Publications by authors named "Fanqi Kong"

25 Publications

  • Page 1 of 1

Ulinastatin Ameliorates IL-1-Induced Cell Dysfunction in Human Nucleus Pulposus Cells via Nrf2/NF-B Pathway.

Oxid Med Cell Longev 2021 21;2021:5558687. Epub 2021 Apr 21.

Department of Orthopedic Surgery, Changzheng Hospital, Navy Medical University (Second Military Medical University), No. 415 Fengyang Road, Shanghai 200003, China.

Low back pain (LBP) has been a wide public health concern worldwide. Among the pathogenic factors, intervertebral disc degeneration (IDD) has been one of the primary contributors to LBP. IDD correlates closely with inflammatory response and oxidative stress, involving a variety of inflammation-related cytokines, such as interleukin 1 beta (IL-1), which could result in local inflammatory environment. Ulinastatin (UTI) is a kind of acidic protein extracted from human urine, which inhibits the release of tumor necrosis factor alpha (TNF-) and other inflammatory factors to protect organs from inflammatory damage. However, whether this protective effect of UTI on human nucleus pulposus (NP) exists, and how UTI affects the biological behaviors of human NP cells during IDD remain elusive. In this current study, we revealed that UTI could improve the viability of NP cells and promote the proliferation of NP cells. Additionally, UTI could protect human NP cells via ameliorating IL-1-induced apoptosis, inflammatory response, oxidative stress, and extracellular matrix (ECM) degradation. Molecular mechanism analysis suggested that the protective effect from UTI on IL-1-treated NP cells were through activating nuclear factor- (erythroid-derived 2-) like 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway and the suppression of NF-B signaling pathway. Therefore, UTI may be a promising therapeutic medicine to ameliorate IDD.
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http://dx.doi.org/10.1155/2021/5558687DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084647PMC
May 2021

Gamabufotalin Inhibits Osteoclastgenesis and Counteracts Estrogen-Deficient Bone Loss in Mice by Suppressing RANKL-Induced NF-κB and ERK/MAPK Pathways.

Front Pharmacol 2021 23;12:629968. Epub 2021 Apr 23.

Department of Spine Surgery, Changzheng Hospital, Naval Medical University, Shanghai, China.

Osteolytic bone disease is a condition of imbalanced bone homeostasis, characterized mainly by excessive bone-resorptive activity, which could predispose these populations, such as the old and postmenopausal women, to developing high risk of skeletal fragility and fracture. The nature of bone homeostasis is the coordination between the osteoblasts (OBs) and osteoclasts (OCs). Abnormal activation of osteoclasts (OCs) could compromise the bone homeostasis, constantly followed by a clutch of osteolytic diseases, including postmenopausal osteoporosis, osteoarthritis, and rheumatoid arthritis. Thus, it is imperatively urgent to explore effective medical interventions for patients. The traditional Chinese medicine (TCM) gamabufotalin (CS-6) is a newly identified natural product from Chansu and has been utilized for oncologic therapies owing to its good clinical efficacy with less adverse events. Previous study suggested that CS-6 could be a novel anti-osteoporotic agent. Nevertheless, whether CS-6 suppresses RANK-(receptor activator of nuclear factor-κ B ligand)/TRAF6 (TNF receptor-associated factor 6)-mediated downstream signaling activation in OCs, as well as the effects of CS-6 on OC differentiation , remains elusive. Therefore, in this present study, we aimed to explore the biological effects of CS-6 on osteoclastogenesis and RANKL-induced activation of related signaling pathways, and further to examine the potential therapeutic application in estrogen-deficient bone loss in the mice model. The results of experiment showed that CS-6 can inhibit RANKL-induced OC formation and the ability of bone resorption in a dose-dependent manner at both the early and late stages of osteoclastogenesis. The gene expression of OC-related key genes such as tartrate-resistant acid phosphatase (TRAP), CTSK, DC-STAMP, MMP9, and β3 integrin was evidently reduced. In addition, CS-6 could mitigate the systemic estrogen-dependent bone loss and pro-inframammary cytokines in mice . The molecular mechanism analysis suggested that CS-6 can suppress RANKL/TRAF6-induced early activation of NF-κB and ERK/MAPK signaling pathways, which consequently suppressed the transcription activity of c-Fos and NFATc1. Taken together, this present study provided ample evidence that CS-6 has the promise to become a therapeutic candidate in treating osteolytic conditions mediated by elevated OC formation and bone resorption.
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http://dx.doi.org/10.3389/fphar.2021.629968DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8104077PMC
April 2021

PD-L1 Improves Motor Function and Alleviates Neuropathic Pain in Male Mice After Spinal Cord Injury by Inhibiting MAPK Pathway.

Front Immunol 2021 15;12:670646. Epub 2021 Apr 15.

Department of Orthopedic Surgery, Spine Center, Changzheng Hospital, Naval Medical University, Shanghai, China.

Background: Traumatic spinal cord injury (SCI) causes severe motor dysfunction and persistent central neuropathic pain (Nep), which has not yet been effectively cured. Programmed cell death ligand-1 (PD-L1) is typically produced by cancer cells and contributes to the immune-suppressive in tumor microenvironment. However, the role of PD-L1 in regulating inflammatory response and Nep after SCI remains unclear. A growing amount of researches have begun to investigate the effect of PD-L1 on macrophages and microglia in recent years. Considering the pivotal role of macrophages/microglia in the inflammatory response after SCI, we proposed the hypothesis that PD-L1 improved the recovery of locomotor and sensory functions after SCI through regulating macrophages and microglia.

Methods: The mice SCI model was established to determine the changes in expression patterns of PD-L1. Meanwhile, we constructed PD-L1 knockout mice to observe differences in functional recovery and phenotypes of macrophages/microglia post-SCI.

Results: In present study, PD-L1 was significantly upregulated after SCI and highly expressed on macrophages/microglia at the injury epicenter. PD-L1 knockout (KO) mice showed worse locomotor recovery and more serious pathological pain compared with wild-type (WT) mice. Furthermore, deletion of PD-L1 significantly increased the polarization of M1-like macrophages/microglia. Mechanistic analysis revealed that PD-L1 may improve functional outcomes following SCI by inhibiting phosphorylation of p38 and ERK1/2.

Conclusions: Our observations implicate the involvement of PD-L1 in recovery of SCI and provide a new treatment strategy for the prevention and treatment of this traumatic condition.
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http://dx.doi.org/10.3389/fimmu.2021.670646DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8081847PMC
April 2021

GIT1 protects traumatically injured spinal cord by prompting microvascular endothelial cells to clear myelin debris.

Aging (Albany NY) 2021 02 17;13(5):7067-7083. Epub 2021 Feb 17.

Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

The clearance of myelin debris is a critical step in the functional recovery following spinal cord injury (SCI). As phagocytes do, microvascular endothelial cells (MECs) participate in myelin debris clearance at the injury site within one week. Our group has verified that G protein-coupled receptor kinase 2 interacting protein-1 (GIT1) is essential in autophagy and angiogenesis, both of which are tightly related to the uptake and degradation of myelin debris by MECs. Here, we analyzed the performance and mechanism of GIT1 in myelin debris clearance after SCI. The SCI contusion model was established and MECs were treated with myelin debris. Better recovery from traumatic SCI was observed in the GIT1 WT mice than in the GIT1 KO mice. More importantly, we found that GIT1 prompted MECs to clear myelin debris and further enhanced MECs angiogenesis and . Mechanistically, GIT1-mediated autophagy contributed to the clearance of myelin debris by MECs. In this study, we demonstrated that GIT1 may prompt MECs to clear myelin debris via autophagy and further stimulate MECs angiogenesis via upregulating VEGF. Our results indicate that GITI may serve as a promising target for accelerating myelin debris clearance and improving SCI recovery.
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http://dx.doi.org/10.18632/aging.202560DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993661PMC
February 2021

Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy.

Oxid Med Cell Longev 2020 23;2020:3549704. Epub 2020 Jul 23.

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

Ischemia-reperfusion injury is the second most common injury of the spinal cord and has the risk of neurological dysfunction and paralysis, which can seriously affect patient quality of life. Salidroside (Sal) is an active ingredient extracted from Herba Cistanche with a variety of biological attributes such as antioxidant, antiapoptotic, and neuroprotective activities. Moreover, Sal has shown a protective effect in ischemia-reperfusion injury of the liver, heart, and brain, but its effect in ischemia-reperfusion injury of the spinal cord has not been elucidated. Here, we demonstrated for the first time that Sal pretreatment can significantly improve functional recovery in mice after spinal cord ischemia-reperfusion injury and significantly inhibit the apoptosis of neurons both and . Neurons have a high metabolic rate, and consequently, mitochondria, as the main energy-supplying suborganelles, become the main injury site of spinal cord ischemia-reperfusion injury. Mitochondrial pathway-dependent neuronal apoptosis is increasingly confirmed by researchers; therefore, Sal's effect on mitochondria naturally attracted our attention. By means of a range of experiments both o and , we found that Sal can reduce reactive oxygen species production through antioxidant stress to reduce mitochondrial permeability and mitochondrial damage, and it can also enhance the PINK1-Parkin signaling pathway and promote mitophagy to eliminate damaged mitochondria. In conclusion, our results show that Sal is beneficial to the protection of spinal cord neurons after ischemia-reperfusion injury, mainly by reducing apoptosis associated with the mitochondrial-dependent pathway, among which Sal's antioxidant and autophagy-promoting properties play an important role.
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http://dx.doi.org/10.1155/2020/3549704DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7396093PMC
May 2021

Exosome-shuttled miR-216a-5p from hypoxic preconditioned mesenchymal stem cells repair traumatic spinal cord injury by shifting microglial M1/M2 polarization.

J Neuroinflammation 2020 Feb 4;17(1):47. Epub 2020 Feb 4.

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

Background: Spinal cord injury (SCI) can lead to severe motor and sensory dysfunction with high disability and mortality. In recent years, mesenchymal stem cell (MSC)-secreted nano-sized exosomes have shown great potential for promoting functional behavioral recovery following SCI. However, MSCs are usually exposed to normoxia in vitro, which differs greatly from the hypoxic micro-environment in vivo. Thus, the main purpose of this study was to determine whether exosomes derived from MSCs under hypoxia (HExos) exhibit greater effects on functional behavioral recovery than those under normoxia (Exos) following SCI in mice and to seek the underlying mechanism.

Methods: Electron microscope, nanoparticle tracking analysis (NTA), and western blot were applied to characterize differences between Exos and HExos group. A SCI model in vivo and a series of in vitro experiments were performed to compare the therapeutic effects between the two groups. Next, a miRNA microarray analysis was performed and a series of rescue experiments were conducted to verify the role of hypoxic exosomal miRNA in SCI. Western blot, luciferase activity, and RNA-ChIP were used to investigate the underlying mechanisms.

Results: Our results indicate that HExos promote functional behavioral recovery by shifting microglial polarization from M1 to M2 phenotype in vivo and in vitro. A miRNA array showed miR-216a-5p to be the most enriched in HExos and potentially involved in HExos-mediated microglial polarization. TLR4 was identified as the target downstream gene of miR-216a-5p and the miR-216a-5p/TLR4 axis was confirmed by a series of gain- and loss-of-function experiments. Finally, we found that TLR4/NF-κB/PI3K/AKT signaling cascades may be involved in the modulation of microglial polarization by hypoxic exosomal miR-216a-5p.

Conclusion: Hypoxia preconditioning represents a promising and effective approach to optimize the therapeutic actions of MSC-derived exosomes and a combination of MSC-derived exosomes and miRNAs may present a minimally invasive method for treating SCI.
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http://dx.doi.org/10.1186/s12974-020-1726-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7001326PMC
February 2020

Hypoxic mesenchymal stem cell-derived exosomes promote bone fracture healing by the transfer of miR-126.

Acta Biomater 2020 02 17;103:196-212. Epub 2019 Dec 17.

Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China. Electronic address:

Increasing evidence has suggested that paracrine mechanisms might be involved in the underlying mechanism of mesenchymal stem cells (MSCs) transplantation, and exosomes are an important component of this paracrine role. However, MSCs are usually exposed to normoxia (21% O) in vitro but experience large differences in oxygen concentration in the body under hypoxia. Indeed, hypoxic precondition of MSCs can enhance their paracrine effects. The main purpose of this study was to determine whether exosomes derived from MSCs under hypoxia (Hypo-Exos) exhibit greater effects on bone fracture healing than those under normoxia (Exos). Using in vivo bone fracture model and in vitro experiments including cell proliferation assay, cell migration assay and so on, we confirmed that Hypo-Exos administration promoted angiogenesis, proliferation and migration to a greater extent when compared to Exos. Furthermore, utilizing a series in vitro and in vivo gain and loss of function experiments, we confirmed a functional role for exosomal miR-126 in the process of bone fracture healing. Meanwhile, we found that knockdown of hypoxia inducible factor 1 (HIF-1α) resulted in a significant decrease of miR-126 in MSCs and exosomes, thereby abolishing the effects of Hypo-Exos. In conclusion, our results demonstrated a mechanism by which Hypo-Exos promote bone fracture healing through exosomal miR-126. Moreover, hypoxia preconditioning mediated enhanced production of exosomal miR-126 through the activation of HIF-1α. Hypoxia preconditioning represents an effective and promising method for the optimization of the therapeutic actions of MSC-derived exosomes for bone fracture healing. STATEMENT OF SIGNIFICANCE: Studies have confirmed that transplantation of exosomes exhibit similar therapeutic effects and functional properties to directly-transplanted stem cells but have less significant adverse effects. However, during in vitro culture conditions, MSCs are usually exposed to normoxia (21% O) which is very different to the oxygen concentrations found in the body under natural physiological conditions. Our results demonstrated a mechanism by which Hypo-Exos promote bone fracture healing through exosomal miR-126 and the SPRED1/Ras/Erk signaling pathway. Moreover, hypoxia preconditioning mediated enhanced production of exosomal miR-126 through the activation of HIF-1α. Hypoxia preconditioning represents an effective and promising method for the optimization of the therapeutic actions of MSC-derived exosomes for bone fracture healing.
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http://dx.doi.org/10.1016/j.actbio.2019.12.020DOI Listing
February 2020

GIT1 regulates angiogenic factor secretion in bone marrow mesenchymal stem cells via NF-κB/Notch signalling to promote angiogenesis.

Cell Prolif 2019 Nov 10;52(6):e12689. Epub 2019 Sep 10.

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

Objectives: Osteogenesis is coupled with angiogenesis during bone remodelling. G-protein-coupled receptor (GPCR) kinase 2-interacting protein-1 (GIT1) is an important protein that participates in fracture healing by regulating angiogenesis. This study investigated whether GIT1 could affect bone mesenchymal stem cells (BMSCs) to secrete angiogenic factors to enhance fracture healing by promoting angiogenesis and its possible mechanism.

Materials And Methods: The angiogenesis of mice post-fracture was detected by micro-CT and immunofluorescence. Subsequently, vascular endothelial growth factor (VEGF) level in mouse and human BMSCs (hBMSCs) under TNF-α stimulation was detected. The hBMSCs were transfected with GIT1 shRNAs to further explore the relationship between GIT1 and VEGF and angiogenesis in vitro. Furthermore, based on previous research on GIT1, possible signal pathways were investigated.

Results: GIT1 knockout mice exhibited impaired angiogenesis and delayed fracture healing. And GIT1 deficiency remarkably reduced the expression of VEGF mRNA in BMSCs, which affected the proliferation and migration of human umbilical vein endothelial cells. GIT1 knockdown inhibited the activation of Notch and NF-κB signals by decreasing nuclear transportation of NICD and P65/P50, respectively. Overexpression of the canonical NF-κB subunits P65 and P50 markedly increased NICD-dependent activation of recombination signal-binding protein-jκ reporter. Finally, GIT1 enhanced the affinity of NF-κB essential modulator (NEMO) for K63-linked ubiquitin chains via interaction with NEMO coiled-coil 2 domains.

Conclusion: These data revealed a positive role for GIT1 by modulating the Notch/NF-κB signals which promoting paracrine of BMSCs to enhance angiogenesis and fracture healing.
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http://dx.doi.org/10.1111/cpr.12689DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6869488PMC
November 2019

Neural stem cell-derived small extracellular vesicles attenuate apoptosis and neuroinflammation after traumatic spinal cord injury by activating autophagy.

Cell Death Dis 2019 04 18;10(5):340. Epub 2019 Apr 18.

Department of Orthopaedics, First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, Jiangsu, China.

Spinal cord injury (SCI) can cause severe irreversible motor dysfunction and even death. Neural stem cell (NSC) transplantation can promote functional recovery after acute SCI in experimental animals, but numerous issues, including low-transplanted cell survival rate, cell de-differentiation, and tumor formation need to be resolved before routine clinical application is feasible. Recent studies have shown that transplanted stem cells facilitate regeneration through release of paracrine factors. Small extracellular vesicles (sEVs), the smallest known membrane-bound nanovesicles, are involved in complex intercellular communication systems and are an important vehicle for paracrine delivery of therapeutic agents. However, the application of NSC-derived small extracellular vesicles (NSC-sEVs) to SCI treatment has not been reported. We demonstrate that NSC-sEVs can significantly reduce the extent of SCI, improve functional recovery, and reduce neuronal apoptosis, microglia activation, and neuroinflammation in rats. Furthermore, our study suggests that NSC-sEVs can regulate apoptosis and inflammatory processes by inducing autophagy. In brief, NSC-sEVs increased the expression of the autophagy marker proteins LC3B and beclin-1, and promoted autophagosome formation. Following NSC-sEV infusion, the SCI area was significantly reduced, and the expression levels of the proapoptotic protein Bax, the apoptosis effector cleaved caspase-3, and the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were significantly reduced, whereas the expression level of the anti-apoptotic protein Bcl-2 was upregulated. In the presence of the autophagy inhibitor 3MA, however, these inhibitory effects of NSC-sEVs on apoptosis and neuroinflammation were significantly reversed. Our results show for the first time that NSC-sEV treatment has the potential to reduce neuronal apoptosis, inhibit neuroinflammation, and promote functional recovery in SCI model rats at an early stage by promoting autophagy.
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http://dx.doi.org/10.1038/s41419-019-1571-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6472377PMC
April 2019

GIT1 is critical for formation of the CD31Emcn vessel subtype in coupling osteogenesis with angiogenesis via modulating preosteoclasts secretion of PDGF-BB.

Bone 2019 05 7;122:218-230. Epub 2019 Mar 7.

Department of Orthopedic, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd., Nanjing 210029, China. Electronic address:

G protein-coupled receptor kinase 2 interacting protein-1 (GIT1) is a scaffold protein that plays a vital role in bone modeling and remodeling during osteogenesis coupled with angiogenesis. Recent studies have shown that a specialized subset of vascular endothelium strongly positive for CD31 and Endomucin (CD31Emcn) is coupled with anabolic bone formation. Based on our previous finding that GIT1 knockout (GIT1 KO) mice have impaired angiogenesis and bone formation, we hypothesized that GIT1 affects formation of the CD31Emcn vessel subtype. In the current study, GIT1 knockout (GIT1 KO) mice displayed a significant decrease in trabecular bone mass and CD31Emcn vessel number, compared to their wild-type counterparts. In the fracture healing mouse model, GIT1 KO mice contained a lower number of CD31Emcn vessels in fracture callus at days 7 and 14. However, no significant differences in the number of preosteoclasts in bone marrow, trabecular bone and callus in GIT1 KO mice were observed, compared with wild-type mice. Notably, concentrations of serum platelet-derived growth factor-BB(PDGF-BB) secreted by preosteoclasts associated with CD31Emcn vessel formation were lower in GIT1 KO mice. In addition, PDGF-BB-associated expression of phosphorylated extracellular signal-regulated kinase- 1/2 (ERK1/2) and specificity protein 1 (SP1) was significantly decreased in preosteoclasts of GIT1 KO mice. These results collectively suggest that GIT1 is a critical participant in formation of the CD31Emcn vessel subtype, highlighting a novel biologic function of this scaffold protein in preosteoclasts.
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http://dx.doi.org/10.1016/j.bone.2019.03.006DOI Listing
May 2019

The miR-15b-5p/PDK4 axis regulates osteosarcoma proliferation through modulation of the Warburg effect.

Biochem Biophys Res Commun 2018 09 6;503(4):2749-2757. Epub 2018 Aug 6.

Department of Orthopedics, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou, Jiangsu, 213003, China. Electronic address:

Blocking aerobic glycolysis has been proposed as an attractive therapeutic strategy for impairing the proliferation of cancer cells. However, the underlying mechanisms are poorly understood. Here, we show that miR-15b-5p was downregulated in osteosarcoma (OS) and that lower expression of miR-15b-5p promoted proliferation and contributed to the Warburg effect in OS cells. Mechanistically, miR-15b-5p acted as a tumor suppressor in OS by directly targeting pyruvate dehydrogenase kinase-4 and inhibiting its expression. These results reveal a previously unknown function of miR-15b-5p in OS, which is associated with metabolic alterations that promote cancer progression. miR-15b-5p may play an essential role in the molecular therapy of patients with OS.
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http://dx.doi.org/10.1016/j.bbrc.2018.08.035DOI Listing
September 2018

Inflammatory cytokines in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation.

Panminerva Med 2018 Sep 24;60(3):86-91. Epub 2018 Apr 24.

Department of Cardiology, The Third Affiliated Hospital of Wenzhou Medical University, Ruian, China -

Background: To investigate the changes of inflammatory cytokines in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation and the effects of metoprolol on them.

Methods: A total of 92 cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation in our hospital from April 2015 to March 2017 were selected and randomly divided into the control group and the observation group, with 46 cases in each group. Three months after pacemaker implantation, the control group was treated with aspirin, the observation group was treated with metoprolol on the basis of aspirin, and the curative effects were compared between the two groups. After treatment, the heart rate, the frequency and duration of atrial fibrillation and the atrial fibrillation load were observed. P-wave dispersion (PD) and cardiac function of the two groups of patients at 6 months after treatment were compared. The changes of serum levels of tumor necrosis factor-α (TNF-α), high sensitive C-reactive protein (Hs-CRP) and interleukin-6 (IL-6) in patients were compared before treatment and at 1, 3 and 6 months after treatment. The quality of life of the two groups of patients was observed.

Results: After treatment, the effective rate of treatment in the observation group was significantly higher than that in the control group (P<0.05). After treatment, the average heart rate and atrial fibrillation load in the observation group were significantly improved compared with those in the control group, and the frequency and duration of atrial fibrillation were significantly lower than those in the control group (P<0.05). After treatment, the maximum P-wave duration (Pmax), the minimum P-wave duration (Pmin) and PD in the observation group were significantly lower than those in the control group (P<0.05). The left ventricular ejection fraction (LVEF) in the observation group was significantly higher than that in the control group, and the left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and E/A in the observation group were significantly lower than those in the control group (P<0.05). After treatment, the levels of TNF-α, Hs-CRP and IL-6 in the two groups of patients were decreased significantly, and those in the observation group were significantly lower than those in the control group (P<0.05). The quality of life score in the observation group was significantly higher than that in the control group (P<0.05).

Conclusions: Metoprolol can effectively reduce the incidence of atrial fibrillation, atrial fibrillation loadand inflammatory cytokine levels in cardiac pacing patients with atrial fibrillation and asymptomatic atrial fibrillation, and improve cardiac function of the patients and their quality of life. It has an important clinical significance.
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http://dx.doi.org/10.23736/S0031-0808.18.03452-3DOI Listing
September 2018

Testing the Role of Recollision in N_{2}^{+} Air Lasing.

Phys Rev Lett 2018 Mar;120(13):133208

University of Ottawa, Ottawa K1N 6N5, Ontario, Canada.

It has been known for many years that during filamentation of femtosecond light pulses in air, gain is observed on the B to X transition in N_{2}^{+}. While the gain mechanism remains unclear, it has been proposed that recollision, a process that is fundamental to much of strong field science, is critical for establishing gain. We probe this hypothesis by directly comparing the influence of the ellipticity of the pump light on gain in air filaments. Then, we decouple filamentation from gain by measuring the gain in a thin gas jet that we also use for high harmonic generation. The latter allows us to compare the dependence of the gain on the ellipticity of the pump with the dependence of the high harmonic signal on the ellipticity of the fundamental. We find that gain and harmonic generation have very different behavior in both filaments and in the jet. In fact, in a jet we even measure gain with circular polarization. Thus, we establish that recollision does not play a significant role in creating the inversion.
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http://dx.doi.org/10.1103/PhysRevLett.120.133208DOI Listing
March 2018

NACHT, LRR and PYD domains-containing protein 3 inflammasome is activated and inhibited by berberine via toll-like receptor 4/myeloid differentiation primary response gene 88/nuclear factor-κB pathway, in phorbol 12-myristate 13-acetate-induced macrophages.

Mol Med Rep 2018 Feb 29;17(2):2673-2680. Epub 2017 Nov 29.

Department of Cardiology, The Key Laboratory of Cardiovascular Disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP-3) inflammasome has recently emerged as a pivotal regulator of chronic inflammation. The present study investigated the expression of NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages, and aimed to identify the effects of berberine on the inflammasome. Human monocytic THP-1 cells were pretreated with berberine for 1 h and then induced with PMA for 48 h. Total RNA and protein were collected for reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Supernatants were collected to determine IL-1β levels by using ELISA. The present study demonstrated that NLRP3 inflammasome and IL-1β were activated in PMA-induced macrophages in a time-dependent manner, whereas berberine significantly inhibited their expression in a dose-dependent manner in PMA-induced macrophages. Furthermore, berberine also suppressed the toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (Myd88)/nuclear factor (NF)-κB signaling pathway which was activated during the conversion of THP-1 cells to macrophages by PMA. In conclusion, berberine reduced NLRP3 inflammasone expression by suppressing the activation of the TLR4/Myd88/NF-κB signaling pathway in PMA-induced macrophages. This inhibitory effect may imply an important role of berberine on chronic inflammation and atherogenic progression in coronary artery disease.
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http://dx.doi.org/10.3892/mmr.2017.8189DOI Listing
February 2018

Change in skin properties over the first 10 years of life: a cross-sectional study.

Arch Dermatol Res 2017 Oct 19;309(8):653-658. Epub 2017 Jul 19.

Johnson & Johnson AP Skin Testing Center, Shanghai, China.

This study investigated skin characteristics in healthy Chinese children aged from 1 to 10 years and compared these findings with similar measures from the child's mothers. Children aged 1, 2, 3, 4, 5, and 10 years (n = 29-30 per age group) and the child's mothers were enrolled in a single-visit cross-sectional study. Clinical parameters evaluated on the face, ventral forearm, and calf were softness, smoothness, erythema, edema, rash, dryness, and scaling. Instrumental evaluations included transepidermal water loss, moisture content, and water-holding capacity. The clinical evaluations indicated a general decrease in softness, smoothness, and overall skin condition with increased child age. In general, the child's clinical scores were better than in adults. Children had a more permeable skin barrier that matured to adult values by approximately 5 years of age. Mothers had greater skin moisture than children. Clinical and instrumental measures were consistent with skin being softer and smoother and in better overall condition in younger children. As the skin matured with age, higher scores were observed. Instrumental measures demonstrated a more permeable skin barrier in younger children compared with older children and with adults.
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http://dx.doi.org/10.1007/s00403-017-1764-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5606948PMC
October 2017

Controlling the orbital angular momentum of high harmonic vortices.

Nat Commun 2017 04 5;8:14970. Epub 2017 Apr 5.

Department of Physics, University of Ottawa, 25 Templeton St, Ottawa, Ontario, Canada K1N 6N5.

Optical vortices, which carry orbital angular momentum (OAM), can be flexibly produced and measured with infrared and visible light. Their application is an important research topic for super-resolution imaging, optical communications and quantum optics. However, only a few methods can produce OAM beams in the extreme ultraviolet (XUV) or X-ray, and controlling the OAM on these beams remains challenging. Here we apply wave mixing to a tabletop high-harmonic source, as proposed in our previous work, and control the topological charge (OAM value) of XUV beams. Our technique enables us to produce first-order OAM beams with the smallest possible central intensity null at XUV wavelengths. This work opens a route for carrier-injected laser machining and lithography, which may reach nanometre or even angstrom resolution. Such a light source is also ideal for space communications, both in the classical and quantum regimes.
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http://dx.doi.org/10.1038/ncomms14970DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5382317PMC
April 2017

Perturbative High Harmonic Wave Front Control.

Phys Rev Lett 2017 Jan 20;118(3):033905. Epub 2017 Jan 20.

Department of Physics, University of Ottawa, 25 Templeton St., Ottawa, ON, Canada K1N 6N5.

We pattern the wave front of a high harmonic beam by intersecting the intense driving laser pulse that generates the high harmonic with a weak control pulse. To illustrate the potential of wave-front control, we imprint a Fresnel zone plate pattern on a harmonic beam, causing the harmonics to focus and defocus. The quality of the focus that we achieve is measured using the spectral wave-front optical reconstruction by diffraction method. We will show that it is possible to enhance the peak intensity by orders of magnitude without a physical optical element in the path of the extreme ultraviolet (XUV) beam. Through perturbative wave-front control, XUV beams can be created with a flexibility approaching what technology allows for visible and infrared light.
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http://dx.doi.org/10.1103/PhysRevLett.118.033905DOI Listing
January 2017

Curcumin Represses NLRP3 Inflammasome Activation via TLR4/MyD88/NF-κB and P2X7R Signaling in PMA-Induced Macrophages.

Front Pharmacol 2016 10;7:369. Epub 2016 Oct 10.

The Key Lab of Cardiovascular Disease of Wenzhou, Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University Wenzhou, China.

In the NOD-like receptor (NLR) family, the pyrin domain containing 3 (NLRP3) inflammasome is closely related to the progression of atherosclerosis. This study aimed to assess the effects of curcumin on NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages and explore its underlying mechanism. Human monocytic THP-1 cells were pretreated with curcumin for 1 h and subsequently induced with PMA for 48 h. Total protein was collected for Western blot analysis. Cytokine interleukin (IL)-1β release and nuclear factor kappa B (NF-κB) p65 translocation were detected by ELISA assay and cellular NF-κB translocation kit, respectively. Curcumin significantly reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1β secretion in PMA-induced macrophages. Moreover, Bay (a NF-κB inhibitor) treatment considerably suppressed the expression of NLRP3 inflammasome in PMA-induced THP-1 cells. Curcumin also markedly inhibited the upregulation of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), phosphorylation level of IκB-α, and activation of NF-κB in PMA-induced macrophages. In addition, purinergic 2X7 receptor (P2X7R) siRNA was administered, and it significantly decreased NLRP3 inflammasome expression in PMA-induced macrophages. Furthermore, curcumin reversed PMA-stimulated P2X7R activation, which further reduced the expression of NLRP3 and cleavage of caspase-1 and IL-1β secretion. Silencing of P2X7R using siRNA also suppressed the activation of NF-κB pathway in PMA-induced macrophages, but P2X7R-silenced cells did not significantly decrease the expression of TLR4 and MyD88. Curcumin inhibited NLRP3 inflammasome through suppressing TLR4/MyD88/NF-κB and P2X7R pathways in PMA-induced macrophages.
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http://dx.doi.org/10.3389/fphar.2016.00369DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5056188PMC
October 2016

MicroRNA-21 protects against cardiac hypoxia/reoxygenation injury by inhibiting excessive autophagy in H9c2 cells via the Akt/mTOR pathway.

J Cell Mol Med 2017 03 29;21(3):467-474. Epub 2016 Sep 29.

Department of Cardiology, The Key Lab of Cardiovascular Disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

MicroRNAs and autophagy play critical roles in cardiac hypoxia/reoxygenation (H/R)-induced injury. Here, we investigated the function of miR-21 in regulating autophagy and identified the potential molecular mechanisms involved. To determine the role of miR-21 in regulating autophagy, H9c2 cells were divided into the following six groups: control group, H/R group, (miR-21+ H/R) group, (miR-21-negative control + H/R) group, (BEZ235+ H/R) group and (miR-21+ BEZ235+ H/R) group. The cells underwent hypoxia for 1 hr and reoxygenation for 3 hrs. Cell count kit-8 was used to evaluate cell function and apoptosis was analysed by Western blotting. Western blotting and transmission electron microscopy were used to investigate autophagy. We found that miR-21 expression was down-regulated, and autophagy was remarkably increased in H9c2 cells during H/R injury. Overexpression of miR-21 with a miR-21 precursor significantly inhibited autophagic activity and decreased apoptosis, accompanied by the activation of the AKT/mTOR pathway. In addition, treatment with BEZ235, a novel dual Akt/mTOR inhibitor, resulted in a significant increase in autophagy and apoptosis. However, we found that miR-21-mediated inhibition of apoptosis and autophagy was partly independent of Akt/mTOR activation, as demonstrated in cells treated with both miR-21 and BEZ235. We showed that miR-21 could inhibit H/R-induced autophagy and apoptosis, which may be at least partially mediated by the Akt/mTOR signalling pathway.
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http://dx.doi.org/10.1111/jcmm.12990DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5323864PMC
March 2017

Combined Treatment with Amlodipine and Atorvastatin Calcium Reduces Circulating Levels of Intercellular Adhesion Molecule-1 and Tumor Necrosis Factor-α in Hypertensive Patients with Prediabetes.

Front Aging Neurosci 2016 25;8:206. Epub 2016 Aug 25.

The Key Laboratory of Cardiovascular Disease of Wenzhou, Department of Cardiology, The First Affiliated Hospital of WenZhou Medical University WenZhou, ZheJiang, China.

Objective: To assess the effect of amlodipine and atorvastatin on intercellular adhesion molecule (ICAM)-1 and tumor necrosis factor (TNF)-α expression, as endothelial function and inflammation indicators, respectively, in hypertensive patients with and without prediabetes.

Methods: Forty-five consecutive patients with hypertension, diagnosed according to JNC7, were divided into two groups based on the presence (HD group, n = 23) or absence (H group, n = 22) of prediabetes, diagnosed according to 2010 ADA criteria, including impaired glucose tolerance (IGT) and fasting glucose tests. All patients simultaneously underwent 12-week treatment with daily single-pill amlodipine besylate/atorvastatin calcium combination (5/10 mg; Hisun-Pfizer Pharmaceuticals Co. Ltd). Serum isolated before and after treatment from overnight fasting blood samples was analyzed by ELISA.

Results: In the HD and H groups after vs. before 12-week amlodipine/atorvastatin treatment, there were significantly (all P < 0.01) lower levels of ICAM-1 (3.06 ± 0.34 vs. 4.07 ± 0.70 pg/ml; 3.26 ± 0.32 vs. 3.81 ± 0.60 pg/ml, respectively) and TNF-α (78.71 ± 9.19 vs. 110.94 ± 10.71 pg/ml; 80.95 ± 9.33 vs. 101.79 ± 11.72 pg/ml, respectively), with more pronounced reductions in HD vs. H group (ICAM-1Δ: 1.01 ± 0.80 vs. 0.55 ± 0.64 pg/ml, respectively, P = 0.037; TNF-αΔ: 32.23 ± 14.33 vs. 20.84 ± 14.89 pg/ml, respectively, P = 0.011), independent of the blood pressure (BP) and cholesterol level reduction.

Conclusions: Amlodipine/atorvastatin improved endothelial function and inflammation, as reflected by lower circulating levels of ICAM-1 and TNF-α, more prominently in hypertensives with than without prediabetes. Starting statin treatment before overt diabetes in hypertensives might thus improve cardiovascular outcomes.
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http://dx.doi.org/10.3389/fnagi.2016.00206DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4996984PMC
September 2016

Atorvastatin suppresses NLRP3 inflammasome activation via TLR4/MyD88/NF-κB signaling in PMA-stimulated THP-1 monocytes.

Biomed Pharmacother 2016 Aug 9;82:167-72. Epub 2016 May 9.

Department of Cardiology, The Key Lab of Cardiovascular disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University, 2 Fuxue Road, Wenzhou, Zhejiang 325000, PR China. Electronic address:

Aims: Increasing evidence shows that NLRP3 inflammasome is closely associated with the progression of atherosclerosis. The purpose of the present study was to evaluate the effects of atorvastatin on NLRP3 inflammasome in PMA-stimulated THP-1 cells and explore its underlying mechanism.

Methods: Human monocytic THP-1 cells were pretreated with atorvastatin for 1h and then induced by PMA for 48h. Total protein was collected for real-time PCR and Western blot analysis. Cytokine IL-1β release was detected by ELISA assay. And the NF-κB p65 translocation was detected by cellular NF-κB translocation kit.

Results: It was shown that atorvastatin significantly reduced the expression of NLRP3, the cleavage of caspase-1 and IL-1β in PMA-induced THP-1 cells. Moreover, Bay (a NF-κB inhibitor) treatment greatly suppressed the expression of NLRP3, the cleavage of caspase-1 and IL-1β in PMA-induced THP-1 cells, suggesting that the activation of NF-κB pathway takes part in regulating the expression of NLRP3 inflammasome. In addition, atorvastatin markedly inhibited the up-regulation of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and the activation of nuclear factor kappa b (NF-κB) in PMA-stimulated THP-1 cells.

Conclusions: Atorvastatin exerts an anti-inflammatory effect by inhibiting NLRP3 inflammasome through suppressing TLR4/MyD88/NF-κB pathway in PMA-induced THP-1 monocytes.
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http://dx.doi.org/10.1016/j.biopha.2016.04.043DOI Listing
August 2016

FABP4-mediated homocysteine-induced cholesterol accumulation in THP-1 monocyte-derived macrophages and the potential epigenetic mechanism.

Mol Med Rep 2016 Jul 19;14(1):969-76. Epub 2016 May 19.

Department of Cardiothoracic Surgery, West China Hospital of Sichuan University, Chengdu, Sichuan 610000, P.R. China.

Hyperhomocysteinemia (HHcy) is an independent risk factor for the development of atherosclerosis (AS), according to overwhelming number of clinical and epidemiological studies. However, the underlying pathogenic molecular mechanisms by which HHcy promotes AS remain to be fully elucidated. Fatty acid binding protein 4 (FABP4) has been shown to be important in macrophage cholesterol trafficking. The objective of the present study was to determine whether homocysteine (Hcy) accelerates AS through regulating FABP4, and then mediates cholesterol accumulation in macrophages. Hcy concentrations of 0, 50, 100, 200 and 500 µM, and 100 µM Hcy+30 µM vitamin B12 (VB12)+30 µM folic acid (FA) were respectively added to cultured THP‑1 monocyte‑derived macrophages for 24 h. The levels of FABP4, which acts as a key factor connecting cellular lipid accumulation to inflammation, were determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analyses in the macrophages. The present study used a nested touchdown methylation‑specific PCR assay to detect the DNA methylation status of the FABP4 promoter region. In addition, the FABP4 gene fragment was inserted into the cloning vector, pcDNA3.1‑EGFP, to construct the recombinant plasmid, pcDNA3.1‑EGFP/FABP4, which was identified using restriction endonuclease digestion analysis and DNA sequencing. The pcDNA3.1‑EGFP/FABP4 expression plasmid was transfected into THP‑1 monocyte‑derived macrophages, mediated by liposome reagent, following which the expression levels of FABP4 were detected using RT‑qPCR and western blot analyses. The present study also determined the intracellular accumulation of total cholesterol in the macrophages. The results indicated that Hcy decreased the levels of FABP4 promoter methylation, but increased the mRNA and protein expression levels of FABP4 in the macrophages, compared with the control group (0 µM Hcy). However, no dose‑dependent changes were observed with increasing concentrations of Hcy. The recombinant fluorescent eukaryotic expression vector, pcDNA3.1‑EGFP/FABP4, was successfully constructed and effectively expressed in the THP‑1 macrophages. The results also showed that FABP4 accelerated the accumulation of cholesterol in the macrophages. Taken together, the results of the present study suggested that FABP4 DNA hypomethylation induced by Hcy may be involved in the overexpression of FABP4, thereby inducing cholesterol accumulation in macrophages.
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http://dx.doi.org/10.3892/mmr.2016.5315DOI Listing
July 2016

Ratio of S-adenosylmethionine to S-adenosylhomocysteine as a sensitive indicator of atherosclerosis.

Mol Med Rep 2016 Jul 9;14(1):289-300. Epub 2016 May 9.

Department of Public Health, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, P.R. China.

The present study aimed to confirm whether the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) is a sensitive indicator, and whether it can be used as a biomarker for the clinical diagnosis of atherosclerosis. Apolipoprotein E (ApoE)-/- mice were randomly divided into four groups and fed with a high methionine diet for 15 weeks. Serum levels of homocysteine (Hcy) were measured using an automatic biochemistry analyzer. The concentrations of SAM and SAH were determined using high‑performance liquid chromatography. The methylation levels of B1 repetitive elements, adipocyte fatty acid binding protein (FABP4), monocyte chemoattractant protein-1 (MCP-1) and extracellular superoxide dismutase (EC‑SOD) were analyzed using nested touchdown-methylation-specific-polymerase chain reaction analysis. After 15 weeks, compared with the normal control group, serum concentrations of Hcy were significantly increased by 1.15‑, 2.54‑ and 1.17‑fold (P<0.05) in the ApoE‑/‑ control group, Meth group and Meth‑F group, respectively. The sizes of the atherosclerotic lesions were increased in the ApoE‑/‑ control group, Meth group and Meth‑F group, by up to 1.44‑, 2.40‑ and 1.45‑fold, respectively, compared with the normal control group (P<0.05). The concentrations of SAM were significantly increased by 3.02‑, 3.42‑ and 2.46‑fold in the ApoE‑/‑ control group, Meth group and Meth‑F group, respectively (P<0.05). The ratios of SAM/SAH were increased by 1.67‑ and 2.75‑fold in the in ApoE‑/‑ control group and Meth group, respectively, compared with the normal control group. The methylation levels of B1 repetitive elements, FABP4, MCP‑1 and EC‑SOD were decreased and exhibited hypomethylation. The methylation statuses of these genes were correlated with the ratio of the serum levels of SAM and SAH. These findings suggested that the SAM/SAH ratio is a biomarker and may provide a sensitive indicator for the clinical diagnosis of atherosclerosis.
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http://dx.doi.org/10.3892/mmr.2016.5230DOI Listing
July 2016

Serum Markers of Endothelial Dysfunction and Inflammation Increase in Hypertension with Prediabetes Mellitus.

Genet Test Mol Biomarkers 2016 Jun 11;20(6):322-7. Epub 2016 May 11.

Department of Cardiology, The Key Lab of Cardiovascular Disease of Wenzhou, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou, P.R. China .

Aims: The aim of this study was to examine endothelial dysfunction and inflammation in hypertension and prediabetes by studying adhesion molecules and inflammatory factors.

Methods And Results: This study included 133 outpatients. Participants were categorized into three groups based on the presence or absence of hypertension and prediabetes: control subjects without prediabetes and hypertension (N group, n = 39); patients with hypertension only (H group, n = 34); and patients with hypertension and prediabetes (HD group, n = 60). Hypertension was diagnosed according to JNC7 criteria. Prediabetes was defined according to 2010 American Diabetes Association criteria. Plasma was isolated from overnight fasting blood samples for enzyme-linked immunosorbent assay (ELISA) analysis of concentrations of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), P-selectin, and interleukin-6 (IL-6) as indicators of endothelial function and inflammation. We found that the H and HD groups showed significantly higher levels of all four biomarkers compared with the N group (all p < 0.01). The HD group also showed significantly higher levels of ICAM-1 (p = 0.042) and TNF-α (p < 0.01) compared with the H group; no significant differences in P-selectin (p = 0.59) and IL-6 (p = 0.70) levels were observed among these groups.

Conclusions: Prediabetes and hypertension induce endothelial dysfunction and inflammation by elevating levels of soluble adhesion molecules and inflammatory cytokines. The comorbidity of these diseases may exacerbate inflammation and endothelial dysfunction by enhancing the expression of ICAM-1 and TNF-α.
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http://dx.doi.org/10.1089/gtmb.2015.0255DOI Listing
June 2016

Transverse load sensing based on a dual-frequency optoelectronic oscillator.

Opt Lett 2013 Jul;38(14):2611-3

Microwave Photonics Research Laboratory, School of Electrical Engineering and Computer Science, University of Ottawa, Ontario, Canada.

We propose and experimentally demonstrate a fiber-optic sensor implemented based on a dual-frequency optoelectronic oscillator (OEO) for transverse load sensing. In the OEO loop, a phase-shifted fiber Bragg grating (PS-FBG) is employed to which a transverse load is applied to introduce a birefringence to create two orthogonally polarized notches, which leads to the generation of two oscillating frequencies. The beat frequency between the two oscillating frequencies is a function of the load force applied to the PS-FBG. The proposed sensor is experimentally demonstrated. The sensitivity and the minimal detectable load are measured to be as high as ~9.73 GHz/(N/mm) and 2.06×10(-4) N/mm, respectively. The high-frequency purity and stability of the generated microwave signal by the OEO permit extremely reliable and high-accuracy measurement. The frequency interrogation allows the system to operate at an ultra-high speed. In addition, the sensing signal is insensitive to the variations of both the environmental temperature and the optical carrier wavelength.
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http://dx.doi.org/10.1364/OL.38.002611DOI Listing
July 2013