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1.
J Transl Med ; 18(1): 187, 2020 May 06.
Artigo em Inglês | MEDLINE | ID: mdl-32375846

RESUMO

BACKGROUND: The prognosis of patients with advanced schistosomiasis is poor. Pre-existing prognosis studies did not differentiate the causes of the deaths. The objectives were to evaluate the 2-year overall survival (OS) and advanced schistosomiasis-specific survival (ASS) in patients with advanced schistosomiasis after discharge through competing risk analysis and to build predictive nomograms. METHODS: Data was extracted from a previously constructed database from Hubei province. Patients were enrolled from September 2014 to January 2015, with follow up to January 2017. OS and ASS were primary outcome measures. Nomograms for estimating 2-year OS and ASS rates after discharge were established based on univariate and multivariate Cox regression model and Fine and Gray's model. Their predictive performances were evaluated using C-index and validated in both internal and external validation cohorts. RESULTS: The training cohort included 1487 patients with advanced schistosomiasis. Two-year mortality rate of the training cohort was 8.27% (123/1487). Competing events accounted for 26.83% (33/123). Older age, splemomegaly clinical classification, abnormal serum DBil, AST, ALP and positive HBsAg were significantly associated with 2-year OS. Older age, splemomegaly clinical classification, abnormal serum AST, ALP and positive HBsAg were significantly associated with 2-year ASS. The established nomograms were well calibrated, and had good discriminative ability, with a C-index of 0.813 (95% CI 0.803-0.823) for 2-year OS prediction and 0.834 (95% CI 0.824-0.844) for 2-year ASS prediction. Their predictive performances were well validated in both internal and external validation cohorts. CONCLUSION: The effective predictors of 2-year OS and ASS were discovered through competing risk analysis. The nomograms could be used as convenient predictive tools in clinical practice to guide follow-up and aid accurate prognostic assessment.

3.
Chem Biodivers ; 2020 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-32249503

RESUMO

The present study investigated the allelopathic effects of aqueous extracts of Castanea henryi litter on the growth and physiological responses of Brassica pekinensis and Zea mays. Treatment with high concentrations of leaf extract (0.05 g/ml for B. pekinensis and 0.10 g/ml for Z. mays) significantly increased malonaldehyde content and reduced seed germination, seedling growth, chlorophyll content, and the activity levels of antioxidant enzymes. These effects generally increased with increasing extract concentration. However, in Z. mays, low extract concentrations actually promoted seed germination, shoot growth, chlorophyll content, and antioxidant enzyme activity. The allelopathic effects of the various C. henryi extracts decreased as follows: leaf extract > twig extract > shell extract. Eleven potential allelochemicals including rutin, quercetin, luteolin, procyanidin A2, kaempferol, allantoin, propionic acid, salicylic acid, jasmonic acid, methylmalonic acid, and gentisic acid were identified in the leaves of C. henryi which were linked to the strongest allelopathic effects. These findings suggest that the allelopathic effects of C. henryi differ depending on receptor plant species, and that leaves are the most allelopathic litter in C. henryi.

4.
Neuroscience ; 433: 174-183, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32198011

RESUMO

Sleep loss or insomnia is among the contributing factors of cognitive deficit, the underlying mechanisms of which remain largely elusive. The endocannabinoid (eCB) system plays a role in sleep, while it is unknown if it is involved in the regulation of memory retrieval by sleep deprivation. In addition, it still controversial how rapid-eye-movement sleep deprivation (REMSD) affects the spatial memory of adolescent mice. Here, we found that 24-h REMSD impairs spatial memory retrieval of adolescent mice in an object-place recognition task, which was rescued by NESS0327, a neutral cannabinoid receptor 1 (CB1R) antagonist. Mechanistically, REMSD induced eCB-mediated short-term and long-term synaptic plasticity changing including depolarization-induced suppression of inhibition (DSI) in the pyramidal neurons of the hippocampus, in which long-term synaptic plasticity changing was rescued by NESS0327. REMSD downregulated monoacylglycerol lipase, a hydrolase for the endocannabinoid 2-arachidonoylglycerol (2-AG), suggesting the involvement of eCB accumulation and the consequent synaptic plasticity in REMSD-elicited memory impairment in adolescent mice. These findings shed light on the role of sleep disorders in learning and memory deficit of adolescents.

5.
Cell Death Dis ; 11(2): 128, 2020 Feb 18.
Artigo em Inglês | MEDLINE | ID: mdl-32071296

RESUMO

Autophagy, a conserved cellular degradation and recycling process, can be enhanced by nutrient depletion, oxidative stress or other harmful conditions to maintain cell survival. 6-Hydroxydopamine/ascorbic acid (6-OHDA/AA) is commonly used to induce experimental Parkinson's disease (PD) lesions by causing oxidative damage to dopaminergic neurons. Activation of autophagy has been observed in the 6-OHDA-induced PD models. However, the mechanism and exact role of autophagy activation in 6-OHDA PD model remain inconclusive. In this study, we report that autophagy was triggered via mucolipin 1/calcium/calcineurin/TFEB (transcription factor EB) pathway upon oxidative stress induced by 6-OHDA/AA. Interestingly, overexpression of TFEB alleviated 6-OHDA/AA toxicity. Moreover, autophagy enhancers, Torin1 (an mTOR-dependent TFEB/autophagy enhancer) and curcumin analog C1 (a TFEB-dependent and mTOR-independent autophagy enhancer), significantly rescued 6-OHDA/AA-induced cell death in SH-SY5Y cells, iPSC-derived DA neurons and mice nigral DA neurons. The behavioral abnormality of 6-OHDA/AA-treated mice can also be rescued by Torin 1 or C1 administration. The protective effects of Torin 1 and C1 can be blocked by autophagy inhibitors like chloroquine (CQ) or by knocking down autophagy-related genes TFEB and ATG5. Taken together, this study supports that TFEB-mediated autophagy is a survival mechanism during oxidative stress and pharmacological enhancement of this process is a neuroprotective strategy against oxidative stress-associated PD lesions.

6.
Sci Rep ; 10(1): 2717, 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32066812

RESUMO

Due to their high specific surface area, graphene oxide and graphene oxide-base nanoparticles have great potential both in dual-drug delivery and combination chemotherapy. Herein, we developed cisplatin (Pt) and doxorubicin (DOX) dual-drug-loaded PEGylated nano-graphene oxide (pGO) to facilitate combined chemotherapy in one system. In this study, nano-sized pGO-Pt/DOX ranged around 161.50 nm was fabricated and characterized using zeta-potential, AFM, TEM, Raman, UV-Vis, and FTIR analyses. The drug delivery efficacy of Pt was enhanced through the introduction of pGO, and the final weight ratio of DOX: Pt: pGO was optimized to 0.376: 0.376: 1. In vitro studies revealed that pGO-Pt/DOX nanoparticles could be effectively delivered into tumor cells, in which they induced prominent cell apoptosis and necrosis and exhibited higher growth inhibition than the single drug delivery system or free drugs. The pGO-Pt/DOX induced the most prominent cancer cell apoptosis and necrosis rate with 18.6%, which was observed almost 2 times higher than that of pGO-Pt or pGO-DOX groups. in the apoptosis and necrotic quadrants In vivo data confirmed that the pGO-Pt/DOX dual-drug delivery system attenuated the toxicity of Pt and DOX to normal organs compared to free drugs. The tumor inhibition data, histopathology observations, and immunohistochemical staining confirmed that the dual-drug delivery system presented a better anticancer effect than free drugs. These results clearly indicated that the pGO-Pt/DOX dual-drug delivery system provided the means for combination drug delivery in cancer treatment.

7.
Int J Mol Sci ; 21(4)2020 Feb 22.
Artigo em Inglês | MEDLINE | ID: mdl-32098449

RESUMO

Abstract: TFEB (transcription factor EB), which is a master regulator of autophagy and lysosome biogenesis, is considered to be a new therapeutic target for Parkinson's disease (PD). However, only several small-molecule TFEB activators have been discovered and their neuroprotective effects in PD are unclear. In this study, a curcumin derivative, named E4, was identified as a potent TFEB activator. Compound E4 promoted the translocation of TFEB from cytoplasm into nucleus, accompanied by enhanced autophagy and lysosomal biogenesis. Moreover, TFEB knockdown effectively attenuated E4-induced autophagy and lysosomal biogenesis. Mechanistically, E4-induced TFEB activation is mainly through AKT-MTORC1 inhibition. In the PD cell models, E4 promoted the degradation of α-synuclein and protected against the cytotoxicity of MPP+ (1-methyl-4-phenylpyridinium ion) in neuronal cells. Overall, the TFEB activator E4 deserves further study in animal models of neurodegenerative diseases, including PD.

8.
Cells ; 9(2)2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-32012902

RESUMO

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aß and Tau) aggregates in the brain, causing progressive dementia. Increasing studies have provided evidence that the defect in protein-degrading systems, especially the autophagy-lysosome pathway (ALP), plays an important role in the pathogenesis of AD. Recent studies have demonstrated that AD-associated protein aggregates can be selectively recognized by some receptors and then be degraded by ALP, a process termed aggrephagy. In this study, we reviewed the role of aggrephagy in AD development and discussed the strategy of promoting aggrephagy using small molecules for the treatment of AD.

9.
Sci Total Environ ; 711: 135184, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32000351

RESUMO

6-Hydroxy-BDE-47 (6-OH-BDE-47) is an important in vivo metabolite derived from 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), a ubiquitous environmental pollutant. The chemical has been widely detected in environmental and biological samples. However, as a potential neurotoxin, whether 6-OH-BDE-47 could promote the development of typical neurodegenerative diseases such as Parkinson's disease (PD) is still unknown. Here, we tested the potential PD-related neurotoxic effect of 6-OH-BDE-47 in rat. The chemical with levels of 0.1, 1 and 10 µg was stereotaxically injected into the right midbrain regions of rat where contain abundant dopaminergic neurons. The resulting deteriorated motor function and decreased levels of striatal dopamine and nigrostriatal tyrosine hydroxylase indicate the dopaminergic neuron loss after the injection. Proteomics study revealed that protein degradation pathways were affected. Western blot analysis confirmed that 6-OH-BDE-47 could inhibit ubiquitination and autophagy, resulting in the increased formation of α-synuclein (α-syn) aggregate, an important pathological hallmark of PD. Overall, our study demonstrated that the 6-OH-BDE-47 administration could induce motor defect by impairing dopaminergic system and promote α-syn aggregation by inhibiting ubiquitination and autophagy, suggesting that the occurrence of 6-OH-BDE-47 in brain could be a risk for developing PD.


Assuntos
Doença de Parkinson , Animais , Neurônios Dopaminérgicos , Bifenil Polibromatos , Ratos , Ratos Sprague-Dawley , alfa-Sinucleína
10.
Redox Biol ; : 101445, 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-32037305

RESUMO

TFEB (transcription factor EB) and TFE3 (transcription factor E3) are "master regulators" of autophagy and lysosomal biogenesis. The stress response p38 mitogen-activated protein (MAP) kinases affect multiple intracellular responses including inflammation, cell growth, differentiation, cell death, senescence, tumorigenesis, and autophagy. Small molecule p38 MAP kinase inhibitors such as SB202190 are widely used in dissection of related signal transduction mechanisms including redox biology and autophagy. Here, we initially aimed to investigate the links between p38 MAP kinase and TFEB/TFE3-mediated autophagy and lysosomal biogenesis. Unexpectedly, we found that only SB202190, rather than several other p38 inhibitors, promotes TFEB and TFE3 to translocate from the cytosol into the nucleus and subsequently enhances autophagy and lysosomal biogenesis. In addition, siRNA-mediated Tfeb and Tfe3 knockdown effectively attenuated SB202190-induced gene expression and lysosomal biogenesis. Mechanistical studies showed that TFEB and TFE3 activation in response to SB202190 is dependent on PPP3/calcineurin rather than on the inhibition of p38 or MTOR signaling, the main pathway for regulating TFEB and TFE3 activation. Importantly, SB202190 increased intracellular calcium levels, and calcium chelator BAPTAP-AM blocked SB202190-induced TFEB and TFE3 activation as well as autophagy and lysosomal biogenesis. Moreover, endoplasmic reticulum (ER) calcium is required for TFEB and TFE3 activation in response to SB202190. In summary, we identified a previously uncharacterized role of SB202190 in activating TFEB- and TFE3-dependent autophagy and lysosomal biogenesis via ER calcium release and subsequent calcium-dependent PPP3/calcineurin activation, leading to dephosphorylation of TFEB and TFE3. Given the importance of p38 MAP kinase invarious conditions including oxidative stress, the findings collectively indicate that SB202190 should not be used as a specific inhibitor for elucidating the p38 MAP kinase biological functions due to its potential effect on activating autophagy-lysosomal axis.

11.
FASEB J ; 34(2): 2011-2023, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31907997

RESUMO

Src Homology 2-containing Inositol Phosphatase-1 (SHIP-1) is a target of miR-155, a pro-inflammatory factor. Deletion of the SHIP-1 gene in mice caused spontaneous lung inflammation and fibrosis. However, the role and function of endothelial miR-155 and SHIP-1 in lung fibrosis remain unknown. Using whole-body miR-155 knockout mice and endothelial cell-specific conditional miR-155 (VEC-Cre-miR-155 or VEC-miR-155) or SHIP-1 (VEC-SHIP-1) knockout mice, we assessed endothelial-mesenchymal transition (EndoMT) and fibrotic responses in bleomycin (BLM) induced lung fibrosis models. Primary mouse lung endothelial cells (MLEC) and human umbilical vein endothelial cells (HUVEC) with SHIP-1 knockdown were analyzed in TGF-ß1 or BLM, respectively, induced fibrotic responses. Fibrosis and EndoMT were significantly reduced in miR-155KO mice and changes in EndoMT markers in MLEC after TGF-ß1 stimulation confirmed the in vivo findings. Furthermore, lung fibrosis and EndoMT responses were reduced in VEC-miR-155 mice but significantly enhanced in VEC-SHIP-1 mice after BLM challenge. SHIP-1 knockdown in HUVEC cells resulted in enhanced EndoMT induced by BLM. Meanwhile, these changes involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways. These studies demonstrate that endothelial miR-155 plays an important role in fibrotic responses in the lung through EndoMT. Endothelial SHIP-1 is essential in controlling fibrotic responses and SHIP-1 is a target of miR-155. Endothelial cells are an integral part in lung fibrosis.

12.
Clin Cancer Res ; 26(1): 110-121, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31527167

RESUMO

PURPOSE: Preclinical data identified the cyclin-dependent kinase 4/6 (CDK4/6) inhibitor palbociclib as synergistic with antiestrogens in inhibiting growth of hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) human breast cancer models. This observation was validated clinically in the randomized, placebo-controlled, phase III PALOMA-2 study. EXPERIMENTAL DESIGN: To determine markers of sensitivity and resistance to palbociclib plus letrozole, we performed comprehensive biomarker analyses, investigating the correlation with progression-free survival (PFS), on baseline tumor tissues from PALOMA-2. RESULTS: Despite a broad biomarker search, palbociclib plus letrozole demonstrated consistent PFS gains versus placebo plus letrozole, with no single biomarker or cassette of markers associated with lack of benefit from combination treatment. Palbociclib plus letrozole confers efficacy on both luminal A and B patients. Higher CDK4 levels were associated with endocrine resistance which was mitigated by the addition of palbociclib, whereas lower PD-1 levels were associated with greater palbociclib plus letrozole benefit. Tumors with more active growth factor signaling, as exemplified by increased expression of FGFR2 and ERBB3 mRNA, appeared to be associated with greater PFS gain from the addition of palbociclib. CONCLUSIONS: These data underscore the importance of CDK4/6 signaling in HR+/HER2- breast cancer and suggest that the interplay between steroid hormone and peptide growth factor signaling could drive dependence on CDK4/6 signaling.See related commentary by Anurag et al., p. 3.

13.
J Neurol Sci ; 409: 116607, 2020 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-31830611

RESUMO

Malignant cerebral edema (MCE) is a life-threatening complication of acute cerebral stroke. To date, the focus has been on symptomatic treatment, rather than on prevention. Therefore, to identify high-risk patients and explore potential therapeutic approaches, we investigated the possible predictors of MCE. Specifically, we performed a meta-analysis to identify the potential predictors of MCE in patients with acute cerebral infarction. We searched the MEDLINE, Embase, Cochrane, China National Knowledge Infrastructure, Wanfang Data, and VIP databases from their inception to July 2018 for cohort and case control studies on the predictors of MCE in patients with cerebral infarction. Forty-seven eligible studies containing a total of 45,826 patients were included. Our results suggest that the risk of MCE is higher in case of severe clinical symptoms and large infarct volumes. Additionally, male sex, older age, and a history of stroke and smoking were protective factors against MCE in cerebral infarction patients. Furthermore, thrombolytic therapy and recanalization substantially decreased the risk of MCE in patients with acute stroke. Higher admission temperature (in the subgroup with admission ≤12 h after onset), higher admission blood pressure, and admission leukocytes were also MCE predictors. Our findings facilitate the early prediction of MCE and may contribute to potential therapeutic approaches.

14.
J Org Chem ; 85(4): 2355-2368, 2020 Feb 21.
Artigo em Inglês | MEDLINE | ID: mdl-31886670

RESUMO

The coenzyme NAD(P)H plays an important role in electron as well as proton transmission in the cell. Thus, a variety of NAD(P)H models have been involved in biomimetic reduction, such as stoichiometric Hantzsch esters and achiral regenerable dihydrophenantheridine. However, the development of a general and new-generation biomimetic asymmetric reduction is still a long-term challenge. Herein, a series of chiral and regenerable NAD(P)H models with central, axial, and planar chiralities have been designed and applied in biomimetic asymmetric reduction using hydrogen gas as a terminal reductant. Combining chiral NAD(P)H models with achiral transfer catalysts such as Brønsted acids and Lewis acids, the substrate scope could be also expanded to imines, heteroaromatics, and electron-deficient tetrasubstituted alkenes with up to 99% yield and 99% enantiomeric excess (ee). The mechanism of chiral regenerable NAD(P)H models was investigated as well. Isotope-labeling reactions indicated that chiral NAD(P)H models were regenerated by the ruthenium complex under hydrogen gas first, and then the hydride of NAD(P)H models was transferred to unsaturated bonds in the presence of transfer catalysts. In addition, density functional theory calculations were also carried out to give further insight into the transition states for the corresponding transfer catalysts.

15.
J Food Drug Anal ; 28(1): 132-146, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31883601

RESUMO

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Amyloid-ß (Aß) and hyper-phosphorylated tau accumulation are accountable for the progressive neuronal loss and cognitive impairments usually observed in AD. Currently, medications for AD offer moderate symptomatic relief but fail to cure the disease; hence development of effective and safe drugs is urgently needed for AD treatment. In this study, we investigated a Chinese medicine (CM) formulation named NeuroDefend (ND), for reducing amyloid ß (Aß) and tau pathology in transgenic AD mice models. Regular oral administration of ND improved cognitive function and memory in 3XTg-AD and 5XFAD mice. In addition, ND reduced beta-amyloid precursor protein (APP), APP C-terminal fragments (CTF-ß/α), Aß and 4G8 positive Aß burden in 3XTg-AD and 5XFAD mice. Furthermore, ND efficiently reduced the levels of insoluble phospho-tau protein aggregates and AT8 positive phospho tau neuron load in 3XTg-AD mice. Hence, ND could be a promising candidate for the treatment of AD in humans.

16.
Aging Cell ; 19(2): e13069, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31858697

RESUMO

Accumulating studies have suggested that targeting transcription factor EB (TFEB), an essential regulator of autophagy-lysosomal pathway (ALP), is promising for the treatment of neurodegenerative disorders, including Alzheimer's disease (AD). However, potent and specific small molecule TFEB activators are not available at present. Previously, we identified a novel TFEB activator named curcumin analog C1 which directly binds to and activates TFEB. In this study, we systematically investigated the efficacy of curcumin analog C1 in three AD animal models that represent beta-amyloid precursor protein (APP) pathology (5xFAD mice), tauopathy (P301S mice) and the APP/Tau combined pathology (3xTg-AD mice). We found that C1 efficiently activated TFEB, enhanced autophagy and lysosomal activity, and reduced APP, APP C-terminal fragments (CTF-ß/α), ß-amyloid peptides and Tau aggregates in these models accompanied by improved synaptic and cognitive function. Knockdown of TFEB and inhibition of lysosomal activity significantly inhibited the effects of C1 on APP and Tau degradation in vitro. In summary, curcumin analog C1 is a potent TFEB activator with promise for the prevention or treatment of AD.

17.
BMC Psychiatry ; 19(1): 386, 2019 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-31805901

RESUMO

BACKGROUND: China has experienced rapid socioeconomic, and health transitions over the last four decades, and urban-rural disparities are becoming increasingly apparent. Research on depression among rural and urban students can provide evidence on the relationship between sociodemographic characteristics and adolescent depression. METHODS: We examined the association between sociodemographic characteristics and adolescent depression among 3605 students from Wuhan city and Jianli county that was recruited from the local junior middle school via a cross-sectional study. Univariate and multivariate logistic regression models were used to explore the sociodemographic characteristics of adolescent depression in urban and rural areas, respectively. Nomograms were constructed to calculate individual depression risk of junior middle school students. RESULTS: 32.47% of rural students and 35.11% of urban students display depressive symptoms. The protective factors of depression in urban students are exercise habit, younger, key class, better academic achievement and males, while Left-behind children (LBC), poor academic achievement and females had higher depression risk in rural area. Two nomograms were constructed to screen the adolescent depression in urban and rural junior middle school students, respectively. The clinical tools were well calibrated. CONCLUSION: The field-based research examined sociodemographic characteristics potentially associated with adolescent depression and offered an effective and convenient tool of individualized depression risk evaluation for junior middle school students. Future longitudinal epidemiologic research on adolescent depression may help to further validate the discovery of present study, which will support developing policies and practices to minimize the factors of adolescent depression.

18.
BMC Neurol ; 19(1): 347, 2019 Dec 29.
Artigo em Inglês | MEDLINE | ID: mdl-31884967

RESUMO

BACKGROUND: Large hemispheric infarction (LHI) is a severe form of stroke with high mortality and disability rates. The purpose of this study was to explore predictive indicators of the in-hospital mortality of LHI patients treated conservatively without decompressive hemicraniectomy. METHOD: We performed a retrospective study of 187 consecutive patients with LHI between January 1, 2016 to May 31, 2019. The receiver operating curves were preformed to evaluate predictive performance of demographics factors, biomarkers and radiologic characteristics. Significant prognostic factors were combined to build a nomogram to predict the risk of in-hospital death of individual patients. RESULT: One hundred fifty-eight patients with LHI were finally enrolled, 58 of which died. Through multivariate logistic regression analysis, we identified that independent prognostic factors for in-hospital death were age (adjusted odds ratio [aOR] = 1.066; 95% confidence interval [CI], 1.025-1.108; P = 0.001), midline shift (MLS, aOR = 1.330, 95% CI, 1.177-1.503; P <  0.001), and neutrophil-to-lymphocyte ratio (NLR, aOR = 3.319, 95% CI, 1.542-7.144; P = 0.002). NLR may serve as a better predictor than white blood count (WBC) and neutrophil counts. Lastly, we used all of the clinical characteristics to establish a nomogram for predicting the prognosis, area under the curve (AUC) of this nomogram was 0.858 (95% CI, 0.794-0.908). CONCLUSION: This study shows that age, MLS, and admission NLR value are independent predictors of in-hospital mortality in patients with LHI. Moreover, nomogram, serve as a precise and convenient tool for the prognosis of LHI patients.


Assuntos
Infarto da Artéria Cerebral Média/mortalidade , Nomogramas , Adulto , Idoso , Área Sob a Curva , Feminino , Mortalidade Hospitalar , Humanos , Infarto da Artéria Cerebral Média/patologia , Masculino , Pessoa de Meia-Idade , Razão de Chances , Prognóstico , Curva ROC , Estudos Retrospectivos , Fatores de Risco
19.
ACS Appl Mater Interfaces ; 11(39): 36141-36153, 2019 Oct 02.
Artigo em Inglês | MEDLINE | ID: mdl-31503444

RESUMO

Wound treatment is a long-lasting clinical issue. Poor angiogenesis leading to delayed wound closure causes huge challenges for healing. Functional electrospun membranes have been established as an efficient strategy to promote wound recovery by protecting and improving vascular regeneration. Here, we aimed to investigate the effect of tazarotene, an active drug for angiogenesis, loaded in aligned electrospun nanofibrous barrier on a soft tissue wound. This aligned membrane was arranged in a single direction, and tazarotene could be released from its nanofibers sustainably. The in vitro study demonstrated that compared with the random drug-loaded or other control groups, the aligned tazarotene-loaded membranes [poly-caprolactone (PCL)/AT] could stimulate proliferation, migration, angiogenesis, and vascular endothelial growth factor secretion and its gene expression of human umbilical vein endothelial cells. Furthermore, the in vivo model showed that the prepared tazarotene-loaded aligned membrane significantly accelerated the speed of healing, improved the neovascularization and re-epithelialization, and inhibited the inflammatory reaction in the wound area. All these results above indicated that the PCL/AT nanofibrous dressing, which could promote angiogenesis because of both stimulation of structure and chemical signals, is a promising wound-caring material.


Assuntos
Sistemas de Liberação de Medicamentos , Membranas Artificiais , Neovascularização Fisiológica/efeitos dos fármacos , Ácidos Nicotínicos , Pele , Cicatrização/efeitos dos fármacos , Animais , Células Endoteliais da Veia Umbilical Humana/metabolismo , Células Endoteliais da Veia Umbilical Humana/patologia , Humanos , Masculino , Ácidos Nicotínicos/química , Ácidos Nicotínicos/farmacologia , Ratos , Ratos Sprague-Dawley , Pele/lesões , Pele/metabolismo , Pele/patologia
20.
Environ Pollut ; 254(Pt A): 113007, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31421570

RESUMO

Parabens are extensively applied in cosmetics, drugs or food as preservatives and have become common pollutants in environmental media. However, data on human exposure to these chemicals is still limited, especially for children. This study aimed to investigate parabens in urine samples of children and to evaluate the cumulative risk of paraben exposure. Five short-chain parabens were measured in 255 urine samples collected from children in a kindergarten and elementary schools from South China. Methyl paraben (MeP), ethyl paraben (EtP) and n-propyl paraben (PrP) were widely detected in urine samples (detection rates > 94.9%), indicating their widespread exposure. The urinary median concentrations of MeP, EtP and PrP were 2.25, 0.33 and 0.50 µg/L, respectively. Significantly positive correlations (p < 0.01) were observed between MeP and PrP in urine, suggesting similar sources and/or metabolic pathways of these two chemicals. The median estimated daily intakes (EDIs) of parabens were determined to be 18.1 and 9.79 µg/kg-bw/day for kindergarten children and elementary school students, respectively. Estimation of human intake and exposure risks indicated potential risks of PrP exposure for elementary school students. This is the first study addressing paraben exposure in South China children.


Assuntos
Exposição Ambiental/estatística & dados numéricos , Poluentes Ambientais/urina , Parabenos/metabolismo , Líquidos Corporais/metabolismo , Criança , China , Cosméticos/análise , Exposição Ambiental/análise , Alimentos , Humanos , Parabenos/análise , Fatores de Risco , Instituições Acadêmicas , Estudantes
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