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1.
Artigo em Inglês | MEDLINE | ID: mdl-32011248

RESUMO

This paper describes derivation of an equivalent circuit for nonlinear responses in film bulk acoustic resonators from the first-order perturbation analysis using the piezoelectric constitutive equations with the h-form. For simplicity, electrodes and piezoelectric layer are regarded as a mass and spring in the derivation. Then it is demonstrated that second- and third-order harmonic responses can be simulated well by the circuit. In addition, nonlinearity in the Si substrate is also taken into account, and its impact is discussed. It is also discussed how the frequency dependences vary with the nonlinearity mechanisms as a finding from the derived equivalent circuit.

2.
J Clin Sleep Med ; 2020 Jan 31.
Artigo em Inglês | MEDLINE | ID: mdl-32003732

RESUMO

BACKGROUND: Obstructive sleep apnea (OSA) is thought to be associated with dyslipidemia. However, differences concerning dyslipidemia during rapid eye movement (REM) and non-REM (NREM) sleep have yet to be determined. OBJECTIVES: This study was designed to explore the association between lipid profiles and OSA during REM or NREM sleep. METHODS: This is a clinical cohort. A total of 2,619 participants with at least 30 min of REM sleep were included. Sleep variables and fasting lipid profiles [total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo)A-I, apoB, apoE, and lipoprotein(a) (Lp(a))] were obtained from each subject. Apnea-hypopnea indices (AHIs) in REM and NREM sleep (AHIREM and AHINREM, respectively) were recorded. Linear regression analysis was used to assess the associations of AHIREM and AHINREM with lipid profiles. RESULTS: When stratified by the AHIREM severity of OSA, all demographics, clinical variables, and sleep parameters differed between the groups except for apoA-I. In fully adjusted multivariate linear regression models, AHIREM was independently associated with increasing levels of TG, HDL-C, and apoE (p = 0.04, p = 0.01 and p = 0.01, respectively). AHINREM was independently associated with increasing levels of TC, TG, LDL and apoB, and lower level of HDL-C (all p < 0.05). In sensitivity analyses by only exploring associations in patients who had an AHINREM < 5 or AHIREM < 5 times per hour in separate regression models, AHIREM was not associated with all lipid profile in almost all adjusted models (all p > 0.05), while AHINREM was associated with elevated TC, LDL-C, and apoB (p = 0.03, p = 0.01 and p = 0.01, respectively). CONCLUSION: AHINREM was independently associated with the greatest alterations in serum lipids, including TC, LDL-C, and apoB.

3.
Cytokine ; 128: 155019, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32018068

RESUMO

BACKGROUND: Previous studies showed that GTS-21, a selective alpha 7 nAchR agonist, can trigger anti-inflammatory effects and improve the survival of septic animals. However, whether GTS-21 affects autophagy responses remains unclear. Here, we tested the hypothesis that GTS-21 ameliorates sepsis-induced hepatic injury by modulating autophagy in mice. METHOD: C57BL/6 male mice were randomly separated and categorized into four groups: the sham group, and CLP group subjected to caecal ligation and puncture (CLP, a model of polymicrobial sepsis). The CLP + GTS-21 group was administered GTS-21 immediately after CLP challenge. α-Bungarotoxin (an alpha 7 nAchR antagonist) was injected before CLP was performed, and then, after CLP challenge, GTS-21 was administered to α-BGT + CLP + GTS-21 group. The hepatic tissue and blood samples were harvested 6 h after the operation. RESULTS: CLP challenge increased TNF-α and IL-6 production, and hepatic enzyme alanine aminotransferase and aspartate transaminase levels. CLP also elevated the expression of hepatic LC3-II, sequestosome-1/p62, Atg7 and Atg5. The administration of GTS-21 inhibited pro-inflammatory cytokine production and hepatic enzymatic marker expression, promoted the expression of LC3-II, Atg7, Atg5, and decreased the expression of p62, which could be reversed by α-BGT treatment. CONCLUSION: Our findings suggested that α7nAchR is involved in diminishing hepatic damage by inhibiting inflammatory responses and improving autophagy in mice with polymicrobial sepsis.

4.
Chem Commun (Camb) ; 56(12): 1831-1834, 2020 Feb 11.
Artigo em Inglês | MEDLINE | ID: mdl-31950935

RESUMO

Catalysts for the N2 reduction reaction (NRR) are at the heart of key alternative technology to the Haber-Bosch process for NH3 synthesis, and are expected to optimize the interplay between efficiency, activity and selectivity. Here, we report our recent finding that P-doped graphene shows superior NRR performances in aqueous media at present, with a remarkably large NH3 yield of 32.33 µg h-1 mgcat.-1 and a high faradaic efficiency of 20.82% at -0.65 V vs. reversible hydrogen electrode. The mechanism is clarified by density functional theory calculations.

5.
J Invest Surg ; : 1-10, 2020 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-31986937

RESUMO

Background: The cytokine TNF-α-stimulated gene-6 (TSG-6) had been verified to have a certain inhibitory effect on the inflammation. During wound healing, fibroblasts increasingly proliferated and deposited collagen fibers, leading to the formation of pathological scars. We sought to elucidate the mechanism by which the TGF-ß1/Smad pathway was mediated by TSG-6 in human keloid fibroblasts.Materials and methods: Human keloid fibroblast cells were isolated from keloid tissue by enzyme digestion and identified by immunocytochemistry. Lentiviral vectors pLVX-puro-TSG-6 and pLVX-shRNA1-TSG-6 were constructed which were then transfected into human keloid fibroblasts. The mRNA and protein levels of TSG-6 were detected respectively by RT-PCR and western blot assay. The intracellular localization of TGF-ß1-induced proteins and phosphorylated (p)-Smad2/3 in keloid fibroblasts were investigated using an immunofluorescence assay. Plasminogen activator inhibitor-1 (PAI-1) transcriptional activity was detected by RT-PCR.Results: TSG-6 could effectively interfere the TGF-ß1/Smad signal transduction pathway in keloid fibroblasts rather than in normal fibroblasts. The phosphorylation levels of Smad2/3 were notably reduced by TSG-6 treatment. TSG-6 blocked the complex formation of Smad2/3/4, and their nuclear translocation. However, it upregulated Smad7 expression, presenting dose dependence. PAI-1 was also suppressed by TSG-6 treatment.Conclusions: TSG-6 inhibits proliferation by inducing apoptosis in keloid fibroblasts, which may be associated with TGF-ß1/Smad pathway.

6.
Inorg Chem ; 59(3): 1622-1632, 2020 Feb 03.
Artigo em Inglês | MEDLINE | ID: mdl-31927910

RESUMO

The formation mechanism and electronic structures of iron porphyrin nitrene intermediates, as well as the nitrene-mediated intermolecular C-H amination, have been studied by performing DFT and ab initio complete active space self-consistent field (CASSCF) calculations. Compared with that of cobalt porphyrin nitrene and iron porphyrin carbene, the formation of iron porphyrin nitrene shows similar but different characteristics. The common feature is that all their formation is required to undergo the "far" or "close" complexes, but these complexes correspond to different energies relative to their respective reactants (isolated metalloporphyrins and azides), which is considered as one main reason to determine the reaction barriers. The overall free energy barrier for the formation of iron porphyrin nitrene was calculated to be 10.6 kcal/mol on a triplet-state surface, which is lower than those of cobalt porphyrin nitrene and iron porphyrin carbene. The departure of N2 from the close complexes formed by iron porphyrin and tosyl azide is nearly barrierless. For iron porphyrin nitrene, both CASSCF and unrestricted DFT calculations revealed that the triplet and open-shell singlet complexes correspond to very similar energies. The triplet nitrene complex can be described as [(por)(-OCH3)FeII═NTs]- ↔ [(por)(-OCH3)FeIII═N•-Ts]- ↔ [(por)(-OCH3)FeIV═N2-Ts]-, while the oss nitrene complex can be described as [(por)(-OCH3)FeIII-N•-Ts]-. Since the N atom bears a similar spin density as in cobalt porphyrin nitrene, the iron porphyrin nitrene exhibits similar activity in hydrogen abstraction. In addition, the intermolecular C-H amination catalyzed by iron porphyrin nitrene follows the hydrogen atom abstraction/radical recombination mechanism with a free energy barrier of 7.1 kcal/mol on the triplet-state surface. In general, the medium reactivity and easily prepared characteristic of iron porphyrin nitrene makes it a potential catalyst for C-H amination.

7.
Brain Res ; 1733: 146680, 2020 Jan 24.
Artigo em Inglês | MEDLINE | ID: mdl-31987731

RESUMO

INTRODUCTION: To explore the underlying mechanism of electroacupuncture (EA) treatment on central post-stroke pain (CPSP), and provide basic evidence for the EA treatment on CPSP. METHODS: Firstly, 40 male SD rats were successfully established with a model of CPSP, under the intervention of different EA frequencies (2 Hz and 15 Hz) and fluoxetine (5 ml/kg and 0.4 mg/ml), whose brain tissue was then removed for paraffin-embedded sectioning; secondly, LPS induced the primary brain cells in the hippocampus to cause inflammation model which were added NS398 (inhibitor of COX-2) and DKK-1 (inhibitor of ß-catenin) later. The lesion sites of brain tissue were observed by Nissl staining and Transmission Electron Microscope (TEM) and autophagy-related proteins (LC3B, p62, LAMP-1), COX-2 and ß-catenin were detected by Western Blot and immunohistochemical staining. Finally, the correlation between LC3B, COX-2, and ß-catenin was calculated by multispectral quantification. RESULTS: (1) In the EA group (15 Hz), the number of Nissl bodies increased, autophagy-related protein LC3B-Ⅱ/Ⅰ, LAMP-1, COX-2, and ß-catenin was lowly expressed, p62 was highly expressed; (2) COX-2, ß-catenin and LC3B are positively correlated with each other (COX-2 & ß-catenin: r = 0.923; COX-2 & LC3B: r = 0.818; ß-catenin & LC3B: r = 0.801); (3) Nissl bodies of primary brain cells of the hippocampus under LPS were like animal experiments; after addition of DKK-1, high expression of ß-catenin and COX-2 induced by LPS was significantly down-regulated, and LC3B-II/I was significantly down-regulated, and p62 protein only had up-regulation trend; after addition of NS398, COX-2 and LC3B-II/I was significantly down-regulated. CONCLUSION: EA may inhibit autophagy in the hippocampus by reducing ß-catenin/COX-2 protein expression and effectively alleviating CPSP. SIGNIFICANCE STATEMENT: Previous studies have found that EA can reduce the expression of NK-1R in damaged rats by inhibition of COX-2 and ß-catenin loops, which controls the activation of glial cells in the damaged area and the apoptosis of neuronal cells, and alleviated pain. In the male SD rat model, we evaluated this effect that EA inhibits autophagy in the hippocampus by reducing ß-catenin/COX-2 protein expression in the brain tissue. In addition, we assessed expression levels of autophagy-related proteins and genes on the inflammatory primary brain cells model. From the experiment, we found EA may inhibit autophagy in the hippocampus by reducing ß-catenin/COX-2 protein expression. These findings provide a foundation for the interpretation of the mechanism of EA on relieving CPSP in clinical practice.

8.
Appl Microbiol Biotechnol ; 104(4): 1785-1793, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31900555

RESUMO

Avian leukosis virus subgroup J (ALV-J) is an important pathogen for various neoplasms and causes significant economic losses in the poultry industry. Serological detection of specific antibodies against ALV-J infection is important for successful clinical diagnosis. Here, a 293F stable cell line was established to stably express gp85 protein. In this cell line, gp85 protein was expressed at approximately 30 mg/L. A subgroup-specific indirect enzyme-linked immunosorbent assay (iELISA) was developed using ALV-J gp85 protein as coated antigen to detect antibodies against ALV-J. The sensitivity of the iELISA (1:51200 diluted in serum) was 16 times more than that of indirect immunofluorescence assay (IFA; 1:3200 diluted in serum). Moreover, there was no crossreactivity with antibodies against other common avian viruses and other avian leukosis virus subgroups, such as subgroups A and B. The practicality of the iELISA was further evaluated by experimental infection and clinical samples. The results from experimental infection indicated that anti-ALV-J antibodies were readily detected by iELISA as early as 4 weeks after ALV-J infection, and positive antibodies were detected until 20 weeks, with an antibody-positive rate of 11.1% to 33.3%. Moreover, analysis of clinical samples showed that 9.49% of samples were positive for anti-ALV-J antibodies, and the concordance rate of iELISA and IFA was 99.24%. Overall, these results suggested that the subgroup-specific iELISA developed in this study had good sensitivity, specificity, and feasibility. This iELISA will be very useful for epidemiological surveillance, diagnosis, and eradication of ALV-J in poultry farms.

9.
Int J Biol Macromol ; 144: 643-655, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31816384

RESUMO

Ras is a key member in the superfamily of small GTPase. Transforming between GTP-bound active state and GDP-bound inactive state in response to exogenous signals, Ras serves as a binary switch in various signaling pathways. One of its downstream effectors is phosphatidylinositol-4,5-bisphosphate 3-kinase α (PI3Kα), which phosphorylates phosphatidylinositol 4,5-bisphosphate into phosphatidylinositol 3,4,5-trisphosphate in the PI3K/Akt/mTOR pathway and mediates an array of important cellular activities including cell growth, migration and survival. Hyperactivation of PI3Kα induced by the Ras isoform K-Ras4B has been unveiled as a key event during the oncogenesis of pancreatic ductal adenocarcinoma, but the underlying mechanism of how K-Ras4B allosterically activates PI3Kα still remains largely unsolved. Here, we employed accelerated molecular dynamic simulations and allosteric pathway analysis to explore into the activation process of PI3Kα by K-Ras4B and unraveled the underlying structural mechanisms. We found that K-Ras4B binding induced more conformational dynamics within PI3Kα and triggered its step-wise transition from a self-inhibited state towards an activated state. Moreover, K-Ras4B binding markedly disrupted the interactions along the p110/p85 interface, especially the ones between nSH2 in p85 and its nearby functional domains in p110 like C2, helical, and kinase domains. The altered inter-domain interactions exposed the kinase domain, which promoted the membrane association and substrate phosphorylation of PI3Kα, thereby facilitating its activation. In particular, the community networks and allosteric pathways analysis further revealed that in PI3Kα/K-Ras4B system, allosteric signaling regulating p110/p85 interaction was rewired from the helical domain to the kinase domain and several important residues and their related allosteric pathways mediating PI3Kα autoinhibition were bypassed. The obtained structural mechanisms provide an in-depth mechanistic insight into the allosteric activation of PI3Kα by K-Ras4B as well as shed light on its drug discovery.

10.
Aesthetic Plast Surg ; 44(1): 207-218, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31637502

RESUMO

OBJECTIVES: At present, there are many therapies for treating keloids and hypertrophic scars, but there is still a lack of treatments that are relatively balanced in efficacy and safety. The study aims to evaluate comprehensively efficacy and safety of common therapies in keloids and hypertrophic scars. METHODS: The literature search was conducted up to May 2019. The traditional meta-analysis was performed on 17 therapies. Bayesian network meta-analysis was conducted on the four most common treatments. The outcome indicators were the numbers of patients with good-to-excellent effect, Vancouver Scar Scale (VSS) and adverse events. RESULTS: There was no significant difference in the efficacy of triamcinolone acetonide (TAC) compared with other monotherapies except for silicone gel sheet and neodymium-yttrium-aluminum-garnet in primary indicator. The combination therapies were superior to TAC, and the results were consistent after the pooled analysis (RR = 0.522, 95% CI 0.332-0.823). The level of VSS in TAC group was higher than that in 5-flurouracil (5-FU) and TAC + 5-FU group, but lower than that in verapamil (VER) group. And the patients treated with TAC were less safe than those treated with verapamil (P = 0.013). Surface under cumulative ranking ranked verapamil and TAC + 5-FU as the favorable efficacy therapies in terms of primary indicator and ranked TAC + 5-FU as the best therapy for VSS, while VER was ranked as the worst. CONCLUSION: This meta-analysis showed that TAC + 5-FU may be the most effective therapy, while verapamil may be a better therapeutic strategy for safety. LEVEL OF EVIDENCE III: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

11.
Nucleic Acids Res ; 48(D1): D394-D401, 2020 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-31665428

RESUMO

Allosteric regulation is one of the most direct and efficient ways to fine-tune protein function; it is induced by the binding of a ligand at an allosteric site that is topographically distinct from an orthosteric site. The Allosteric Database (ASD, available online at http://mdl.shsmu.edu.cn/ASD) was developed ten years ago to provide comprehensive information related to allosteric regulation. In recent years, allosteric regulation has received great attention in biological research, bioengineering, and drug discovery, leading to the emergence of entire allosteric landscapes as allosteromes. To facilitate research from the perspective of the allosterome, in ASD 2019, novel features were curated as follows: (i) >10 000 potential allosteric sites of human proteins were deposited for allosteric drug discovery; (ii) 7 human allosterome maps, including protease and ion channel maps, were built to reveal allosteric evolution within families; (iii) 1312 somatic missense mutations at allosteric sites were collected from patient samples from 33 cancer types and (iv) 1493 pharmacophores extracted from allosteric sites were provided for modulator screening. Over the past ten years, the ASD has become a central resource for studying allosteric regulation and will play more important roles in both target identification and allosteric drug discovery in the future.

12.
Nutr Metab Cardiovasc Dis ; 30(1): 23-32, 2020 Jan 03.
Artigo em Inglês | MEDLINE | ID: mdl-31753787

RESUMO

BACKGROUND AND AIMS: The apolipoprotein B/apolipoprotein A-I (ApoB/ApoA-I) and insulin resistance has been recognized as common cardiovascular diseases (CVD) risk factors. However, whether they were biomarkers for 10-year CVD risk in obstructive sleep apnea (OSA) had been rarely studied. Besides, interrelationships between the ApoB/ApoA-I, insulin resistance and OSA remain unclear. METHODS AND RESULTS: A total of 4010 subjects were finally included. Anthropometric, fasting biochemical, and polysomnographic parameters were collected. 10-year Framingham CVD risk score (FRS) was calculated for each subjects. The relationships between insulin resistance, OSA risk and the ApoB/ApoA-I was evaluated through logistic regressions analysis, restricted cubic spline (RCS) analysis and mediation analysis. ApoB/ApoA-I, HOMA-IR and AHI were all risk factors for high10-year CVD risk as assessed by FRS (odds ratios (OR) = 5.365, 1.094, 1.010, respectively, all P < 0.001)). The fully adjusted OR (95% confidence intervals) for both OSA [1 (reference), 1.308 (1.027-1.665), 1.517 (1.178-1.953), and 1.803 (1.371-2.372)] and insulin resistance [1 (reference), 1.457 (1.173-1.711), 1.701 (1.369-2.113), 2.051(1.645-2.558)] increased from the first to the fourth quartiles of the ApoB/ApoA-I. The RCS mapped a nonlinear dose-effect relationship between the ApoB/ApoA-I and risk of insulin resistance and OSA. Mediation analyses showed HOMA-IR explain 9.7%, 4.7% and 10.8% of the association between apnea-hypopnea index, oxygen desaturation index, micro-arousal index and ApoB/ApoA-I, respectively. CONCLUSIONS: Our study revealed that ApoB/ApoA-I, insulin resistance and OSA were risk factors for CVD. Insulin resistance may serve as a potential mediator in OSA-related lipoprotein disorders and further increase CVD risk.

13.
Expert Opin Pharmacother ; 21(2): 167-172, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31762335

RESUMO

Introduction: Obesity is considered to be a chronic disease. Currently there are five prescription-only medications on the US market for the long-term management of obesity. However, these medications are underutilized by obese or overweight individuals seeking medical assistance for weight management.Areas covered: This special report provides an overview of the emerging obesity pharmacotherapies based on the data available from recruiting and active phase II/III trials from a registry of clinical trials. The authors also give their expert opinion and provide their future perspectives on the treatment of obesity based on what is known.Expert opinion: Despite obesity being a chronic condition affecting 40% of the US population, there is a low demand for obesity medications in the US market. Although the potential obesity medications that are currently being investigated in phase II/III clinical trials are promising, it is unclear whether the future pharmacotherapies will be enough to meet the health care need.

14.
J Cell Physiol ; 235(3): 2310-2324, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31489649

RESUMO

Radiation-induced pulmonary fibrosis (RIPF) is a life-threatening complication of thoracic radiotherapy, which contributes to continued deterioration in pulmonary function. Sphingosine-1 phosphate receptor 3 (S1PR3) has been identified as a crucial molecule in fibrosis. Accumulating evidence indicated that the inhibition of the S1PRs ameliorates fibrogenesis. Thus, this study aims to explore whether S1PR3 participates in RIPF and elucidates the molecular mechanisms underlying S1PR3-modulated epithelial-mesenchymal transition (EMT) in transforming growth factor-ß1-induced pulmonary epithelia. A recombinant adeno-associated viral-mediated S1PR3 (AAV-S1PR3) gene therapy analyzed the effect of S1PR3 gene deficiency on the altered histology structure and molecular mechanisms in the lung of mice with whole-lung irradiation. Compared with the AAV-negative control mice, AAV-mediated S1PR3 knockdown in the lung of mice attenuated pulmonary fibrosis induced by the radiation, as indicated by the alleviation of collagen accumulation, lessened histopathological alterations, and the suppression of inflammatory cells infiltration. S1PR3 deficiency reversed the RIPF concomitantly with abrogated EMT-related protein (α-smooth muscle actin). Consistently, S1PR3-deficient pulmonary epithelia inhibited the EMT process changes and fibrosis formation. Furthermore, S1PR3 was designated as one of the target genes for microRNA-495-3p (miR-495-3p). The inhibition of miR-495-3p promoted the expression of S1PR3 in pulmonary epithelia, whereas the overexpression of miR-495-3p inhibited the S1PR3/SMAD2/3 pathway and suppressed the EMT process. Collectively, miR-495-3p might be a negative regulator of the EMT process in fibrosis formation by inhibiting the targeted S1PR3 gene. These results established a link between the S1PR3 gene, the EMT process, and the fibrosis, suggesting the pharmacological blockage of S1PR3 as a potential therapeutic strategy for RIPF.

15.
Talanta ; 208: 120385, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31816798

RESUMO

A novel dummy molecularly imprinted polymers (DMIPs) for aminoglycoside antibiotics (AAs) was prepared for the first time by precipitation polymerization using raffinose as template molecule, methacrylic acid as functional monomer and trimethylolpropane triacrylate as cross-linker. The obtained DMIPs were characterized in detail, and their adsorbing and recognition performance were evaluated. The results showed that the DMIPs exhibited specific recognition towards six AAs with large adsorption capacity. The dummy molecularly imprinted solid phase extraction (DMISPE) conditions including elution/washing solutions and sample loading volumes were optimized. Under optimum conditions, a convenient and efficient method for the determination of AAs in environmental water samples based on DMISPE coupling with hydrophilic interaction-high performance liquid chromatography-tandem mass spectrometry was established. The developed method showed good linearity with correlation coefficients higher than 0.9921 for all the analytes and good recoveries (70.8-108.3%) with relative standard deviations from 2.6 to 11.4% spiked at three different concentration levels in water samples. The limit of detection (S/N = 3) ranged from 0.006 to 0.6 ng/mL. The results demonstrated good potential of DMIPs for sample pretreatment of trace AAs in environmental water samples.

16.
Analyst ; 2019 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-31825412

RESUMO

Rapid detection of physiological changes of neuropeptides is of great importance as they are involved in a wide range of physiological processes and behaviors. Abnormalities in their expression level are correlated with various neurological diseases. However, current methods such as radioimmunoassay, enzyme-linked immunosorbent assays and liquid chromatography tandem mass spectrometry relied on cumbersome operation steps and could not rapidly provide the information of their concentration fluctuations. Thus motivated, we developed a target-driven DNA-based molecular machine that could be triggered only in the presence of a specific target neuropeptide. Using arginine-vasopressin (AVP) as a model neuropeptide, we integrated the DNA-based molecular machine with fluorescence signal transduction and amplification technology. The assay was rapid and homogeneous, which offered a linear range of 75-700 pM and a limit-of-detection as low as 75 pM. It holds great potential for further applications in real-time monitoring of the variations of the AVP level in biological samples.

17.
Am J Chin Med ; 47(8): 1755-1780, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31801357

RESUMO

Considering the heavy burden of migraine, it is essential to update insufficient and/or outdated clinical evidence supporting electroacupuncture (EA) in migraine therapy. In this study, a literature search of seven medical databases was performed. After data extraction and quality evaluation, 13 randomized controlled trials, including 1559 patients, were assessed in this analysis. Results demonstrated that EA was superior to control treatment (Western medicine, sham-EA, blank control, acupuncture, and acupoint catgut embedding) according to the visual analog scale (VAS) score, frequency of headache attack (Western medicine, sham-EA, blank control), self-rating anxiety scale (SAS [blank control]), self-rating depression score (SDS [Western medicine and blank control]), and clinical efficiency (Western medicine and sham-EA) after treatment (P<0.05). Results of network meta-analysis (for VAS, SAS, and SDS) demonstrated statistically significant differences in VAS scores for EA compared with sham-EA, acupuncture with sham-EA, acupoint catgut embedding with sham-EA, and acupoint catgut embedding with blank control. Rank probability analysis of VAS, SAS, and SDS scores all demonstrated that EA ranked first. Most studies were symmetrically distributed on both sides of the midline in funnel plots for VAS, SAS, and SDS, which indicated a low likelihood of small sample effects. Sensitivity analysis confirmed the stability of the studies included in this research. EA is one of several effective treatments for migraine pain symptoms, and, to some extent, anxiety and depression. Nevertheless, multi-center studies with large sample sizes and/or well-designed randomized controlled trials (RCTs) will be needed in the future.

18.
Respir Res ; 20(1): 276, 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31801522

RESUMO

BACKGROUND: Obstructive sleep apnea (OSA) and excessive daytime sleepiness (EDS) were considered to contribute to MetS. This study was performed to assess the association between MetS and EDS in two independent large-scale populations, and in subjects who underwent upper-airway surgery. METHODS: A total of 6312 patients without self-reported depression and 3578 suspected OSA patients were consecutively recruited, during health screening examinations and from our sleep center, respectively. A total of 57 subjects with OSA who underwent upper-airway surgery were also included. Demographic, anthropometric, biochemical, and polysomnographic data were obtained. RESULTS: In the health screening examination group, 233 (9.23%) women and 350 (10.93%) men had complaints of EDS. A total of 229 (7.04%) women and 1182 (36.88%) men met the criteria for MetS. In the OSA group, 147 (21.18%) women and 1058 (36.69%) men reported EDS. In addition, 93 (13.4%) women and 1368 (47.43%) men reported MetS. In the health screening examination group, EDS did not contribute significantly to MetS (OR = 1.125, 95% CI: 0.907-1.395; p = 0.283). In the OSA group, EDS significantly contributed to MetS (OR = 1.249, 95% CI: 1.063-1.468; p = 0.007); however, the results were not significant after adjusting for sleep variables (OR = 1.071, 95% CI: 0.905-1.268; p = 0.423). Upper-airway surgery did not affect cardio-metabolic variables in OSA patients with or without EDS. CONCLUSIONS: EDS was not associated with MetS in two independent large-scale cohorts. In addition, upper-airway surgery did not affect components of MetS in OSA patients with and without EDS.

19.
Pain Res Manag ; 2019: 5930627, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31781318

RESUMO

Objectives: To review the evidence of acupuncture for acute and preventive treatment of migraine for further awareness of the effect of acupuncture for migraine. Design: An overview of systematic reviews and meta-analyses (SR/MAs) for randomized controlled trials. Material and Methods: We searched PubMed, Embase, the Cochrane Library, China Knowledge Resource Integrated Database, VIP Chinese Journal Full Text Database, WANFANG Data, and China Biology Medicine disc from their establishment to May 27, 2018. SR/MAs of randomized controlled trials comparing the effect of the acupuncture intervention with another treatment control in migraine patients were included. Results: 428 SRs were identified, and 15 of them were included. Only 4 SR/MAs were assessed by GRADE, which showed certainty of most evidence being low or very low. Assessed by AMSTAR-2, fourteen was critically low rating overall confidence in the results, and 1 was low rating overall confidence in the results. Evidence suggested that acupuncture has a significant advantage of pain improvement, efficacy, and safety relative to blank control, sham acupuncture, or drug treatment, but some of these results are contradictory. Conclusions: We found that acupuncture on treating migraine has the advantage for pain improvement and safety, but the quality of SR/MAs of acupuncture for migraine remains to be improved.

20.
Front Pharmacol ; 10: 1220, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31680983

RESUMO

Background: Bilirubin (BR) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1) through glucuronidation in the liver. Some studies have shown that several subtypes of cytochrome P450 (CYP) enzymes, including CYP1A2, are upregulated by inducers and proposed to be alternative BR degradation enzymes. However, no information is available on the BR degradation ability of CYP in normal rats without manipulation by CYP inducers. Methods: Quantitative real-time polymerase chain reaction (QRT-PCR), western blot, immunofluorescence, and confocal microscopy were used to find expression of CYP1A2 in the brain and the liver. BR metabolites in microsomal fractions during development were examined by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (LC-MS/MS). Results: In the present study, we observed that CYP1A2 mRNA levels increased at postnatal days (P)14 and P30 with respect to the level at P7 both in liver and brain, this increment was especially pronounced in the brain at P14. The expression of CYP1A2 in the brainstem (BS) was higher than that in the cerebellum (CLL) and cortex (COR). Meanwhile, the CYP1A2 protein level was significantly higher in the COR than in the brainstem and CLL at P14. The levels of BR and its metabolites (m/z values 301, 315, 333 and biliverdin) were statistically unaltered by incubation with liver and brain microsomal fractions. Conclusion: Our results indicated that the region-specific expression of CYP1A2 increased during development, but CYP family enzymes were physiologically incapable of metabolizing BR. The ability of CYPs to oxidize BR may be triggered by CYP inducers.

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