends and perspectives on commercialization-driven electrodes are offered. These design principles and potential strategies are also promising to be applied in other energy storage and conversion systems, such as supercapacitors, and other metal-ion batteries.
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http://dx.doi.org/10.1002/smll.202102233DOI Listing
October 2021

Urinary phenols and parabens metabolites associated with cardiovascular disease among adults in the United States.

Environ Sci Pollut Res Int 2021 Aug 3. Epub 2021 Aug 3.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China.

The field of environmental health has begun to examine the effects of higher-order chemical combinations. The current literature lacks studies exploring associations between multiple organic chemical mixtures and cardiometabolic diseases (CVDs). This study aimed to evaluate associations between urinary phenols, parabens metabolites, and total and individual CVDs among a nationally representative sample of adults in the US. This cross-sectional study analyzed 7 urinary chemicals detected among the general population from the 2005-2016 National Health and Nutrition Examination Survey (NHANES, n=10,428). Multivariate logistic regression and weighted quantile sum (WQS) regression were applied to examine relationships between phenols and parabens metabolites, alone and in combination, and total and individual CVDs prevalence. Compared with the lowest quartile, URBPA (OR: 1.52; 95% CI: 1.20-1.91; P=0.001) levels in the highest quartile were independently associated with increased total CVD. The WQS index of phenols and parabens mixtures were independently correlated with total CVD (adjusted odds ratios [OR]: 1.16; 95% confidence interval [CI]:1.06-1.28; P=0.002), angina (adjusted OR: 1.30; 95% CI: 1.07-1.59; P=0.009), and heart attack (adjusted OR: 1.30; 95% CI: 1.12-1.51, P<0.001). Urinary bisphenol A (URBPA, weight=0.636) was the most heavily weighted component in the total CVD model. Restricted cubic spline regression demonstrated positive correlations and nonlinear associations between URBPA and both total CVD (P for nonlinearity=0.032) and individual CVD (heart attack; P for nonlinearity=0.031). Our findings suggested that high combined levels of phenols, and parabens are associated with an increased CVD risk, with URBPA contributing the highest risk.
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http://dx.doi.org/10.1007/s11356-021-15589-5DOI Listing
August 2021

Inhibition of LOXL1-AS1 alleviates oxidative low-density lipoprotein induced angiogenesis via downregulation of miR-590-5p mediated KLF6/VEGF signaling pathway.

Cell Cycle 2021 09 31;20(17):1663-1680. Epub 2021 Jul 31.

Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou Henan, China.

Increasing evidences have confirmed that long non-coding RNA LOXL1-AS1 functions in multiple human diseases. Here, we aim to explore the function and mechanism of LOXL1-AS1 in modulating oxidized low-density lipoprotein (ox-LDL)-induced angiogenesis of endothelial cells (ECs). Presently, we found that LOXL1-AS1 and KLF6 were upregulated in ECs treated by Ox-LDL in a dose- and time-dependent manner while miR-590-5p was downregulated. Overexpression of LOXL1-AS1 aggravated Ox-LDL mediated ECs proliferation and migration, and promoted angiogenesis both and . On the contrary, enhancing miR-590-5p or inhibiting LOXL1-AS1 level led to suppressive effects on the proliferation, migration and angiogenesis of ECs. Moreover, LOXL1-AS1 upregulation promoted the expression of vascular endothelial growth factor (VEGF), MMPs (including MMP2, MMP9 and MMP14) and also activated VEGF/VEGFR2/PI3K/Akt/eNOS pathway. Mechanistically, LOXL1-AS1 works as a competitive endogenous RNA (ceRNA) by sponging miR-590-5p, which targeted at the 3'-untranslated region (3'UTR) of KLF6. Additionally, the proliferation, migration and angiogenesis of ECs were elevated following KLF6 upregulation. By detecting the expression of LOXL1-AS1 and miR-590-5p in the serum of healthy donors and atherosclerosis patients, it was found that LOXL1-AS1 was upregulated in atherosclerosis patients (compared with healthy donors) and had a negative relationship with miR-590-5p. Taken together, LOXL1-AS1 promoted Ox-LDL induced angiogenesis via regulating miR-590-5p-modulated KLF6/VEGF signaling pathway. The LOXL1-AS1-miR-590-5p axis exerts a novel role in the progression of atherosclerosis.
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http://dx.doi.org/10.1080/15384101.2021.1958484DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489901PMC
September 2021

Association of urinary phthalate metabolites with cardiovascular disease among the general adult population.

Environ Res 2021 11 27;202:111764. Epub 2021 Jul 27.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China; Department of Cardiology, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, 215002, China. Electronic address:

Objective: This study aims to explore the relationship between urinary phthalate metabolites and total and specific cardiovascular disease (CVD) among the general adult population.

Methods: This cross-sectional study analyzed 11 urinary phthalates in the general population from the 2005-2016 National Health and Nutrition Examination Survey (NHANES) (n = 10,427). Multivariate logistic regression and weighted quantile sum (WQS) regression were applied to examine the relationship between phthalate metabolites and mixtures and the prevalence rates of total and specific CVD.

Results: Compared to the lowest quartile, mono-isobutyl phthalate (MiBP) (OR 1.37; 95% CI 1.03-1.83, P for trend = 0.032) and mono-benzyl phthalate (MBzP) (OR 1.44; 95% CI 1.10-1.88, P for trend = 0.013) in the highest quartile were independently associated with increased total CVD. The WQS index of phthalate mixtures was independently correlated with total CVD (adjusted OR 1.17; 95% CI 1.01-1.36, P = 0.039), and MBzP (weight = 0.392) was the most heavily weighted component. In addition, restricted cubic spline regression demonstrated that the MBzP level had a positive correlation and linear association with total CVD (P for nonlinearity = 0.182).

Conclusions: Our findings suggest that high phthalate mixture levels are associated with an increased prevalence of CVD, with the greatest influence coming from MBzP.
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http://dx.doi.org/10.1016/j.envres.2021.111764DOI Listing
November 2021

The Role of Mitochondria in Liver Ischemia-Reperfusion Injury: From Aspects of Mitochondrial Oxidative Stress, Mitochondrial Fission, Mitochondrial Membrane Permeable Transport Pore Formation, Mitophagy, and Mitochondria-Related Protective Measures.

Oxid Med Cell Longev 2021 5;2021:6670579. Epub 2021 Jul 5.

Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, China.

Ischemia-reperfusion injury (IRI) has indeed been shown as a main complication of hepatectomy, liver transplantation, trauma, and hypovolemic shock. A large number of studies have confirmed that microvascular and parenchymal damage is mainly caused by reactive oxygen species (ROS), which is considered to be a major risk factor for IRI. Under normal conditions, ROS as a kind of by-product of cellular metabolism can be controlled at normal levels. However, when IRI occurs, mitochondrial oxidative phosphorylation is inhibited. In addition, oxidative respiratory chain damage leads to massive consumption of adenosine triphosphate (ATP) and large amounts of ROS. Additionally, mitochondrial dysfunction is involved in various organs and tissues in IRI. On the one hand, excessive free radicals induce mitochondrial damage, for instance, mitochondrial structure, number, function, and energy metabolism. On the other hand, the disorder of mitochondrial fusion and fission results in further reduction of the number of mitochondria so that it is not enough to clear excessive ROS, and mitochondrial structure changes to form mitochondrial membrane permeable transport pores (mPTPs), which leads to cell necrosis and apoptosis, organ failure, and metabolic dysfunction, increasing morbidity and mortality. According to the formation mechanism of IRI, various substances have been discovered or synthesized for specific targets and cell signaling pathways to inhibit or slow the damage of liver IRI to the body. Here, based on the development of this field, this review describes the role of mitochondria in liver IRI, from aspects of mitochondrial oxidative stress, mitochondrial fusion and fission, mPTP formation, and corresponding protective measures. Therefore, it may provide references for future clinical treatment and research.
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http://dx.doi.org/10.1155/2021/6670579DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275408PMC
December 2021
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