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1.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 37(4): 412-416, 2019 Aug 01.
Artigo em Chinês | MEDLINE | ID: mdl-31512836

RESUMO

OBJECTIVE: We aim to determine the thickness of the labial plate, the distance between the cement-enamel junction (CEJ) and alveolar crest, and the inclination angle of the long axis of healthy maxillary anterior teeth by using cone- beam computed tomography (CBCT). METHODS: A total of 345 CBCT volumes obtained by Newtom VGI® CBCT were analyzed by using the NNT software. The digital measurements of the labial bone plate thickness at level 4 mm below the CEJ, the midpoint of tooth root and the radiological tooth apex, the distance between the CEJ and alveolar crest, and the angle between the long axis of the teeth and the long axis of alveolar process were obtained from the mid-sagittal planes of maxillary incisors and canines. Plate thickness 4 mm below the CEJ was measured, and values below ≥1 mm were recorded. RESULTS: In the central incisor, 1) the angle between the long axis of the teeth and alveolar bone was 15.2°±6.2°, the distance between the CEJ and alveolar crest was (1.5±1.0) mm, labial bone plate thick-ness at 4 mm below the CEJ was (0.8±0.4) mm, the midpoint of tooth root was (0.6±0.4) mm, and the radiological tooth apex was (1.3±0.7) mm; in the lateral incisor, 16.2°±8.8°, (1.6±1.0) mm, (0.7±0.5) mm, (0.4±0.6) mm, and (1.1±0.7) mm, respectively; and in the canine, 19.0°±6.2°, (1.8±1.0) mm, (0.9±0.6) mm, (0.4±0.6) mm, and (1.2±0.7) mm, respectively. 2) The frequencies of plate thickness ≥1 mm were 28.3%, 25.8%, and 42.7% in the central incisor, lateral incisor, and canine, respectively. 3) The distance between the CEJ and alveolar crest was positively correlated with age. The correlation coefficients was 0.42 (P<0.01) in the central incisor, 0.50 (P<0.01) in the lateral incisor, and 0.62 (P<0.01) in the canine. CONCLUSIONS: The thickness of labial bone plate is thin, the distance from CEJ to alveolar crest increases with age, and the long axis of the teeth is more inclined than the long axis of alveolar process. Knowledge of these special morphological characteristics can improve the safety and result for many dental procedures.


Assuntos
Placas Ósseas , Maxila , Processo Alveolar , Tomografia Computadorizada de Feixe Cônico , Incisivo
2.
BMC Urol ; 19(1): 74, 2019 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-31382939

RESUMO

BACKGROUND: Strong evidence comparing effectiveness between nephron-sparing intervention (NSI) and active surveillance (AS) is lacking. Thus, we aim to compare the outcomes of survival, including cancer-specific survival (CSS), overall survival (OS), and cardiovascular-specific survival (CVSS), in patients with renal masses who underwent NSI or AS. METHODS: A systematic literature search of PubMed, Web of Science, and EMBASE was performed for citations published prior to September 2018 that described NSI, partial nephrectomy and thermal ablation included, and AS for patients with renal masses and a standard meta-analysis on survival outcomes was then conducted. RESULTS: The meta-analysis included seven studies containing 5809 patients. The results comparing NSI with AS were as follows: CSS (hazard ratio (HR) = 0.64, 95% confidence interval (CI): 0.46-0.89, P < 0.001), OS (HR = 0.46, 95%CI: 0.39-0.53, P < 0.001), and CVSS (HR = 0.37, 95%CI: 0.24-0.57, P < 0.001). CONCLUSIONS: This systematic review and meta-analysis indicates that NSI is associated with better OS, CSS and CVSS when compared with AS for patients with renal masses. Further better prospective cohort studies are needed to make definitive statements about these different treatment methods.

3.
ACS Appl Mater Interfaces ; 11(35): 32449-32459, 2019 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-31405273

RESUMO

A series of Cr-doped In2-xCrxO3 (ICO) semiconductor thin films were epitaxially grown on (111)-oriented 0.71Pb(Mg1/3Nb2/3)O3-0.29PbTiO3 (PMN-0.29PT) single-crystal substrates by the pulsed laser deposition. Upon the application of an electric field to the PMN-0.29PT substrate along the thickness direction, we realized in situ, reversible, and nonvolatile control of the electronic properties and Fermi level of the films, which are manifested by abundant physical phenomena such as the n-type to p-type transformation, metal-semiconductor transition, metal-insulator transition, crossover of the magnetoresistance (MR) from negative to positive, and a large nonvolatile on-and-off ratio of 5.5 × 104% at room temperature. We also strictly disclose that both the sign and the magnitude of MR are determined by the electron carrier density of ICO films, which could modify the s-d exchange interaction and weak localization effect. Our results demonstrate that the ferroelectric gating approach using PMN-PT can be utilized to gain deeper insight into the carrier-density-related electronic properties of In2O3-based semiconductors and provide a simple and energy efficient way to construct multifunctional devices which can utilize the unique properties of composite materials.

4.
Autophagy ; : 1-18, 2019 Jun 28.
Artigo em Inglês | MEDLINE | ID: mdl-31223056

RESUMO

Macroautophagy/autophagy deficit induces intracellular MAPT/tau accumulation, the hallmark pathology in Alzheimer disease (AD) and other tauopathies; however, the reverse role of MAPT accumulation in autophagy and neurodegeneration is not clear. Here, we found that overexpression of human wild-type full-length MAPT, which models MAPT pathologies as seen in sporadic AD patients, induced autophagy deficits via repression of autophagosome-lysosome fusion leading to significantly increased LC3 (microtubule-associated protein 1 light chain 3)-II and SQSTM1/p62 (sequestosome 1) protein levels with autophagosome accumulation. At the molecular level, intracellular MAPT aggregation inhibited expression of IST1 (IST1 factor associated with ESCRT-III), a positive modulator for the formation of ESCRT (the Endosomal Sorting Complex Required for Transport) complex that is required for autophagosome-lysosome fusion. Upregulating IST1 in human MAPT transgenic mice attenuated autophagy deficit with reduced MAPT aggregation and ameliorated synaptic plasticity and cognitive functions, while downregulating IST1 per se induced autophagy deficit with impaired synapse and cognitive function in naïve mice. IST1 can facilitate association of CHMP2B (charged multivesicular body protein 2B) and CHMP4B/SNF7-2 to form ESCRT-III complex, while lack of IST1 impeded the complex formation. Finally, we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation. Our findings suggest that the AD-like MAPT accumulation can repress autophagosome-lysosome fusion by deregulating ANP32A-INHAT-IST1-ESCRT-III pathway, which also reveals a vicious cycle of MAPT accumulation and autophagy deficit in the chronic course of AD neurodegeneration.Abbreviations: AAV: adeno-associated virus; Aß: ß-amyloid; aCSF: artificial cerebrospinal fluid; AD: Alzheimer disease; ANP32A: acidic nuclear phosphoprotein 32 family member A; ATG: autophagy related; AVs: autophagic vacuoles; CEBPB: CCAAT enhancer binding protein beta; CHMP: charged multivesicular body protein; DMEM: Dulbecco's modified eagle's medium; EBSS: Earle's balanced salt solution; EGFR: epidermal growth factor receptor; ESCRT: endosomal sorting complex required for transport; fEPSPs: field excitatory postsynaptic potentials; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GSK3B: glycogen synthase kinase 3 beta; HAT: histone acetyl transferase; HDAC: histone deacetylase; INHAT: inhibitor of histone acetyl transferase; IST1: IST1 factor associated with ESCRT-III; LAMP2: lysosomal associated membrane protein 2; LTP: long-term potentiation; MAP1LC3: microtubule associated protein 1 light chain 3; MAPT/tau: microtubule associated protein tau; MVB: multivesicular bodies; MWM: Morris water maze; PBS: phosphate-buffered saline solution; RAB7: member RAS oncogene family; SNAREs: soluble N-ethylmaleimide-sensitive factor attachment protein receptors; SQSTM1/p62: sequestosome 1.

5.
J Med Primatol ; 48(6): 320-328, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31148186

RESUMO

BACKGROUND: The relatively tiny spinal cord of non-human primate (NHP) causes increased challenge in diffusion tensor imaging (DTI) post-processing. This study aimed to establish a reliable correction strategy applied to clinical DTI images of NHP. METHODS: Six normal and partial spinal cord injury (SCI) rhesus monkeys underwent 3T MR scanning. A correction strategy combining multiple iterations and non-rigid deformation was used for DTI image post-processing. Quantitative evaluations were then conducted to investigate effects of distortion correction. RESULTS: After correction, longitudinal geometric distortion, global distortion, and residual distance errors were all significantly decreased (P < 0.05). Fractional anisotropy at the injured site was remarkably lower than that at the contralateral site (P = 0.0488) and was substantially lower than those at the adjacent superior (P = 0.0157) and inferior (P = 0.0128) areas at the same side. CONCLUSIONS: Our image correction strategy can improve the quality of the DTI images of NHP thoracic cords, contributing to the development of SCI preclinical research.

6.
EMBO Rep ; 20(6)2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31085626

RESUMO

Intracellular tau accumulation forming neurofibrillary tangles is hallmark pathology of Alzheimer's disease (AD), but how tau accumulation induces synapse impairment is elusive. By overexpressing human full-length wild-type tau (termed hTau) to mimic tau abnormality as seen in the brain of sporadic AD patients, we find that hTau accumulation activates JAK2 to phosphorylate STAT1 (signal transducer and activator of transcription 1) at Tyr701 leading to STAT1 dimerization, nuclear translocation, and its activation. STAT1 activation suppresses expression of N-methyl-D-aspartate receptors (NMDARs) through direct binding to the specific GAS element of GluN1, GluN2A, and GluN2B promoters, while knockdown of STAT1 by AAV-Cre in STAT1flox/flox mice or expressing dominant negative Y701F-STAT1 efficiently rescues hTau-induced suppression of NMDAR expression with amelioration of synaptic functions and memory performance. These findings indicate that hTau accumulation impairs synaptic plasticity through JAK2/STAT1-induced suppression of NMDAR expression, revealing a novel mechanism for hTau-associated synapse and memory deficits.

7.
Medicine (Baltimore) ; 98(17): e15308, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31027096

RESUMO

This retrospective study investigated the effectiveness and safety of acupuncture as an adjunctive therapy to topical ibuprofen (TIP) for patients with chronic knee pain (CKP) due to osteoarthritis.This retrospective study analyzed medical records of 84 patients with CKP due to osteoarthritis. These patients were divided into a treatment group (n = 42) and a control group (n = 42). The patients in the treatment group were treated with acupuncture plus TIP, while the subjects in the control group received TIP monotherapy. The primary effectiveness endpoint was assessed by Western Ontario and McMaster Universities osteoarthritis index (WOMAC). The secondary effectiveness endpoints were evaluated by the numeric rating scale (NRS), 12-item Short FormHealth Survey (SF-12, mainly including mental component summary [MCS], and physical component summary [PCS]), and adverse events. All patients received an 8-week treatment. All endpoints were measured pre-treatment and posttreatment.The patients who received acupuncture plus TIP showed better effectiveness in both primary endpoint of WOMAC scale (pain, P < .01; function, P < .01; and stiffness, P < .01) and secondary endpoints of NRS (P < .01), and SF-12 (MCS, P < .01; and PCS, P < .01), than patients who received TIP monotherapy. In addition, both groups had similar safety profile.The results of this study showed that the effectiveness of acupuncture plus TIP may be better than TIP monotherapy for patients with CKP due to osteoarthritis.


Assuntos
Terapia por Acupuntura/métodos , Ibuprofeno/uso terapêutico , Osteoartrite do Joelho/terapia , Manejo da Dor/métodos , Administração Cutânea , Idoso , Idoso de 80 Anos ou mais , Doença Crônica , Terapia Combinada , Feminino , Humanos , Ibuprofeno/administração & dosagem , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
8.
Exp Anim ; 68(3): 341-349, 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-30930341

RESUMO

Walking is characterized by repetitive limb movements associated with highly structured patterns of muscle activity. The causal relationships between the muscle activities and hindlimb segments of walking are difficult to decipher. This study investigated these particular relationships and clarified whether they are correlated with speed to further understand the neuromuscular control pattern. Four adult female rhesus monkeys (Macaca mulatta) were selected to record gait parameters while walking on a bipedal treadmill at speeds of 0.2, 0.8, 1.4, and 2.0 km/h. We recorded 3 ipsilateral hindlimb muscles by surface recording. In this study, we calculated the correlations between electromyography (EMG) and kinematic parameters (24 EMG*17 kinematic parameters). Of the 408 calculated coefficients, 71.6% showed significant linear correlations. Significant linear correlations were found between muscle activity, such as burst amplitudes and the integral of muscle activity, and the corresponding kinematic parameters of each joint. Most of these relationships were speed independent (91.7% of all variables). Through correlation analysis, this study demonstrated a causal association between kinematic and EMG patterns of rhesus monkey locomotion. Individuals have particular musculoskeletal control patterns, and most of the relationships between hindlimb segments and muscles are speed independent. The current findings may enhance our understanding of neuromusculoskeletal control strategies.


Assuntos
Macaca mulatta/fisiologia , Músculo Esquelético/fisiologia , Caminhada/fisiologia , Animais , Fenômenos Biomecânicos , Eletromiografia , Feminino
9.
Biochim Biophys Acta Mol Basis Dis ; 1865(6): 1477-1489, 2019 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-30826466

RESUMO

BACKGROUND: Maternal immune activation (MIA) is an independent risk factor for psychiatric disorders including depression spectrum in the offsprings, but the molecular mechanism is unclear. Recent studies show that interferon-stimulated gene-15 (ISG15) is involved in inflammation and neuronal dendrite development; here we studied the role of ISG15 in MIA-induced depression and the underlying mechanisms. METHODS: By vena caudalis injecting polyinosinic: polycytidylic acid (poly I:C) into the pregnant rats to mimic MIA, we used AAV or lentivirus to introduce or silence ISG15 expression. Synaptic plasticity was detected by confocal microscope and Golgi staining. Cognitive performances of the offspring were measured by Open field, Forced swimming and Sucrose preference test. RESULTS: We found that MIA induced depression-like behaviors with dendrite impairments in the offspring with ISG15 level increased in the offsprings' brain. Overexpressing ISG15 in the prefrontal cortex of neonatal cubs (P0) could mimic dendritic pathology and depressive like behaviors, while downregulating ISG15 rescued these abnormalities in the offsprings. Further studies demonstrated that MIA-induced upregulation of inflammatory cytokines promoted ISG15 expression in the offspring' brain which suppressed Rap2A ubiquitination via NEDD4 and thus induced Rap2A accumulation, while upregulating NEDD4 abolished ISG15-induced dendrite impairments. CONCLUSIONS: These data reveal that MIA impedes offsprings' dendrite development and causes depressive like behaviors by upregulating ISG15 and suppressing NEDD4/Rap2A signaling. The current findings suggest that inhibiting ISG15 may be a promising intervention of MIA-induced psychiatric disorders in the offsprings.

10.
Medicine (Baltimore) ; 98(8): e14589, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30813181

RESUMO

This retrospective study investigated the efficacy and safety of extracorporeal shock wave (EPSW) combined with hyaluronic acid (HA) for patients with knee osteoarthritis (KOA).This retrospective study included 70 patients with KOA. Of those subjects, 35 of them received EPSW combined HA, and were allocated to a treatment group, while the other 35 participants received HA alone and were allocated to a control group. Patients in both groups were treated for a total of 8 weeks. The primary outcome was measured by visual analog scale (VAS). The secondary outcomes were measured by Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), and knee injury and osteoarthritis outcome score (KOOS). In addition, adverse events (AEs) were also evaluated. All outcomes were measured before and after the treatment.After the treatment, patients in the treatment group exhibited better efficacy in VAS (P < .01), WOMAC scale (pain, P < .01; function, P < .01; and stiffness, P < .01), and KOOS scores (pain, P < .01; function in daily living, P < .01; symptoms, P < .01; sport and recreation, P < .01; and quality of life, P < .01), than patients in the control group. In addition, no significant differences regarding the AEs were found between 2 groups.The findings of this study demonstrated that the efficacy of EPSW combined with HA is superior to the HA alone for patients with KOA.


Assuntos
Tratamento por Ondas de Choque Extracorpóreas/métodos , Ácido Hialurônico/administração & dosagem , Osteoartrite do Joelho/terapia , Viscossuplementos/administração & dosagem , Idoso , Idoso de 80 Anos ou mais , Terapia Combinada , Tratamento por Ondas de Choque Extracorpóreas/efeitos adversos , Feminino , Humanos , Ácido Hialurônico/efeitos adversos , Injeções Intra-Articulares , Articulação do Joelho/fisiopatologia , Masculino , Pessoa de Meia-Idade , Medição da Dor , Qualidade de Vida , Estudos Retrospectivos , Índice de Gravidade de Doença , Resultado do Tratamento , Viscossuplementos/efeitos adversos
11.
ACS Appl Mater Interfaces ; 11(9): 9548-9556, 2019 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-30724082

RESUMO

Single-phase (00 l)-oriented Bi2Te3 topological insulator thin films have been deposited on (111)-oriented ferroelectric 0.71Pb(Mg1/3Nb2/3)O3-0.29PbTiO3 (PMN-PT) single-crystal substrates. Taking advantage of the nonvolatile polarization charges induced by the polarization direction switching of PMN-PT substrates at room temperature, the carrier density, Fermi level, magnetoconductance, conductance channel, phase coherence length, and quantum corrections to the conductance can be in situ modulated in a reversible and nonvolatile manner. Specifically, upon the polarization switching from the positively poled Pr+ state (i.e., polarization direction points to the film) to the negatively poled Pr- (i.e., polarization direction points to the bottom electrode) state, both the electron carrier density and the Fermi wave vector decrease significantly, reflecting a shift of the Fermi level toward the Dirac point. The polarization switching from Pr+ to Pr- also results in significant increase of the conductance channel α from -0.15 to -0.3 and a decrease of the phase coherence length from 200 to 80 nm at T = 2 K as well as a reduction of the electron-electron interaction. All these results demonstrate that electric-voltage control of physical properties using PMN-PT as both substrates and gating materials provides a simple and a straightforward approach to realize reversible and nonvolatile tuning of electronic properties of topological thin films and may be further extended to study carrier density-related quantum transport properties of other quantum matter.

12.
Cancer Manag Res ; 10: 5881-5894, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30510456

RESUMO

Purpose: TNBC is generally more aggressive than other BC subtypes and has limited therapeutic options. We aimed to construct comprehensive and reliable nomograms to predict the OS and BCSS of TNBC patients to offer clinicians therapeutic guidance for improving the prognosis of TNBC patients. Patients and methods: We used the SEER 19 Cancer Registry to identify 21,419 eligible TNBC patients diagnosed from January 1, 2010 to December 31, 2015, and divided the database randomly into a training cohort (n=10,709) and a validation cohort (n=10,710). The log-rank test and Cox analysis together with a competing risk model were utilized to identify independent prognostic factors for OS and BCSS, which were then integrated to construct nomograms. Results: According to the training cohort, except for laterality, the following factors were all predictive of OS and BCSS: age at diagnosis, race, tumor size, number of positive lymph nodes, grade, and histological subtype. The 1-, 3-, and 5-year probabilities of BC-specific mortality were 2.7%, 12.5%, and 17.1%, respectively. The precision of the nomograms was assessed by the C-index value and calibration plot diagrams. The C-index value were 0.779 for OS and 0.793 for BCSS in the internal validation and 0.774 for OS and 0.792 for BCSS in the external validation. Both internal and external calibration plot diagrams showed good consistency between the actual and predicted outcomes, especially for 3- and 5-year OS and BCSS. Conclusion: These nomograms hold promise as a novel and accurate tool in predicting OS and BCSS of TNBC patients and could be used in clinical practice to assist clinicians in developing more effective therapeutic strategies and to evaluate prognostic personally.

13.
Mol Psychiatry ; 2018 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-30382187

RESUMO

δ-Secretase, an age-dependent asparagine protease, cleaves both amyloid precursor protein (APP) and Tau and is required for amyloid plaque and neurofibrillary tangle pathologies in Alzheimer's disease (AD). However, whether δ-secretase activation is sufficient to trigger AD pathogenesis remains unknown. Here we show that the fragments of δ-secretase-cleavage, APP (586-695) and Tau(1-368), additively drive AD pathogenesis and cognitive dysfunctions. Tau(1-368) strongly augments BACE1 expression and Aß generation in the presence of APP. The Tau(1-368) fragment is more robust than full-length Tau in binding active STAT1, a BACE1 transcription factor, and promotes its nuclear translocation, upregulating BACE1 and Aß production. Notably, Aß-activated SGK1 or JAK2 kinase phosphorylates STAT1 and induces its association with Tau(1-368). Inhibition of these kinases diminishes stimulatory effect of Tau(1-368). Knockout of STAT1 abolishes AD pathologies induced by δ-secretase-generated APP and Tau fragments. Thus, we show that Tau may not only be a downstream effector of Aß in the amyloid hypothesis, but also act as a driving force for Aß, when cleaved by δ-secretase.

14.
J Alzheimers Dis ; 66(1): 333-345, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30282353

RESUMO

Extracellular accumulation of amyloid-ß (Aß) forming senile plaques is one of the hallmark pathologies in Alzheimer's disease (AD), while the mechanisms underlying the neuronal toxic effect of Aß are not fully understood. Here, we found that intracerebroventricular infusion of the aged Aß42 in mice only induces memory deficit at 24 h but not at 7 days. Interestingly, a remarkably increased CREB (cAMP response element-binding protein) Ser133-phosphorylation (pS133-CREB) with microglial activation was detected at 24 h but not at 7 days after Aß infusion. Aß treatment for 24 h increased pS133-CREB level in microglia of the hippocampal non-granular cell layers with remarkably decreased pS133-CREB immunoreactivity in neurons of the hippocampal granular cell layers, including CA1, CA3, and DG subsets. Inhibition of microglia activation by minocycline or CREB phosphorylation by H89, an inhibitor of protein kinase A (PKA), abolished Aß-induced microglia CREB hyperphosphorylation with restoration of neuronal function and attenuation of inflammatory response, i.e., reduced levels of interleukin-6 (IL6) and pCREB binding of matrix metalloproteinase-9 (MMP9) DNA. Finally, treatment of the primary hippocampal neurons with Aß-potentiated microglia media decreased neuronal GluN1 and GluA2 levels, while simultaneous inhibition of PKA restored the levels. These novel findings reveal that intracerebroventricular infusion of Aß only induces transient memory deficit in mice and the molecular mechanisms involve a stimulated microglial CREB phosphorylation.

15.
ACS Appl Mater Interfaces ; 10(38): 32809-32817, 2018 Sep 26.
Artigo em Inglês | MEDLINE | ID: mdl-30156403

RESUMO

We report the fabrication of 0.71Pb(Mg1/3Nb2/3)O3-0.29PbTiO3 (PMN-0.29PT)-based ferroelectric field effect transistors (FeFETs) by the epitaxial growth of cobalt-doped tin dioxide (SnO2) semiconductor thin films on PMN-0.29PT single crystals. Using such FeFETs we realized in situ, reversible, and nonvolatile manipulation of the electron carrier density and achieved a large nonvolatile modulation of the resistance (∼330%) of the SnO2:Co films through the polarization switching of PMN-0.29PT at 300 K. Particularly, combining the ferroelectric gating with piezoresponse force microscopy, X-ray diffraction, Hall effect, and magnetoresistance (MR), we rigorously disclose that both sign and magnitude of the MR are intrinsically determined by the electron carrier density, which could modify the s-d exchange interaction of the SnO2:Co films. Furthermore, we realized multilevel resistance states of the SnO2:Co films by combining the ferroelectric gating with ultraviolet light illumination, demonstrating that the FeFETs have potential applications in multistate resistive memories and electro-optical devices.

16.
Neurobiol Aging ; 71: 267.e1-267.e4, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30093141

RESUMO

NEK1 was recently identified as an amyotrophic lateral sclerosis (ALS) gene through rare variant burden analysis, and its role in ALS in various populations is still unclear. The aim of this study was to determine the frequency and spectrum of NEK1 mutations in an ALS cohort from mainland China. All exons and their flanking intron regions of NEK1 were screened by direct nucleotide sequencing in 377 unrelated ALS patients. These patients were also screened with a massive parallel sequencing gene panel for 24 known ALS genes and C9orf72 hexanucleotide repeat expansion. In totality, we detected 9 variants, comprising 3 novel heterozygous loss-of-function mutations and 6 rare missense variants (MAF < 0.1%) in NEK1. The patient with splice site mutation also carried another probably damaging variant in SOD1. Our study established a NEK1 mutant frequency of 0.8% in Chinese ALS patients, further expanded its spectrum of variants, and highlighted the possibility of coexistence with variants in additional ALS genes in NEK1 loss-of-function carriers.

17.
Thorac Cancer ; 9(9): 1194-1208, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30039918

RESUMO

Lung cancer ranks first in incidence and mortality in China. Surgery is the primary method to cure cancer, but only 20-30% of patients are eligible for curative resection. In recent years, in addition to surgery, other local therapies have been developed for patients with numerous localized primary and metastatic pulmonary tumors, including stereotactic body radiation therapy and thermal ablative therapies through percutaneously inserted applicators. Percutaneous thermal ablation of pulmonary tumors is minimally invasive, conformal, repeatable, feasible, cheap, has a shorter recovery time, and offers reduced morbidity and mortality. Radiofrequency ablation (RFA), the most commonly used thermal ablation technique, has a reported 80-90% rate of complete ablation, with the best results obtained in tumors < 3 cm in diameter. Because the clinical efficacy of RFA of pulmonary tumors has not yet been determined, this clinical guideline describes the techniques used in the treatment of localized primary and metastatic pulmonary tumors in nonsurgical candidates, including mechanism of action, devices, indications, techniques, potential complications, clinical outcomes, post-ablation surveillance, and use in combination with other therapies. In the future, the role of RFA in the treatment of localized pulmonary tumors should ultimately be determined by evidence from prospective randomized controlled trials comparing sublobar resection or stereotactic body radiation therapy.

18.
Exp Anim ; 67(4): 431-440, 2018 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-29769463

RESUMO

After incomplete spinal cord injury (SCI), neural circuits may be plastically reconstructed to some degree, resulting in extensive functional locomotor recovery. The present study aimed to observe the post-SCI locomotor recovery of rhesus monkey hindlimbs and compare the recovery degrees of different hindlimb parts, thus revealing the recovery process of locomotor function. Four rhesus monkeys were chosen for thoracic hemisection injury. The hindlimb locomotor performance of these animals was recorded before surgery, as well as 6 and 12 weeks post-lesion. Via principal component analysis, the relevant parameters of the limb endpoint, pelvis, hindlimb segments, and joints were processed and analyzed. Twelve weeks after surgery, partial kinematic recovery was observed at the limb endpoint, shank, foot, and knee joints, and the locomotor performance of the ankle joint even recovered to the pre-lesion level; the elevation angle of the thigh and hip joints showed no obvious recovery. Generally, different parts of a monkey hindlimb had different spontaneous recovery processes; specifically, the closer the part was to the distal end, the more extensive was the locomotor function recovery. Therefore, we speculate that locomotor recovery may be attributed to plastic reconstruction of the motor circuits that are mainly composed of corticospinal tract. This would help to further understand the plasticity of motor circuits after spinal cord injury.


Assuntos
Membro Posterior/fisiopatologia , Atividade Motora , Regeneração Nervosa/fisiologia , Recuperação de Função Fisiológica/fisiologia , Traumatismos da Medula Espinal/fisiopatologia , Animais , Fenômenos Biomecânicos , Feminino , Macaca mulatta , Plasticidade Neuronal/fisiologia , Tratos Piramidais/fisiopatologia
19.
J Alzheimers Dis ; 63(4): 1537-1546, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29782322

RESUMO

There is accumulating evidence that decreased histone acetylation is involved in normal aging and neurodegenerative diseases. Recently, we found that ANP32A, a key component of INHAT (inhibitor of acetyltransferases) that suppresses histone acetylation, increased in aged and cognitively impaired C57 mice and expressing wild-type human full length tau (htau) transgenic mice. Downregulating ANP32A restored cognitive function and synaptic plasticity through upregulation of the expressions of synaptic-related proteins via increasing histone acetylation. However, there is no direct evidence that ANP32A can induce neurodegeneration and memory deficits. In the present study, we overexpressed ANP32A in the hippocampal CA3 region of C57 mice and found that ANP32A overexpression induced cognitive abilities and synaptic plasticity deficits, with decreased synaptic-related protein expression and histone acetylation. Combined with our recent studies, our findings reveal that upregulated ANP32A induced-suppressing histone acetylation may underlie the cognitive decline in neurodegenerative disease, and suppression of ANP32A may represent a promising therapeutic approach for neurodegenerative diseases including Alzheimer's disease.

20.
Am J Hypertens ; 31(9): 1013-1023, 2018 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-29767672

RESUMO

BACKGROUND: Toll-like receptor 4 (TLR4) has been implicated in the progression of cardiovascular disease, including hypertension. However, the role of TLR4 in the development of prehypertension is uncertain. METHODS: Prehypertensive rats were treated with 8% salt for 12 weeks to induce prehypertension. These rats were then given either TAK-242 selective TLR4 blocker, or vehicle by bilateral micro-injection to the paraventricular nucleus (PVN). Blood pressure (BP) and renal sympathetic nerve activity were recorded. PVN expression of TLR4, myeloid differentiation factor 88 (Myd88), nuclear factor-kappa B (NF-κB) p65, proinflammation cytokines (PICs), interleukin (IL)-1ß, IL-6, tumor necrosis factor-alpha (TNF-α), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), NADPH oxidase 4 (NOX4), Cu/Zn superoxide dismutase (SOD) level, tyrosine hydroxylase, and 67 kDa isoform of glutamate decarboxylase (GAD67) were tested to determine the influence of TLR4 blockade. RESULTS: TLR4 expression increased significantly in the PVN of high-salt groups with a corresponding increase in reactive oxygen species (ROS) and PICs. TLR4 blockade significantly reduced the signaling molecules downstream TLR4 and the expression of TNF-α, IL-6, IL-1ß, decreased ROS, NOX2, NOX4 level, increased Cu/Zn-SOD, re-balanced neurotransmitters, and regulated sympathetic nerve activity in the PVN of prehypertensive rats. CONCLUSIONS: Salt-induced prehypertension is partly due to the upregulation of TLR4 in PVN. Blockade of TLR4 in the brain reduced salt-induced prehypertension response, possibly through downregulation of ROS and PICs expression, and the restorage of neurotransmitter balance in the PVN.

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