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1.
J Transl Med ; 17(1): 349, 2019 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-31640726

RESUMO

BACKGROUND: Subarachnoid hemorrhage (SAH) accounts for 4.4% of cerebral vascular disease, which is one of the leading causes of death in China. Rupture of intracranial aneurysms (IAs) is the most common cause of SAH. The natural history of unruptured IAs (UIAs) and the risk factors for rupture are among the key issues regarding the pathogenesis of IA and SAH that remain unclear in the Chinese population. METHODS: The China Intracranial Aneurysm Project (CIAP) is a prospective, observational, multicenter registry study of the natural courses, risk factors for the onset and rupture, treatment methods, comorbidity management and other aspects of intracranial aneurysms. To date, there are five studies in the CIAP. CIAP-1 is a prospective observational cohort study of UIAs. More than 5000 patients who will be followed for at least 1 year are expected to be enrolled in this cohort. These participants come from more than 20 centers that represent different regions in China. Enrollment began on May 1, 2017, and will take approximately 5 years. A nationwide online database of UIAs will be built. Participants' basic, lifestyle, clinical and follow-up information will be collected. The blood samples will be stored in the Central Biological Specimen Bank. Strict standards have been established and will be followed in this study to ensure efficient implementation. DISCUSSION: The natural course of UIAs in the Chinese population will be explored in this registry study. In addition, the risk factors for the rupture of the UIAs and the joint effect of those factors will be analyzed. The present study aims to create a nationwide database of UIAs and investigate the natural course of UIAs in China. Trial registration The Natural Course of Unruptured Intracranial Aneurysms in a Chinese Cohort (ClinicalTrials.gov Identifier: NCT03117803). Registered: July 5, 2017.

2.
J Hazard Mater ; : 121354, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31615709

RESUMO

This work is to systematically study the mercury-removal behavior of activated coke (AC), regeneration of spent AC by microwave treatment and subsequent recycling of Hg0. The powdery (AC) was obtained under coal-fired hot gas conditions in a drop-tube reactor. The adsorption mechanism and capacity of the AC for Hg0 removal in a H2O + SO2 + O2 atmosphere were investigated. The regeneration of the AC by microwave heating and recovery of Hg0 were studied. The results showed that this AC preparation method can greatly simplify the process, and the AC's large surface area, developed pore structure, and abundant functional groups played a key role in the adsorption of Hg0. The adsorption mechanism and the optimum reaction conditions were determined, with a highest average Hg0-adsorption efficiency of 91% obtained at 70 °C in 3 h. Desorption of Hg0 was also studied, in which the alkaline-functional-group content and pore structure were enhanced, and S was detected by X-ray photoelectron spectroscopy in microwave-regenerated AC, which could improve the Hg0 removal efficiency increased to 96% after five adsorption/desorption cycles. The Hg0 could subsequently be recovered from the desorbed gas by condensation with an efficiency of 87.4% using ice-water.

3.
Sci Total Environ ; 695: 133811, 2019 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-31419687

RESUMO

Nitrification and denitrification are the most important nitrogen transformation processes in the environment. Recently, due to widespread use, antibiotics have been reported to lead to environmental risks. Tetracycline (TC) is one of the most extensively used antibiotics in many areas. However, its reported effects on nitrogen transformations were conflicting in previous studies. In this study, the effects of TC on nitrogen transformations in sediment were investigated by analyzing TC transport and bacterial activity. It was found that the adsorption of TC onto the sediment was favorable and spontaneous, with adsorption capacity 54.3 mg/kg. The adsorption kinetics of TC onto the sediment and the isotherm fitted the Elvoich and Freundlich models, respectively, indicating that the adsorption was a chemisorption process, including electrostatic interactions and chemical bonding between TC and the sediment. TC showed no effect on nitrification in the sediment, but significantly inhibited the reduction of nitrate and nitrite during denitrification, consistent with observations made for the model denitrifier Paracoccus denitrificans under TC stress. Mechanistic study indicated that TC at 130 µg/g-cell inhibited 50.7% of P. denitrificans growth and 61.6% of cell viability. Meanwhile, the catalytic activities of the key denitrifying enzymes, nitrate reductase (NAR) and nitrite reductase (NIR), decreased to 29.1% and 68.0% of the control levels when the TC concentration was 130 µg/g-cell, suggesting that NAR was more sensitive to the TC than NIR, which contributed to a delay in nitrite accumulation.

4.
Acta Biomater ; 97: 177-186, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31352107

RESUMO

Long-segmental tracheal defects constitute an intractable clinical problem, due to the lack of satisfactory tracheal substitutes for surgical reconstruction. Tissue engineered artificial substitutes could represent a promising approach to tackle this challenge. In our current study, tissue-engineered trachea, based on a 3D-printed poly (l-lactic acid) (PLLA) scaffold with similar morphology to the native trachea of rabbits, was used for segmental tracheal reconstruction. The 3D-printed scaffolds were seeded with chondrocytes obtained from autologous auricula, dynamically pre-cultured in vitro for 2 weeks, and pre-vascularized in vivo for another 2 weeks to generate an integrated segmental trachea organoid unit. Then, segmental tracheal defects in rabbits were restored by transplanting the engineered tracheal substitute with pedicled muscular flaps. We found that the combination of in vitro pre-culture and in vivo pre-vascularization successfully generated a segmental tracheal substitute with bionic structure and mechanical properties similar to the native trachea of rabbits. Moreover, the stable blood supply provided by the pedicled muscular flaps facilitated the survival of chondrocytes and accelerated epithelialization, thereby improving the survival rate. The segmental trachea substitute engineered by a 3D-printed scaffold, in vitro pre-culture, and in vivo pre-vascularization enhanced survival in an early stage post-operation, presenting a promising approach for surgical reconstruction of long segmental tracheal defects. STATEMENT OF SIGNIFICANCE: We found that the combination of in vitro pre-culture and in vivo pre-vascularization successfully generated a segmental tracheal substitute with bionic structure and mechanical properties similar to the native trachea of rabbits. Moreover, the stable blood supply provided by the pedicled muscular flaps facilitated the survival of chondrocytes and accelerated epithelialization, thereby improving the survival rate of the rabbits. The segmental trachea substitute engineered by a 3D-printed scaffold, in vitro pre-culture, and in vivo pre-vascularization enhanced survival in an early stage post-operation, presenting a promising approach for surgical reconstruction of long segmental tracheal defects.

5.
J Neurointerv Surg ; 2019 Jul 12.
Artigo em Inglês | MEDLINE | ID: mdl-31300535

RESUMO

BACKGROUND: The main surgical techniques for spontaneous basal ganglia hemorrhage include stereotactic aspiration, endoscopic aspiration, and craniotomy. However, credible evidence is still needed to validate the effect of these techniques. OBJECTIVE: To explore the long-term outcomes of the three surgical techniques in the treatment of spontaneous basal ganglia hemorrhage. METHODS: Five hundred and sixteen patients with spontaneous basal ganglia hemorrhage who received stereotactic aspiration, endoscopic aspiration, or craniotomy were reviewed retrospectively. Six-month mortality and the modified Rankin Scale score were the primary and secondary outcomes, respectively. A multivariate logistic regression model was used to assess the effects of different surgical techniques on patient outcomes. RESULTS: For the entire cohort, the 6-month mortality in the endoscopic aspiration group was significantly lower than that in the stereotactic aspiration group (odds ratio (OR) 4.280, 95% CI 2.186 to 8.380); the 6-month mortality in the endoscopic aspiration group was lower than that in the craniotomy group, but the difference was not significant (OR=1.930, 95% CI 0.835 to 4.465). A further subgroup analysis was stratified by hematoma volume. The mortality in the endoscopic aspiration group was significantly lower than in the stereotactic aspiration group in the medium (≥40-<80 mL) (OR=2.438, 95% CI 1.101 to 5.402) and large hematoma subgroup (≥80 mL) (OR=66.532, 95% CI 6.345 to 697.675). Compared with the endoscopic aspiration group, a trend towards increased mortality was observed in the large hematoma subgroup of the craniotomy group (OR=8.721, 95% CI 0.933 to 81.551). CONCLUSION: Endoscopic aspiration can decrease the 6-month mortality of spontaneous basal ganglia hemorrhage, especially in patients with a hematoma volume ≥40 mL.

6.
Curr Med Chem ; 2019 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-31267851

RESUMO

Molecular imaging techniques apply sophisticated technologies to monitor, directly or indirectly, the spatiotemporal distribution of molecular or cellular processes for biomedical, diagnostic, or therapeutic purposes. For example, single-photon emission computed tomography (SPECT) and positron emission tomography (PET) imaging, the most representative modalities of molecular imaging, enable earlier and more accurate diagnosis of cancer and cardiovascular diseases. New possibilities for noninvasive molecular imaging in vivo have emerged with advances in bioorthogonal chemistry. For example, tetrazine-related inverse electron demand Diels-Alder (IEDDA) reactions can rapidly generate short-lived radioisotope probes in vivo that provide strong contrast for SPECT and PET. Here we review pretargeting strategies for molecular imaging and novel radiotracers synthesized via tetrazine bioorthogonal chemistry. We systematically describe advances in direct radiolabeling and pretargeting approaches in SPECT and PET using metal and nonmetal radioisotopes based on tetrazine bioorthogonal reactions, and we discuss prospects for the future of such contrast agents.

7.
Microbiome ; 7(1): 98, 2019 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-31255176

RESUMO

BACKGROUND: Western-style diets arouse neuroinflammation and impair emotional and cognitive behavior in humans and animals. Our previous study showed that a high-fructose diet caused the hippocampal neuroinflammatory response and neuronal loss in animals, but the underlying mechanisms remained elusive. Here, alterations in the gut microbiota and intestinal epithelial barrier were investigated as the causes of hippocampal neuroinflammation induced by high-fructose diet. RESULTS: A high-fructose diet caused the hippocampal neuroinflammatory response, reactive gliosis, and neuronal loss in C57BL/6N mice. Depletion of the gut microbiota using broad-spectrum antibiotics suppressed the hippocampal neuroinflammatory response in fructose-fed mice, but these animals still exhibited neuronal loss. Gut microbiota compositional alteration, short-chain fatty acids (SCFAs) reduction, intestinal epithelial barrier impairment, NOD-like receptor family pyrin domain-containing 6 (NLRP6) inflammasome dysfunction, high levels of serum endotoxin, and FITC-dextran were observed in fructose-fed mice. Of note, SCFAs, as well as pioglitazone (a selective peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist), shaped the gut microbiota and ameliorated intestinal epithelial barrier impairment and NLRP6 inflammasome dysfunction in fructose-fed mice. Moreover, SCFAs-mediated NLRP6 inflammasome activation was inhibited by histamine (a bacterial metabolite) in ex vivo colonic explants and suppressed in murine CT26 colon carcinoma cells transfected with NLRP6 siRNA. However, pioglitazone and GW9662 (a PPAR-γ antagonist) exerted no impact on SCFAs-mediated NLRP6 inflammasome activation in ex vivo colonic explants, suggesting that SCFAs may stimulate NLRP6 inflammasome independently of PPAR-γ activation. SCFAs and pioglitazone prevented fructose-induced hippocampal neuroinflammatory response and neuronal loss in mice. Additionally, SCFAs activated colonic NLRP6 inflammasome and increased DCX+ newborn neurons in the hippocampal DG of control mice. CONCLUSIONS: Our findings reveal that gut dysbiosis is a critical factor for a high-fructose diet-induced hippocampal neuroinflammation in C57BL/6N mice possibly mediated by impairing intestinal epithelial barrier. Mechanistically, the defective colonic NLRP6 inflammasome is responsible for intestinal epithelial barrier impairment. SCFAs can stimulate NLRP6 inflammasome and ameliorate the impairment of intestinal epithelial barrier, resulting in the protection against a high-fructose diet-induced hippocampal neuroinflammation and neuronal loss. This study addresses a gap in the understanding of neuronal injury associated with Western-style diets. A new intervention strategy for reducing the risk of neurodegenerative diseases through SCFAs supplementation or dietary fiber consumption is emphasized.

8.
J Neurol Surg A Cent Eur Neurosurg ; 80(6): 498-502, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31075809

RESUMO

BACKGROUND: Cranioplasty is a common procedure in neurosurgery. It is usually performed following decompressive craniectomy (DC). However, complications may occur after the operation, such as massive brain swelling. Up to now, far too little attention has been given to this severe complication. We report one case of fatal cerebral swelling after cranioplasty and analyze the possible mechanism of this complication. CASE DESCRIPTION: The patient was a 40-year-old man who had a severe right basal ganglia cerebral hemorrhage and underwent DC ∼ 2 months before. One day before scheduled cranioplasty, a lumbar cerebrospinal fluid drainage was placed. The cranioplasty itself was uneventful. However, he gradually fell into a coma, and his right pupil was moderately dilated 20 hours after the surgery. A brain computed tomography (CT) scan indicated massive right cerebral edema with compressed right midbrain. The patient did not regain consciousness, and he remained quadriplegic. CONCLUSION: It is necessary to increase awareness of complications of cranioplasty in high-risk patients. The lessons learned from this case include avoiding excessive drainage of cerebrospinal fluid. Patients with low-density lesions in the brain need to be treated with caution. Once the CT scan shows massive cerebral swelling, the patient has a poor prognosis.

9.
Opt Lett ; 44(9): 2232-2235, 2019 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-31042191

RESUMO

We report an ultralow-voltage, electrothermal (ET) micro-electro-mechanical system (MEMS) based probe for forward-viewing endoscopic optical coherence tomography (OCT) imaging. The fully assembled probe has a diameter of 5.5 mm and a length of 55 mm, including the imaging optics and a 40 mm long fiber-optic cantilever attached on a micro-platform of the bimorph ET MEMS actuator. The ET MEMS actuator provides a sufficient mechanical actuation force as well as a large vertical displacement, achieving up to a 3 mm optical scanning range with only a 3 VACp-p drive voltage with a 1.5 VDC offset. The imaging probe was integrated with a swept-source OCT system of a 100 kHz A-scan rate, and its performance was successfully demonstrated with cross-sectional imaging of biological tissues ex vivo and in vivo at a speed up to 200 frames per second.

10.
Neuropeptides ; 76: 101934, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31130301

RESUMO

Corticotropin-releasing factor (CRF) is a neuropeptide mainly synthesized in the hypothalamic paraventricular nucleus and has been traditionally implicated in stress and anxiety. Intriguingly, genetic or pharmacological manipulation of CRF receptors affects locomotor activity as well as motor coordination and balance in rodents, suggesting an active involvement of the central CRFergic system in motor control. Yet little is known about the exact role of CRF in central motor structures and the underlying mechanisms. Therefore, in the present study, we focused on the effect of CRF on the lateral vestibular nucleus (LVN) in the brainstem vestibular nuclear complex, an important center directly contributing to adjustment of muscle tone for both postural maintenance and the alternative change from the extensor to the flexor phase during locomotion. The results show that CRF depolarizes and increases the firing rate of neurons in the LVN. Tetrodotoxin does not block the CRF-induced depolarization and inward current on LVN neurons, suggesting a direct postsynaptic action of the neuropeptide. The CRF-induced depolarization on LVN neurons was partly blocked by antalarmin or antisauvagine-30, selective antagonists for CRF receptors 1 (CRFR1) and 2 (CRFR2), respectively. Furthermore, combined application of antalarmin and antisauvagine-30 totally abolished the CRF-induced depolarization. Immunofluorescence results show that CRFR1 and CRFR2 are co-localized in the rat LVN. These results demonstrate that CRF excites the LVN neurons by co-activation of both CRFR1 and CRFR2, suggesting that via the direct modulation on the LVN, the central CRFergic system may actively participate in the central vestibular-mediated postural and motor control.

11.
Medicine (Baltimore) ; 98(21): e15758, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31124961

RESUMO

BACKGROUND: For cancer, it is common that there is usually a dysregulation of the long noncoding RNA regulator of reprogramming (LncRNA ROR). To illustrate the application of LncRNA ROR, which serves as the prognostic marker for the malignant tumors, it is of great importance to conduct a meta-analysis. METHODS: There were 3 databases being applied. The data used were collected before January 5, 2018. These 3 databases include the OVID, PubMed, and Science databse. To further explore the association between the expression and survival of LncRNA ROR, it calculated the 95% confidence intervals (CIs) and hazard ratios (HRs). Meanwhile, the odds ratios (ORs) have been calculated for the evaluation of the correlation between the pathological and expression parameters of LncRNA ROR. RESULTS: There were 8 researches participated by 720 patients. According to the HR, it has been implied that there was a high LncRNA ROR expression related with the weak disease-free survival (DFS) (HR = 3.48, 95% CI, 2.24-5.41) and overall survival (OS) (HR = 2.47, 95% CI, 1.76-3.47) among the cancer patients with none dramatic heterogeneity. There was also a correlation among lymph node metastasis (OR = 5.38, 95% CI, 2.21-13.12), high tumor stage (OR = 3.80, 95% CI, 1.95-7.41), and larger tumor size (OR = 4.43, 95% CI, 1.26-15.51). CONCLUSIONS: Thus, it can be predicted about the lymph node metastasis and high tumor stage, larger tumor size, DFS, and poor OS based on the high LncRNA ROR. This suggests that high LncRNA ROR can be used as a new indicator of poor prognosis in cancer.


Assuntos
Neoplasias/genética , Neoplasias/patologia , RNA Longo não Codificante/genética , Biomarcadores Tumorais , China , Humanos , Metástase Linfática , Estadiamento de Neoplasias , Análise de Sobrevida , Carga Tumoral
12.
Cell Mol Gastroenterol Hepatol ; 7(4): 763-781, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30831319

RESUMO

BACKGROUND & AIMS: Obesity promotes the development of nonalcoholic fatty liver diseases (NAFLDs), yet not all obese patients develop NAFLD. The underlying causes for this discrepancy remain elusive. LPGAT1 is an acyltransferase that catalyzes the remodeling of phosphatidylglycerol (PG), a mitochondrial phospholipid implicated in various metabolic diseases. Here, we investigated the role of LPGAT1 in regulating the onset of diet-induced obesity and its related hepatosteatosis because polymorphisms of the LPGAT1 gene promoter were strongly associated with susceptibility to obesity in Pima Indians. METHODS: Mice with whole-body knockout of LPGAT1 were generated to investigate the role of PG remodeling in NAFLD. RESULTS: LPGAT1 deficiency protected mice from diet-induced obesity, but led to hepatopathy, insulin resistance, and NAFLD as a consequence of oxidative stress, mitochondrial DNA depletion, and mitochondrial dysfunction. CONCLUSIONS: This study identified an unexpected role of PG remodeling in obesity, linking mitochondrial dysfunction to NAFLD.

13.
Aging Cell ; 18(3): e12941, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30838774

RESUMO

Cardiolipin (CL) is a mitochondrial signature phospholipid that is required for membrane structure, respiration, dynamics, and mitophagy. Oxidative damage of CL by reactive oxygen species is implicated in the pathogenesis of Parkinson's disease (PD), but the underlying cause remains elusive. This work investigated the role of ALCAT1, an acyltransferase that catalyzes pathological remodeling of CL in various aging-related diseases, in a mouse model of PD induced by 1-methyl-4-phenyl-1,2,4,6-tetrahydropyridine (MPTP). We show that MPTP treatment caused oxidative stress, mtDNA mutations, and mitochondrial dysfunction in the midbrain. In contrast, ablation of the ALCAT1 gene or pharmacological inhibition of ALCAT1 prevented MPTP-induced neurotoxicity, apoptosis, and motor deficits. ALCAT1 deficiency also mitigated mitochondrial dysfunction by modulating DRP1 translocation to the mitochondria. Moreover, pharmacological inhibition of ALCAT1 significantly improved mitophagy by promoting the recruitment of Parkin to dysfunctional mitochondria. Finally, ALCAT1 expression was upregulated by MPTP and by α-synucleinopathy, a key hallmark of PD, whereas ALCAT1 deficiency prevented α-synuclein oligomerization and S-129 phosphorylation, implicating a key role of ALCAT1 in the etiology of mouse models of PD. Together, these findings identify ALCAT1 as a novel drug target for the treatment of PD.

14.
Pediatr Cardiol ; 40(4): 762-767, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30868185

RESUMO

Congenital heart defect (CHD) is one of the most common birth defects in China, while pulmonary atresia with intact ventricular septum (PA-IVS) is the life-threatening form of CHD. Numerous previous studies revealed that rare copy number variants (CNVs) play important roles in CHD, but little is known about the prevalence and role of rare CNVs in PA-IVS. In this study, we conducted a genome-wide scanning of rare CNVs in an unselected cohort consisted of 54 Chinese patients with PA-IVS and 20 patients with pulmonary atresia with ventricular septal defect (PA-VSD). CNVs were identified in 6/20 PA-VSD patients (30%), and three of these CNVs (15%) were considered potentially pathogenic. Two pathogenic CNVs occurred at a known CHD locus (22q11.2) and one likely pathogenic deletion located at 13q12.12. However, no rare CNVs were detected in patients with PA-IVS. Potentially pathogenic CNVs were more enriched in PA-VSD patients than in PA-IVS patients (p = 0.018). No rare CNVs were detected in patients with PA-IVS in our study. PA/IVS might be different from PA/VSD in terms of genetics as well as anatomy.


Assuntos
Grupo com Ancestrais do Continente Asiático/genética , Variações do Número de Cópias de DNA/genética , Cardiopatias Congênitas/genética , Comunicação Interventricular/genética , Atresia Pulmonar/genética , Criança , Pré-Escolar , China , Feminino , Estudo de Associação Genômica Ampla/métodos , Cardiopatias Congênitas/etnologia , Humanos , Lactente , Recém-Nascido , Masculino , Fenótipo , Prevalência , Atresia Pulmonar/etnologia
15.
Glob Chang Biol ; 25(6): 2174-2188, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30897264

RESUMO

Climate change has substantial influences on autumn leaf senescence, that is, the end of the growing season (EOS). Relative to the impacts of temperature and precipitation on EOS, the influence of drought is not well understood, especially considering that there are apparent cumulative and lagged effects of drought on plant growth. Here, we investigated the cumulative and lagged effects of drought (in terms of the Standardized Precipitation-Evapotranspiration Index, SPEI) on EOS derived from the normalized difference vegetation index (NDVI3g) data over the Northern Hemisphere extra-tropical ecosystems (>30°N) during 1982-2015. The cumulative effect was determined by the number of antecedent months at which SPEI showed the maximum correlation with EOS (i.e., Rmax-cml ) while the lag effect was determined by a month during which the maximum correlation between 1-month SPEI and EOS occurred (i.e., Rmax-lag ). We found cumulative effect of drought on EOS for 27.2% and lagged effect for 46.2% of the vegetated land area. For the dominant time scales where the Rmax-cml and Rmax-lag occurred, we observed 1-4 accumulated months for the cumulative effect and 2-6 lagged months for the lagged effect. At the biome level, drought had stronger impacts on EOS in grasslands, savannas, and shrubs than in forests, which may be related to the different root functional traits among vegetation types. Considering hydrological conditions, the mean values of both Rmax-cml and Rmax-lag decreased along the gradients of annual SPEI and its slope, suggesting stronger cumulative and lagged effects in drier regions as well as in areas with decreasing water availability. Furthermore, the average accumulated and lagged months tended to decline along the annual SPEI gradient but increase with increasing annual SPEI. Our results revealed that drought has strong cumulative and lagged effects on autumn phenology, and considering these effects could provide valuable information on the vegetation response to a changing climate.


Assuntos
Mudança Climática , Secas , Desenvolvimento Vegetal , Folhas de Planta , Ecossistema , Florestas , Imagens de Satélites , Estações do Ano , Temperatura Ambiente , Água
16.
BMJ Open ; 9(2): e025218, 2019 02 19.
Artigo em Inglês | MEDLINE | ID: mdl-30782928

RESUMO

OBJECTIVE: This study aimed to assess the registration quality of clinical trials (CTs) with traditional Chinese medicine (TCM) in the WHO International Clinical Trials Registry Platform (ICTRP) and identify the common problems if any. METHODS: The ICTRP database was searched for all TCM CTs that were registered up to 31 December 2017. Registered information of each trial was collected from specific registry involved in ICTRP through hyperlink. The primary analysis was to assess the reporting quality of registered trials with TCM interventions, which is based on the minimum 20 items of WHO Trial Registration Data Set (TRDS, V.1.2.1) plus optional additional three items recommended by ICTRP, and some specific items for TCM information (including TCM intervention, diagnosis, outcome and rationale). Descriptive statistics were additionally used to analyse the baseline characteristics of TCM trial registrations. RESULTS: A total of 3339 records in 15 registries were examined. The number of TCM registered trials has increased rapidly after the requirement of mandatory trial registration proposed by International Committee of Medical Journal Editors on 1 July 2005, and the top two registries were Chinese Clinical Trial Registry and ClincialTrials.gov. Of 3339 trials, 61% were prospective registration and 12.8% shared resultant publications. There were 2955 interventional trials but none of them had a 100% reporting rate of the minimum 20 items and additional three items. The reporting quality of these 23 items was not optimal due to 11 of them had a lower reporting rate (<65%). For TCM details, 49.2% lacked information on description of TCM intervention(s), 85.9% did not contain TCM diagnosis criteria, 92.6% did not use TCM outcome(s) and 67.1% lacked information on TCM background and rationale. CONCLUSION: The registration quality of TCM CTs should be improved by prospective registration, full completion of WHO TRDS, full reporting of TCM information and results sharing. Further full set of trial registration items for TCM trials should be developed thus to standardise the content of TCM trial registration.

17.
FASEB J ; 33(4): 5641-5653, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30694703

RESUMO

Cartilage engineering strategies using mesenchymal stem cells (MSCs) could provide preferable solutions to resolve long-segment tracheal defects. However, the drawbacks of widely used chondrogenic protocols containing TGF-ß3, such as inefficiency and unstable cellular phenotype, are problematic. In our research, to optimize the chondrogenic differentiation of human umbilical cord MSCs (hUCMSCs), kartogenin (KGN) preconditioning was performed prior to TGF-ß3 induction. hUCMSCs were preconditioned with 1 µM of KGN for 3 d, sequentially pelleted, and incubated with TGF-ß3 for 28 d. Then, the expression of chondrogenesis- and ossification-related genes was evaluated by immunohistochemistry and RT-PCR. The underlying mechanism governing the beneficial effects of KGN preconditioning was explored by phosphorylated kinase screening and validated in vitro and in vivo using JNK inhibitor (SP600125) and ß-catenin activator (SKL2001). After KGN preconditioning, expression of fibroblast growth factor receptor 3, a marker of precartilaginous stem cells, was up-regulated in hUCMSCs. Furthermore, the KGN-preconditioned hUCMSCs efficiently differentiated into chondrocytes with elevated chondrogenic gene ( SOX9, aggrecan, and collagen II) expression and reduced expression of ossific genes (collagen X and MMP13) compared with hUCMSCs treated with TGF-ß3 only. Phosphokinase screening indicated that the beneficial effects of KGN preconditioning are directly related to an up-regulation of JNK phosphorylation and a suppression of ß-catenin levels. Blocking and activating tests revealed that the prochondrogenic effects of KGN preconditioning was achieved mainly by activating the JNK/Runt-related transcription factor (RUNX)1 pathway, and antiossific effects were imparted by suppressing the ß-catenin/RUNX2 pathway. Eventually, tracheal patches, based on KGN-preconditioned hUCMSCs and TGF-ß3 encapsulated electrospun poly( l-lactic acid-co-ε-caprolactone)/collagen nanofilms, were successfully used for restoring tracheal defects in rabbit models. In summary, KGN preconditioning likely improves the chondrogenic differentiation of hUCMSCs by committing them to a precartilaginous stage with enhanced JNK phosphorylation and suppressed ß-catenin. This novel protocol consisting of KGN preconditioning and subsequent TGF-ß3 induction might be preferable for cartilage engineering strategies using MSCs.-Jing, H., Zhang, X., Gao, M., Luo, K., Fu, W., Yin, M., Wang, W., Zhu, Z., Zheng, J., He, X. Kartogenin preconditioning commits mesenchymal stem cells to a precartilaginous stage with enhanced chondrogenic potential by modulating JNK and ß-catenin-related pathways.

18.
J Neurosci ; 2018 Nov 09.
Artigo em Inglês | MEDLINE | ID: mdl-30413645

RESUMO

Vestibular compensation is responsible for the spontaneous recovery of postural, locomotor and oculomotor dysfunctions in patients with peripheral vestibular lesion or posterior circulation stroke. Mechanism investigation of vestibular compensation is of great importance in both facilitating recovery of vestibular function and understanding the post-lesion functional plasticity in the adult central nervous system. Here, we report that postsynaptic histamine H1 receptor contributes greatly to facilitating vestibular compensation. The expression of H1 receptor is restrictedly increased in the ipsilesional rather than contralesional GABAergic projection neurons in the medial vestibular nucleus (MVN), one of the most important centers for vestibular compensation, in unilateral labyrinthectomized male rats. Furthermore, H1 receptor mediates an asymmetric excitation of the commissural GABAergic but not glutamatergic neurons in the ipsilesional MVN, which may help to rebalance bilateral vestibular systems and promote vestibular compensation. Selective blockage of H1 receptor in the MVN significantly retards the recovery of both static and dynamic vestibular symptoms following unilateral labyrinthectomy, and remarkably attenuates the facilitation of betahistine, whose effect has traditionally been attributed to its antagonistic action on the presynaptic H3 receptor, on vestibular compensation. These results reveal a previously unknown role for histamine H1 receptor in vestibular compensation and amelioration of vestibular motor deficits, as well as an involvement of H1 receptor in potential therapeutic effects of betahistine. The findings provide not only a new insight into the post-lesion neuronal circuit plasticity and functional recovery in the central nervous system, but also a novel potential therapeutic target for vestibular disorders.Significance statementVestibular disorders manifest postural imbalance, nystagmus and vertigo. Vestibular compensation is critical for facilitating recovery from vestibular disorders, and of great importance in understanding the post-lesion functional plasticity in the adult central nervous system. Here, we show that postsynaptic H1 receptor in the medial vestibular nucleus (MVN) contributes greatly to the recovery of both static and dynamic symptoms following unilateral vestibular lesion. H1 receptor selectively mediates the asymmetric activation of commissural inhibitory system in the ipsilesional MVN and actively promotes vestibular compensation. The findings provide not only a new insight into the post-lesion neuronal circuit plasticity and functional recovery of central nervous system, but also a novel potential therapeutic target for promoting vestibular compensation and ameliorating vestibular disorders.

19.
J Clin Invest ; 128(12): 5413-5427, 2018 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-30226827

RESUMO

The subthalamic nucleus (STN) is an effective therapeutic target for deep brain stimulation (DBS) for Parkinson's disease (PD), and histamine levels are elevated in the basal ganglia in PD patients. However, the effect of endogenous histaminergic modulation on STN neuronal activities and the neuronal mechanism underlying STN-DBS are unknown. Here, we report that STN neuronal firing patterns are more crucial than firing rates for motor control. Histamine excited STN neurons, but paradoxically ameliorated parkinsonian motor deficits, which we attributed to regularizing firing patterns of STN neurons via the hyperpolarization-activated cyclic nucleotide-gated channel 2 (HCN2) channel coupled to the H2 receptor. Intriguingly, DBS increased histamine release in the STN and regularized STN neuronal firing patterns under parkinsonian conditions. HCN2 contributed to the DBS-induced regularization of neuronal firing patterns, suppression of excessive ß oscillations, and alleviation of motor deficits in PD. The results reveal an indispensable role for regularizing STN neuronal firing patterns in amelioration of parkinsonian motor dysfunction and a functional compensation for histamine in parkinsonian basal ganglia circuitry. The findings provide insights into mechanisms of STN-DBS as well as potential therapeutic targets and STN-DBS strategies for PD.

20.
Anal Bioanal Chem ; 410(29): 7663-7670, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30267271

RESUMO

Novel porous Co3O4 nanosheets (NSs) were synthesized on the flexible carbon cloth (CC) substrate by a facile hydrothermal method and applied to construct a non-enzymatic sensor for glucose detection. The sensor is based on the electro-catalytic oxidation of glucose on the surface of Co3O4 NSs. Since this particular nanostructure can provide large surface area and more active sites, the Co3O4 NSs non-enzymatic sensor exhibits excellent analytical performance, such as a high sensitivity (8506 µA mM-1 cm-2), a fast response time (less than 6 s), low detection limit of 1 µM, good selectivity, and long-term stability. The results suggest that the porous Co3O4 NSs have great potential applications in the development of sensors for enzyme-free detection of glucose.

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