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1.
Bioresour Technol ; 294: 122151, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31557652

RESUMO

Filamentous sludge bulking poses great threats to operational stability of aerobic granular sludge. Exploration of the microbial community aids knowledge of the causative factors to sludge bulking and guides directions for corresponding actions for prevention and controlling. Detailed changes of bacterial community within the non-bulking and bulking were performed and compared with a non-specific method through 1‰ (v/v) hydrogen peroxide (H2O2) addition. Results revealed that non-bulking/bulking granules maintained effective carbon and nitrogen removal, while bulking completely deteriorated enhanced biological phosphorus removal (EBPR). Excess extracellular polymeric substances (EPS) especially polysaccharide (PS) were directly linked with sludge bulking and abundant PS contributed to subsequent granular re-stability. Filamentous bulking dramatically altered the bacterial populations and 1‰ H2O2 effectively controlled bulking by eliminating causative filaments Singulisphaera and Thiothrix. Together, this study provides new insights into the non-bulking/bulking granules and could direct the prevention and control of filamentous bulking in aerobic granules.

2.
J Mol Endocrinol ; 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31404910

RESUMO

Neuropathic pain represents one of the most common complications associated with diabetes mellitus (DM) that impacts quality of life. Accumulating studies have highlighted the involvement of microRNAs (miRNAs) in DM. Thus, the current study aimed to investigate the roles of microRNA-155 (miR-155) in diabetic peripheral neuropathy (DPN). In vitro DPN models were established using rat Schwann cells (SCs) by treatment with 5.5 mM glucose. Gain- or loss-of-function studies were conducted to determine the effect of miR-155 on Nrf2, cellular function, reactive oxygen species, and inflammation. Rat DNP models were established by streptozotocin injection and damage of sciatic nerve. Next, miR-155 antagomir or agomir was employed to investigate the effects associated with miR-155 on motor and sciatic nerve conduction velocity (MNCV, SNCV), angiogenesis and inflammatory response in vivo. Nrf2 was identified to be a target of miR-155 by dual-luciferase reporter gene assay. Silencing of miR-155 or restoration of Nrf2 promoted cell proliferation, inhibited apoptosis and alleviated inflammation in vitro. miR-155 antagomir-induced inhibition increased MNCV and SNCV, strengthened angiogenesis and alleviated inflammation in DPN rats. Additionally, the effects exerted by miR-155 were reversed when Nrf2 was restored both in vitro and in vivo. Taken together, the key findings of our study provide evidence indicating that miR-155 targeted and suppressed Nrf2 in DPN. miR-155 silencing was found to alleviate sciatic nerve injury in DPN, highlighting its potential as a therapeutic target for DPN.

3.
Pharm Biol ; 57(1): 453-459, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31311385

RESUMO

Context: Neuroligin-1 (NLGN1) is a cell adhesion protein located on the excitatory postsynaptic membrane. ß-Amyloid (Aß)-induced neuroinflammation decreases NLGN1 expression through epigenetic mechanisms. Triptolide (T10) and tripchlorolide (T4) exert protective effects on synapses in Alzheimer's disease (AD) mice, but the mechanisms remain unclear. Objective: The effects of T10 and T4 on hippocampal NLGN1 expression in AD mice and the epigenetic mechanisms were assessed using chromatin immunoprecipitation and methylated DNA immunoprecipitation. Materials and methods: Sixty APP/PS1 transgenic mice were randomly divided into an AD model group, a T10-treated group and a T4-treated group (n = 20); 20 wild-type littermates served as the control group. APP/PS1 transgenic mice were intraperitoneally injected with T10 (0.1 mg/kg) and T4 (25 µg/kg) once per day for 60 days. NLGN1 expression was examined using western blotting and quantitative PCR. Results: T10 and T4 increased the levels of the NLGN1 protein and mRNA in hippocampus of AD mice. T10 and T4 inhibited the binding of HDAC2 (p< 0.01) and MeCP2 (p< 0.01 and p< 0.05, respectively) to the NLGN1 promoter, and cytosine methylation (1.2305 ± 0.1482/1.2554 ± 0.3570 vs. 1.6578 ± 0.1818, p< 0.01) at the NLGN1 promoter in the hippocampus of AD mice. T10 and T4 increased the level of acetylated histone H3 (0.7733 ± 0.1611/0.8241 ± 0.0964 vs. 0.5587 ± 0.0925, p< 0.01) at the NLGN1 promoter in the hippocampus of AD mice. Conclusions: T10 and T4 may increase hippocampal NLGN1 expression in AD mice through epigenetic mechanisms, providing a new explanation for the mechanism underlying the protective effects of T10 and T4 on synapses.

4.
J Org Chem ; 84(16): 10490-10500, 2019 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-31333031

RESUMO

A versatile protocol for the direct thiolation of an inert sp2 C-H bond is presented via a catalytic amount of copper catalysis, by switching related Brønsted bases and regulating the reaction time, and the corresponding mono- and dithiolation products can be obtained selectively in moderate to good yields. The reaction exhibits a relatively broad substrate scope and a good functional group tolerance, even with different heterocyclic amides and alkyl thiols.

5.
Biomed Pharmacother ; 117: 109092, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31203134

RESUMO

BACKGROUND: 17ß-Estradiol (E2) is a critical regulator of trophoblast function during pregnancy. Serum- and glucocorticoid-inducible kinase (SGK1) has been shown to regulate specific cellular targets downstream of E2. However, whether and how SGK1 directly mediates the regulatory effects of E2 on trophoblasts functions remain unknown. METHODS: SGK1 expression in human villous samples and serum E2 levels were measured in women with early pregnancy loss (EPL) and healthy pregnant women. The effect of E2 on SGK1 regulation was assessed using luciferase reporter gene assay and Chromatin Immunoprecipitation assay. The mediation of regulatory effects of E2 by SGK1 on trophoblast functions including cell viability, invasion and related signaling molecules such as B cell leukemia/lymphoma 6, E-cadherin, matrix metalloproteinase 2, α-ENaC, vascular endothelial growth factor, and the phosphorylation status of FOXO1 and AKT were evaluated in HTR8/SVneo cells transfected with SGK1 knockdown plasmid with/without E2 treatment. RESULTS: SGK1 protein levels in human villous samples and serum E2 levels were decreased in patients with EPL compared to controls. E2 (10 nM) increased SGK1 promoter activity directly through estrogen receptor. E2-activated SGK1 enhanced cell viability, invasion and downstream targets in trophoblast cells. SGK1 knockdown abrogated the above responses to E2 treatment. CONCLUSIONS: SGK1 mediates the effects of E2 on trophoblast viability and invasion, suggesting that SGK1 acts as a key node in regulating the cross-talk at the feto-maternal interface during the development of placenta and might be a potential therapeutic target for EPL.

6.
J Neuroeng Rehabil ; 16(1): 64, 2019 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-31159822

RESUMO

BACKGROUND: Different mechanical supporting strategies to the joints in the upper extremity (UE) may lead to varied rehabilitative effects after stroke. This study compared the rehabilitation effectiveness achieved by electromyography (EMG)-driven neuromuscular electrical stimulation (NMES)-robotic systems when supporting to the distal fingers and to the proximal (wrist-elbow) joints. METHODS: Thirty subjects with chronic stroke were randomly assigned to receive motor trainings with NMES-robotic support to the finger joints (hand group, n = 15) and with support to the wrist-elbow joints (sleeve group, n = 15). The training effects were evaluated by the clinical scores of Fugl-Meyer Assessment (FMA), Action Research Arm Test (ARAT), and Modified Ashworth Scale (MAS) before and after the trainings, as well as 3 months later. The cross-session EMG monitoring of EMG activation level and co-contraction index (CI) were also applied to investigate the recovery progress of muscle activations and muscle coordination patterns through the training sessions. RESULTS: Significant improvements (P < 0.05) in FMA full score, FMA shoulder/elbow (FMA-SE) and ARAT scores were found in both groups, whereas significant improvements (P < 0.05) in FMA wrist/hand (FMA-WH) and MAS scores were only observed in the hand group. Significant decrease of EMG activation levels (P < 0.05) of UE flexors was observed in both groups. Significant decrease in CI values (P < 0.05) was observed in both groups in the muscle pairs of biceps brachii and triceps brachii (BIC&TRI) and the wrist-finger flexors (flexor carpi radialis-flexor digitorum) and TRI (FCR-FD&TRI). The EMG activation levels and CIs of the hand group exhibited faster reductions across the training sessions than the sleeve group (P < 0.05). CONCLUSIONS: Robotic supports to either the distal fingers or the proximal elbow-wrist could achieve motor improvements in UE. The robotic support directly to the distal fingers was more effective than to the proximal parts in improving finger motor functions and in releasing muscle spasticity in the whole UE. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov , identifier NCT02117089; date of registration: April 10, 2014. https://clinicaltrials.gov/ct2/show/NCT02117089.

7.
Mol Med Rep ; 20(2): 1306-1312, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31173216

RESUMO

17ß­estradiol (E2) and aquaporin 2 (AQP2) are associated with endometrial receptivity, and E2 directly regulates AQP2 expression in endometrial cancer cells. The present study aimed to investigate the role of AQP2 in embryo implantation. Normal endometrial samples were collected at the Women's Hospital (Hangzhou, China) from women seeking in vitro fertilization and embryo transfer; women with endometrial abnormalities were excluded from the study. Samples were categorized into early­mid proliferative, late proliferative, early secretory, mid­secretory and late secretory phase groups, according to the menstrual cycle. The mRNA and protein expression levels of AQP2 were assessed in normal human endometrium in response to E2 via reverse transcription­quantitative polymerase chain reaction and western blotting, respectively. The effects of AQP2 on spheroid attachment were assessed using an in vitro co­culture assay with small interfering (si)RNA against AQP2. The highest expression levels of AQP2 were observed in the late proliferative and mid­secretory phases, with the lowest levels detected in the early proliferative and late secretory phases. In addition, treatment with 10­9 or 10­7 M E2 for 24 h upregulated AQP2 in the cultured endometrium. Knockdown of AQP2 by siRNA significantly decreased JAr spheroid attachment; however, this effect was significantly reversed when AQP2 siRNA­transfected cells were treated with 10­7 M E2. The results of the present study suggested that AQP2 expression levels in human endometrium may be mediated by estrogen, and low AQP2 expression levels may be a potential cause of impaired uterine receptivity.

8.
Cell Rep ; 27(10): 3034-3048.e5, 2019 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-31167146

RESUMO

Dermal γδT cells play critical roles in skin homeostasis and inflammation. However, the underlying molecular mechanisms by which these cells are activated have not been fully understood. Here, we show that the mechanistic or mammalian target of rapamycin (mTOR) and STAT3 pathways are activated in dermal γδT cells in response to innate stimuli such as interleukin-1ß (IL-1ß) and IL-23. Although both mTOR complex 1 (mTORC1) and mTORC2 are essential for dermal γδT cell proliferation, mTORC2 deficiency leads to decreased dermal γδT17 cells. It appears that mitochondria-mediated oxidative phosphorylation is critical in this process. Notably, although the STAT3 pathway is critical for dermal Vγ4T17 effector function, it is not required for Vγ6T17 cells. Transcription factor IRF-4 activation promotes dermal γδT cell IL-17 production by linking IL-1ß and IL-23 signaling. The absence of mTORC2 in dermal γδT cells, but not STAT3, ameliorates skin inflammation. Taken together, our results demonstrate that the mTOR-STAT3 signaling differentially regulates dermal γδT cell effector function in skin inflammation.

9.
Macromol Rapid Commun ; 40(17): e1900096, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31111979

RESUMO

Molecular imprinting is an approach of generating imprinting cavities in polymer structures that are compatible with the target molecules. The cavities have memory for shape and chemical recognition, similar to the recognition mechanism of antigen-antibody in organisms. Their structures are also called biomimetic receptors or synthetic receptors. Owing to the excellent selectivity and unique structural predictability of molecularly imprinted materials (MIMs), practical MIMs have become a rapidly evolving research area providing key factors for understanding separation, recognition, and regenerative properties toward biological small molecules to biomacromolecules, even cell and microorganism. In this review, the characteristics, morphologies, and applicability of currently popular carrier materials for molecular imprinting, especially the fundamental role of hydrogels, porous materials, hierarchical nanoparticles, and 2D materials in the separation and recognition of biological templates are discussed. Moreover, through a series of case studies, emphasis is given on introducing imprinting strategies for biological templates with different molecular scales. In particular, the differences and connections between small molecular imprinting (bulk imprinting, "dummy" template imprinting, etc.), large molecular imprinting (surface imprinting, interfacial imprinting, etc.), and cell imprinting strategies are demonstrated in detail. Finally, future research directions are provided.

10.
Cell Rep ; 27(8): 2335-2353.e6, 2019 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-31116980

RESUMO

Zinc-finger E-box binding homeobox 1 (Zeb1) is a key regulator of epithelial-mesenchymal transition and cancer metastasis. Mutation of ZEB1 is associated with human diseases and defective brain development. Here we show that downregulation of Zeb1 expression in embryonic cortical neural progenitor cells (NPCs) is necessary for proper neuronal differentiation and migration. Overexpression of Zeb1 during neuronal differentiation, when its expression normally declines, blocks NPC lineage progression and disrupts multipolar-to-bipolar transition of differentiating neurons, leading to severe migration defects and subcortical heterotopia bands at postnatal stages. ZEB1 regulates a cohort of genes involved in cell differentiation and migration, including Neurod1 and Pard6b. The interaction between ZEB1 and CTBP2 in the embryonic cerebral cortex is required for ZEB1 to elicit its effect on the multipolar-to-bipolar transition, but not its suppression of Neurod1. These findings provide insights into understanding the complexity of transcriptional regulation during neuronal differentiation.

11.
Mol Pain ; 15: 1744806919842464, 2019 Jan-Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30987515

RESUMO

Neuropathic pain is a type of chronic pain induced by either central or peripheral nerve injury. MicroRNAs have been recently linked to many diseases, including neuropathic pain. However, the role of miR-7a in neuropathic pain still remains elusive. Thus, we aim to investigate the effects of miR-7a on neuropathic pain based on the spinal nerve ligation rat model. After establishment of spinal nerve ligation rat models, rats were infected with adeno-associated virus-neurofilament light polypeptide, adeno-associated virus-miR-7a or treated with metformin. The paw withdrawal threshold and paw withdrawal latency were assessed afterward, and the expression of miR-7a and neurofilament light polypeptide as well as their interaction was determined. Subsequently, miR-7a was overexpressed or silenced in dorsal root ganglion cells to investigate the role of miR-7a in neuropathic pain. Furthermore, the regulatory effect of neurofilament light polypeptide on neuropathic pain was detected using plasmid overexpressing neurofilament light polypeptide. Spinal nerve ligation rat model exhibited upregulation of neurofilament light polypeptide but downregulation of miR-7a. In addition, neurofilament light polypeptide accumulation or miR-7a inhibition decreased paw withdrawal threshold and paw withdrawal latency. Then, neurofilament light polypeptide accumulation or miR-7a inhibition was observed to increase the phosphorylation level of signal transducer and activator of transcription. miR-7a was found to directly target neurofilament light polypeptide and downregulate neurofilament light polypeptide. In addition, inhibiting the signal transducer and activator of transcription signaling pathway was also revealed to increase paw withdrawal threshold and paw withdrawal latency. Collectively, our study demonstrated that miR-7a ameliorated neuropathic pain via blocking the signal transducer and activator of transcription signaling pathway by repressing neurofilament light polypeptide. These findings, if taken further, can be of important clinical significance in treating patients with neuropathic pain.

12.
Environ Sci Pollut Res Int ; 26(13): 13221-13234, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30903476

RESUMO

In this work, a novel biochar was prepared from the Artemisia argyi stem at 300 °C (AS300), 450 °C (AS450), and 600 °C (AS600). The structural properties of these biochars were characterized with various tools. The sorption kinetic processes of Cr(VI) and Cu(II) onto these biochars were better described by the pseudo-second order. The sorption isotherm processes of Cr(VI) onto these biochars were better described by the Freundlich model while the adsorption processes of Cu(II) were consistent with the Langmuir model. Batch sorption experiments showed that AS600 had the maximum adsorption capacity to Cr(VI) and Cu(II) with 161.92 and 155.96 mg/g, respectively. AS600 was selected for the follow-up batch and dynamic adsorption experiments. Results showed that AS600 had larger adsorption capacity for Cr(VI) at lower pH while the larger adsorption capacity for Cu(II) was found at higher pH. The effect of ionic strength on the adsorption of Cu(II) by AS600 was greater than that on the adsorption of Cr(VI). Dynamic adsorption experiments showed that Cu(II) had a higher affinity for the adsorption sites on the AS600 compared with Cr(VI). The adsorption mechanisms mainly involved electrostatic attraction, ion exchange, pore filling, and chemical bonding effect. Graphical abstract.


Assuntos
Artemisia/química , Carvão Vegetal/química , Cromo/química , Cobre/química , Adsorção
13.
Chem Commun (Camb) ; 55(21): 3089-3092, 2019 Mar 07.
Artigo em Inglês | MEDLINE | ID: mdl-30785464

RESUMO

Efficient access to evodiamine and its analogues is presented via Lewis acid catalysis. In this reaction, three chemical bonds and two heterocyclic-fused rings are constructed in one step. The reaction shows good functional group tolerance and atom economy, and various heteroatom-containing evodiamine analogues are obtained in moderate to excellent yields even on a gram scale. An anti-tumor study in vitro demonstrates compound 2b possesses potent efficacy against hepatoma cell line (IC50 = 5.7 µM).


Assuntos
Antineoplásicos Fitogênicos/química , Antineoplásicos Fitogênicos/farmacologia , Evodia/química , Quinazolinas/química , Quinazolinas/farmacologia , Antineoplásicos Fitogênicos/síntese química , Apoptose/efeitos dos fármacos , Carcinoma Hepatocelular/tratamento farmacológico , Linhagem Celular Tumoral , Técnicas de Química Sintética , Humanos , Neoplasias Hepáticas/tratamento farmacológico , Quinazolinas/síntese química
14.
Org Biomol Chem ; 17(9): 2341-2345, 2019 02 27.
Artigo em Inglês | MEDLINE | ID: mdl-30758028

RESUMO

Here, we present an unprecedented pathway to α-sulfenylated carbonyl compounds from commercially available thiols and universally employed TEMPO and its analogues, which act as C3 synthons through skeletal rearrangement under simple and metal-free conditions. Mechanism studies suggest that this reaction involves a consecutive radical oxidation and cation coupling process. TEMPO analogues and thiols serve as oxidants and reductive reagents, respectively, along the radical process, while in the coupling process, the former ones afford C3 synthons to couple with related sulfur sources.

15.
J Immunol ; 202(5): 1623-1634, 2019 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-30665937

RESUMO

The role of the mTOR signaling pathway in different myeloid cell subsets is poorly understood in the context of tumor development. In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the roles of mechanistic target of rapamycin complex 1 (mTORC1) in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis. We found no difference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, although depletion of mTORC1 decreased the immunosuppressive function of tumor-associated macrophages (TAM). Despite the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on macrophages. In addition, TNF-α production by mTORC1-deficient myeloid cells was also decreased in the s.c. LLC tumors. On the contrary, disruption of mTORC1 in myeloid cells promoted lung cancer metastasis. Accordingly, immunosuppressive interstitial macrophages/metastasis-associated macrophages (CD11b+F4/80high) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 responses. Taken together, our results demonstrate that differential tumor microenvironment dictates the immunological outcomes of myeloid cells, with mTORC1 disruption leading to different tumor growth phenotypes.

16.
J Invest Dermatol ; 2018 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-30120937

RESUMO

The IL-1 signaling pathway has been shown to play a critical role in the pathogenesis of chronic, autoinflammatory skin diseases such as psoriasis. However, the exact cellular and molecular mechanisms have not been fully understood. Here, we show that IL-1ß is significantly elevated in psoriatic lesional skin and imiquimod-treated mouse skin. In addition, IL-1R signaling appears to correlate with psoriasis disease progression and treatment response. IL-1 signaling in both dermal γδ T cells and other cells such as keratinocytes is essential to an IMQ-induced skin inflammation. IL-1ß induces dermal γδ T cell proliferation and IL-17 production in mice. In addition, IL-1ß stimulates keratinocytes to secrete chemokines that preferentially chemoattract peripheral CD27- CCR6+IL-17 capable of producing γδ T cells (γδT17). Further studies showed that endogenous IL-1ß secretion is regulated by skin commensals to maintain dermal γδT17 homeostasis in mice. Mouse skin associated with Corynebacterium species, bacteria enriched in human psoriatic lesional skin, has increased IL-1ß and dermal γδT17 cell expansion. Thus, the IL-1ß-IL-1R signaling pathway may contribute to skin inflammation and psoriasis pathogenesis via the direct regulation of dermal IL-17-producing cells and stimulation of keratinocytes for amplifying inflammatory cascade.

17.
Cell Physiol Biochem ; 48(3): 1164-1176, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30045011

RESUMO

BACKGROUND/AIMS: Deguelin is a natural rotenoid that shows anti-inflammatory and antimicrobial activities. Rotenoids prevent oxidative damage and potentiate natural antioxidant activity in diabetic conditions, suggesting utility in treating diabetes and its complications. Here, we evaluate the potential efficacy of deguelin against diabetic neuropathy (DN). METHODS: DN was induced by streptozotocin followed by daily treatment with deguelin (4, 6 or 8 mg/kg) for 14 days. Blood glucose was measured, neurobehavioral tests for nociception and motor coordination were performed, and neuron conduction velocities were analysed electrophysiologically. We also assessed (Na+-K+) ATPase activity, performed a reactive oxygen species assay, measured the levels of various markers of oxidative stress, and of hydrogen sulphide (H2S) in dorsal root ganglion (DRG) neurons, conducted immunoblotting studies for proteins and ELISA for inflammatory cytokines. RESULTS: Deguelin significantly suppressed mechanical and thermal hyperalgesia, as well as cold allodynia, and partially restored the conduction velocities of neurons in DN rats. Significantly decreased expression levels of capspase-3 in DRG neurons, and increased (Na+-K+) ATPase activity in sciatic nerves, were observed. In addition, deguelin decreased glucose levels, attenuated oxidative stress and neuroinflammation, and elevated levels of H2S, nuclear respiratory factor 2 (Nrf2) and heme oxygenase-1, suggesting a disease-attenuating effect of deguelin in DN rats. To shed light on the underlying mechanism of action of deguelin, insulin- and dimethyl fumarate (BG-12)-treated groups were also included. Insulin suppressed glucose levels and BG-12 produced effects on Nrf2 levels similar to 8 mg/kg deguelin, confirming involvement of the Nrf2 pathway in the beneficial effects of deguelin against DN. CONCLUSIONS: Deguelin attenuated DN by decreasing oxidative stress and plasma glucose levels via the Nrf2 signalling pathway.


Assuntos
Antioxidantes/uso terapêutico , Diabetes Mellitus Experimental/tratamento farmacológico , Neuropatias Diabéticas/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Rotenona/análogos & derivados , Animais , Glicemia/análise , Glicemia/metabolismo , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/metabolismo , Neuropatias Diabéticas/sangue , Neuropatias Diabéticas/metabolismo , Masculino , Ratos Sprague-Dawley , Rotenona/uso terapêutico , Transdução de Sinais/efeitos dos fármacos
18.
Nanotechnology ; 29(37): 375604, 2018 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-29926809

RESUMO

In order to facilitate the broad applications of molecular recognition materials in biomedical areas, it is critical to enhance their adsorption capacity while maintaining their excellent recognition performance. In this work, we designed and synthesized well-defined peptide-imprinted mesoporous silica (PIMS) for specific recognition of an immunostimulating hexapeptide from human casein (IHHC) by using amphiphilic ionic liquid as the surfactant to anchor IHHC via a combination of one-step sol-gel method and docking oriented imprinting approach. Thereinto, theoretical calculation was employed to reveal the multiple binding interactions and dual-template configuration between amphiphilic ionic liquid and IHHC. The fabricated PIMS was characterized and an in-depth analysis of specific recognition mechanism was conducted. Results revealed that both adsorption and recognition capabilities of PIMS far exceeded that of the NIMS's. More significantly, the PIMS exhibited a superior binding capacity (60.5 mg g-1), which could increase 18.9% than the previous work. The corresponding imprinting factor and selectivity coefficient could reach up to 4.51 and 3.30, respectively. The PIMS also possessed lickety-split kinetic binding for IHHC, where the equilibrium time was only 10 min. All of these merits were due to the high surface area and the synergistic effect of multiple interactions (including hydrogen bonding, π-π stacking, ion-ion electrostatic interactions and van der Waals interactions, etc) between PIMS and IHHC in imprinted sites. The present work suggests the potential application of PIMS for large-scale and high-effective separation of IHHC, which may lead to their broad applications in drug/gene deliver, biosensors, catalyst and so on.

19.
Biomed Eng Online ; 17(1): 91, 2018 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-29941043

RESUMO

BACKGROUND: Rehabilitation robots can provide intensive physical training after stroke. However, variations of the rehabilitation effects in translation from well-controlled research studies to clinical services have not been well evaluated yet. This study aims to compare the rehabilitation effects of the upper limb training by an electromyography (EMG)-driven robotic hand achieved in a well-controlled research environment and in a practical clinical service. METHODS: It was a non-randomized controlled trial, and thirty-two participants with chronic stroke were recruited either in the clinical service (n = 16, clinic group), or in the research setting (n = 16, lab group). Each participant received 20-session EMG-driven robotic hand assisted upper limb training. The training frequency (4 sessions/week) and the pace in a session were fixed for the lab group, while they were flexible (1-3 sessions/week) and adaptive for the clinic group. The training effects were evaluated before and after the treatment with clinical scores of the Fugl-Meyer Assessment (FMA), Action Research Arm Test (ARAT), Functional Independence Measure (FIM), and Modified Ashworth Scale (MAS). RESULTS: Significant improvements in the FMA full score, shoulder/elbow and wrist/hand (P < 0.001), ARAT (P < 0.001), and MAS elbow (P < 0.05) were observed after the training for both groups. Significant improvements in the FIM (P < 0.05), MAS wrist (P < 0.001) and MAS hand (P < 0.05) were only obtained after the training in the clinic group. Compared with the lab group, higher FIM improvement in the clinic group was observed (P < 0.05). CONCLUSIONS: The functional improvements after the robotic hand training in the clinical service were comparable to the effectiveness achieved in the research setting, through flexible training schedules even with a lower training frequency every week. Higher independence in the daily living and a more effective release in muscle tones were achieved in the clinic group than the lab group.


Assuntos
Eletromiografia , Laboratórios , Robótica , Reabilitação do Acidente Vascular Cerebral/métodos , Extremidade Superior , Doença Crônica , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Resultado do Tratamento
20.
Technol Cancer Res Treat ; 17: 1533033818781405, 2018 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-29950151

RESUMO

Esophageal squamous cell carcinoma is the sixth most lethal cancer worldwide and the fourth most lethal cancer in China. Tissue-specific transplantation antigen P35B codifies the enzyme GDP-d-mannose-4,6-dehydratase, which participates in the biosynthesis of GDP-l-fucose. GDP-l-fucose is an important substrate involved in the biosynthesis of many glycoproteins. Cancer cells are often accompanied by the changes in glycoprotein structure, which affects the adhesion, invasion, and metastasis of cells. It is not clear whether tissue-specific transplantation antigen P35B has any effect on the development of esophageal squamous cell carcinoma. We used an immunohistochemical method to assess the expression of tissue-specific transplantation antigen P35B in 104 esophageal squamous cell carcinoma samples. The results showed tissue-specific transplantation antigen P35B expression was associated with some clinical features in patients, such as age ( P = .017), clinical stage ( P = .010), and lymph node metastasis ( P = .043). Kaplan-Meier analysis and log-rank test showed that patients with esophageal squamous cell carcinoma having high tissue-specific transplantation antigen P35B expression had a worse prognosis compared to the patients with low expression ( P = .048). Multivariate Cox proportional hazards regression model showed that high expression of tissue-specific transplantation antigen P35B could predict poor prognosis for patients with esophageal squamous cell carcinoma independently. In conclusion, abnormal fucosylation might participate in the progress of esophageal squamous cell carcinoma and tissue-specific transplantation antigen P35B may serve as a novel biomarker for prognosis of patients with esophageal squamous cell carcinoma.

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