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Staphylococcus aureus is a gram-positive bacterium that can easily cause outbreaks of food-borne diseases. In this work, a signal-enhanced three-dimensional paper-based photoelectrochemical (PEC) aptsensor for the rapid and sensitive determination of S. aureus was developed. Specifically, gold nanoparticles (AuNPs) were electrodeposited on a paper-based working electrode to provide binding sites for a sulfhydryl-functionalized aptamer. Subsequently, S. aureus was captured with high specificity by a carboxyl-functionalized aptamer modified with amino-functionalized AgBiS2 nanoflowers (NH2-AgBiS2 NFs), which functionalized as PEC probes that generated strong photocurrent under irradiation with 980-nm light. By exploiting the "aptamer-target-aptamer" PEC sensing platform, the rapid and ultrasensitive detection of S. aureus was achieved. The sensor had a wide linear range of 20 to 2 × 107 CFU/mL and low limit of detection of 4 CFU/mL. Further, the applicability of the as-prepared aptsensor was successfully certified for the analysis of pork samples artificially contaminated with S. aureus.
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Nanopartículas Metálicas , Carne de Porco , Carne Vermelha , Infecções Estafilocócicas , Suínos , Animais , Staphylococcus aureus , Ouro , Infecções Estafilocócicas/diagnóstico , OligonucleotídeosRESUMO
The dichotomized brain system is a concept that was generalized from the 'dual syndrome hypothesis' to explain the heterogeneity of cognitive impairment, in which anterior and posterior brain systems are independent but partially overlap. The dopaminergic system acts on the anterior brain and is responsible for executive function, working memory, and planning. In contrast, the cholinergic system acts on the posterior brain and is responsible for semantic fluency and visuospatial function. Evidence from dopaminergic/cholinergic imaging or functional neuroimaging has shed significant insight relating to the involvement of the cerebellum in the cognitive process of patients with Parkinson's disease. Previous research has reported evidence that the cerebellum receives both dopaminergic and cholinergic projections. However, whether these two neurotransmitter systems are associated with cognitive function has yet to be fully elucidated. Furthermore, the precise role of the cerebellum in patients with Parkinson's disease and cognitive impairment remains unclear. Therefore, in this review, we summarize the cerebellar dopaminergic and cholinergic projections and their relationships with cognition, as reported by previous studies, and investigated the role of the cerebellum in patients with Parkinson's disease and cognitive impairment, as determined by functional neuroimaging. Our findings will help us to understand the role of the cerebellum in the mechanisms underlying cognitive impairment in Parkinson's disease.
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Recent studies have demonstrated that neuroplasticity, such as synaptic plasticity and neurogenesis, exists throughout the normal lifespan but declines with age and is significantly impaired in individuals with Alzheimer's disease. Hence, promoting neuroplasticity may represent an effective strategy with which Alzheimer's disease can be alleviated. Due to their significant ability to self-renew, differentiate, and migrate, neural stem cells play an essential role in reversing synaptic and neuronal damage, reducing the pathology of Alzheimer's disease, including amyloid-ß, tau protein, and neuroinflammation, and secreting neurotrophic factors and growth factors that are related to plasticity. These events can promote synaptic plasticity and neurogenesis to repair the microenvironment of the mammalian brain. Consequently, neural stem cells are considered to represent a potential regenerative therapy with which to improve Alzheimer's disease and other neurodegenerative diseases. In this review, we discuss how neural stem cells regulate neuroplasticity and optimize their effects to enhance their potential for treating Alzheimer's disease in the clinic.
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Chronic obstructive pulmonary disease (COPD) is a persistent and progressive respiratory disorder characterized by expiratory airflow limitation caused by chronic inflammation. Evidence has shown that COPD is correlated with neutrophil chemotaxis towards the airways, resulting in neutrophilic airway inflammation. This study aimed to evaluate neutrophil chemotaxis in bronchoalveolar lavage fluid (BALF) from COPD patients using a high-throughput nine-unit microfluidic platform and explore the possible correlations between neutrophil migratory dynamics and COPD development. The results showed that BALF from COPD patients induced stronger neutrophil chemotaxis than the Control BALF. Our results also showed that the chemotactic migration of neutrophils isolated from the blood of COPD patients was not significantly different from neutrophils from healthy controls, and neutrophil migration in three known chemoattractants (fMLP, IL-8, and LTB4) was not affected by glucocorticoid treatment. Moreover, comparison with clinical data showed a trend of a negative relationship between neutrophil migration chemotactic index (C. I.) in COPD BALF and patient's spirometry data, suggesting a potential correlation between neutrophil migration and the severity of COPD. The present study demonstrated the feasibility of using the microfluidic platform to assess neutrophil chemotaxis in COPD pathogenesis, and it may serve as a potential marker for COPD evaluation in the future.
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Autologous cell therapy manufacturing timeframes constitute bottlenecks in clinical management pathways of severe burn patients. While effective temporary wound coverings exist for high-TBSA burns, any means to shorten the time-to-treatment with cytotherapeutic skin grafts could provide substantial therapeutic benefits. This study aimed to establish proofs-of-concept for a novel combinational cytotherapeutic construct (autologous/allogeneic DE-FE002-SK2 full dermo-epidermal graft) designed for significant cutaneous cell therapy manufacturing timeframe rationalization. Process development was based on several decades (four for autologous protocols, three for allogeneic protocols) of in-house clinical experience in cutaneous cytotherapies. Clinical grade dermal progenitor fibroblasts (standardized FE002-SK2 cell source) were used as off-the-freezer substrates in novel autologous/allogeneic dermo-epidermal bilayer sheets. Under vitamin C stimulation, FE002-SK2 primary progenitor fibroblasts rapidly produced robust allogeneic dermal templates, allowing patient keratinocyte attachment in co-culture. Notably, FE002-SK2 primary progenitor fibroblasts significantly outperformed patient fibroblasts for collagen deposition. An ex vivo de-epidermalized dermis model was used to demonstrate the efficient DE-FE002-SK2 construct bio-adhesion properties. Importantly, the presented DE-FE002-SK2 manufacturing process decreased clinical lot production timeframes from 6-8 weeks (standard autologous combined cytotherapies) to 2-3 weeks. Overall, these findings bear the potential to significantly optimize burn patient clinical pathways (for rapid wound closure and enhanced tissue healing quality) by combining extensively clinically proven cutaneous cell-based technologies.
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OBJECTIVES: Childhood adversity and lifestyle have been associated with frailty in later life, but not much is known about factors that may explain these associations. Therefore, this study aims to investigate the association of childhood adversity with frailty, and the mediating role of unhealthy lifestyle in the association. METHODS: This lifespan analysis included 152,914 adults aged 40-69 years old from the UK Biobank. We measured childhood adversity with five items: physical neglect, emotional neglect, sexual abuse, physical abuse, and emotional abuse through online mental health survey. Frailty was measured by the frailty index; an unhealthy lifestyle score (range: 0-5) was calculated based on unhealthy body mass index, smoking, alcohol consumption, physical inactivity, and unhealthy diet at the baseline survey. Multiple logistic regression and mediation analysis were performed. RESULTS: A total of 10,078 participants (6.6%) were defined as having frailty. Participants with any childhood adversity had higher odds of frailty. For example, in the fully adjusted model, with a one-point increase in cumulative score of childhood adversity, the odds of frailty increased by 38% (odds ratio: 1.38; 95% Confidence Interval: 1.36, 1.40). Unhealthy lifestyle partially mediated the associations of childhood adversity with frailty (mediation proportion: 4.4%-7.0%). The mediation proportions were largest for physical (8.2%) and sexual (8.1%) abuse. CONCLUSIONS: Childhood adversity was positively associated with frailty, and unhealthy lifestyle partially mediated the association. This newly identified pathway highlights the potential of lifestyle intervention strategies among those who experienced childhood adversity (in particular, physical, and sexual abuse) to promote healthy aging.
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BACKGROUND: Concomitant diseases often occur in cancer patients and are important in decision-making regarding treatments. However, information regarding the prognostic relevance of comorbidities for mortality risk is still limited among Chinese gastric cancer (GC) patients. This study aimed to investigate the association between comorbidities and 3-year mortality risk. METHODS: This retrospective study enrolled 376 GC patients undergoing radical gastrectomy at the Affiliated Zhongshan Hospital of Dalian University from January 2011 to December 2019. Demographic and clinicopathological information and treatment outcomes were collected. Patients were divided into low-, moderate- and high-risk comorbidity groups based on their Charlson Comorbidity Index (CCI) and age-adjusted CCI (ACCI) scores. Kaplan-Meier survival and Cox regression analyses were used to examine 3-year overall survival (OS) and mortality risk for each group. RESULTS: The median follow-up time was 43.5 months, and 40.2% (151/376) of GC patients had died at the last follow-up. There were significant differences in OS rates between ACCI-based comorbidity groups (76.56; 64.51; 54.55%, log-rank P = 0.011) but not between CCI-based comorbidity groups (log-rank P = 0.16). The high-risk comorbidity group based on the ACCI remained a significant prognostic factor for 3-year OS in multivariate analysis, with an increased mortality risk (hazard ratio [HR], 1.99; 95% CI, 1.15-3.44). Subgroup analysis revealed that this pattern only held for male GC patients but not for female patients. CONCLUSION: The present study suggested that high-risk comorbidities were significantly associated with a higher mortality risk, particularly in Chinese male GC patients. Moreover, the ACCI score was an independent prognostic factor of long-term mortality.
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BACKGROUND: Triple-negative breast cancer (TNBC) is a subtype of breast cancer with higher aggressiveness and poorer outcomes. Recently, long non-coding RNAs (lncRNAs) have become the crucial gene regulators in the progression of human cancers. However, the function and underlying mechanisms of lncRNAs in TNBC remains unclear. METHODS: Based on public databases and bioinformatics analyses, the low expression of lncRNA MIDEAS-AS1 in breast cancer tissues was detected and further validated in a cohort of TNBC tissues. The effects of MIDEAS-AS1 on proliferation, migration, invasion were determined by in vitro and in vivo experiments. RNA pull-down assay and RNA immunoprecipitation (RIP) assay were carried out to reveal the interaction between MIDEAS-AS1 and MATR3. Luciferase reporter assay, Chromatin immunoprecipitation (ChIP) and qRT-PCR were used to evaluate the regulatory effect of MIDEAS-AS1/MATR3 complex on NCALD. RESULTS: LncRNA MIDEAS-AS1 was significantly downregulated in TNBC, which was correlated with poor overall survival (OS) and progression-free survival (PFS) in TNBC patients. MIDEAS-AS1 overexpression remarkably inhibited tumor growth and metastasis in vitro and in vivo. Mechanistically, MIDEAS-AS1 mainly located in the nucleus and interacted with the nuclear protein MATR3. Meanwhile, NCALD was selected as the downstream target, which was transcriptionally regulated by MIDEAS-AS1/MATR3 complex and further inactivated NF-κB signaling pathway. Furthermore, rescue experiment showed that the suppression of cell malignant phenotype caused by MIDEAS-AS1 overexpression could be reversed by inhibition of NCALD. CONCLUSIONS: Collectively, our results demonstrate that MIDEAS-AS1 serves as a tumor-suppressor in TNBC through modulating MATR3/NCALD axis, and MIDEAS-AS1 may function as a prognostic biomarker for TNBC.
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Rationale: In the healthy lung, the pseudostratified conducting airway epithelium is anchored to the reticular basement membrane (RBM) via hemidesmosome junction complexes formed between basal cells and the extracellular matrix (ECM). The RBM within the healthy lung is composed of the ECM proteins laminin and collagen-IV. In patients with asthma, the RBM is remodeled with collagen-I, -III and fibronectin deposition. The goal of this study was to assess the effect of RBM ECM proteins on basal airway epithelial cell attachment, spreading and barrier formation using real-time electrical cell-substrate impedance sensing (ECIS). Methods: ECIS 8-well arrays were coated with 50 µg/mL of fibronectin, collagen-I, collagen-III, collagen-IV, or laminin and compared to bovine serum albumin (BSA) or uncoated controls. The airway epithelial cell line (1HAEo-) was seeded 40, 50, 60, and 70 k cells/well and continuously monitored over 70 h to assess cell attachment, spreading and barrier formation using high (64 k Hz) and low (500 Hz) frequency resistance and capacitance. Data were analyzed using a one-phase decay model from which half-life (time cells cover half of the electrode area) and rate-constant (cell-spreading rate/h) were determined and a generalized additive mixed effect model (GAMM) was used to assess ECM proteins over the entire experiment. Results: High-frequency (64 kHz) capacitance measures demonstrated the half-life for 1HAEo-cells to attach was fastest when grown on fibronectin (6.5 h), followed by collagen-I (7.2 h) and collagen-III (8.1 h), compared to collagen-IV (11.3 h), then laminin (13.2 h) compared to BSA (12.4 h) and uncoated (13.9 h) controls. High-frequency (64 kHz) resistance measures demonstrated that the rate of 1HAEo- cell spreading was significantly faster on fibronectin and collagen-I compared to collagen-III, collagen-IV, laminin, BSA and the uncoated control. Low-frequency (500 Hz) resistance measures demonstrated that 1HAEo-cells formed a functional barrier fastest when grown on fibronectin and collagen-I, compared to the other ECM conditions. Lastly, the distance of 1HAEo-cells from the ECM substrates was the smallest when grown on fibronectin reflecting high cell-matrix adhesion. Conclusion: Airway epithelial cells attach, spread and form a barrier fastest on fibronectin, and collagen-I and these reticular basement membrane ECM proteins may play a protective role in preserving the epithelial barrier during airway remodeling in asthma.
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The prognosis of lung metastatic osteosarcoma (OS) remains disappointing. siRNA-based gene silencing of VEGFR2 is a promising treatment strategy for lung metastatic OS, but there is a lack of safe and efficient delivery systems to encapsulate siRNAs for in vivo administration. This study presented a synthetic biological strategy that remolds the host liver with synthesized genetic circuits for efficient in vivo VEGFR2 siRNA delivery. After being taken-up by hepatocytes, the genetic circuit (in the form of a DNA plasmid) reprogrammed the liver to drive the autonomous intrahepatic assembly and encapsulation of VEGFR2 siRNAs into secretory small extracellular vesicles (sEVs), thus allowing for the transport of self-assembled VEGFR2 siRNAs towards the lung. The results showed that our strategy was superior to the positive medicine (Apatinib) for OS lung metastasis in terms of therapeutic efficacy and toxic adverse effects and may provide a feasible and viable therapeutic solution for lung metastatic OS.
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Neoplasias Ósseas , Vesículas Extracelulares , Osteossarcoma , Humanos , RNA Interferente Pequeno/genética , Osteossarcoma/genética , Osteossarcoma/terapia , Neoplasias Ósseas/genética , Neoplasias Ósseas/terapia , PulmãoRESUMO
OBJECTIVE: This study aimed primarily to analyze the three-dimensional (3D) changes in the pharyngeal airway (PA), and secondarily, the hyoid bone (HB) and the craniocervical (CC) following stabilization splint (SS) therapy in adult patients with temporomandibular joint disorders (TMD) and mandibular deviation (MD). METHODS: Thirty-five adult patients with TMD and MD, who were treated using SS with a mean age of 25.14 years, were enrolled in this retrospective clinical study. Pre- and post-therapeutic cone beam computed tomography (CBCT) scans were analyzed. PA dimension (nasopharyngeal, oropharyngeal, hypopharyngeal, sub- hypopharyngeal, and total pharyngeal airway spaces were measured in surface area, volume, minimum constricted area (MCA) and width), HB position and CC posture were analyzed three-dimensionally using InVivo 6.0.3 and Dolphin 11.95 software. Wilcoxon rank-sum or Paired t-test was conducted, and P< 0.05 was considered significant. RESULTS: SS therapy was administered for a period of 9.49±4.02 months. The oropharyngeal airway space showed a significant decrease in sagittal width. The hypopharyngeal surface area, volume, MCA and sagittal width decreased significantly. In terms of HB, hyoid-mandibular plane (H-MP), retrognathia-third vertebra's most inferior-anterior (RGN-C3ia) and retrognathia-Sella (RGN-S) distances significantly decreased. The Nasion-Sella line and the line that passes through C2ip to the odontoid process posterior tangent (NSL-OPT) angle in CC posture also decreased significantly. CONCLUSION: SS therapy in TMD patients with MD mainly results in narrowing of the hypopharyngeal region, no change in HB position and improvement in head posture. These results undoubtedly assist in diagnosis and treatment of clinical conditions.
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Electrocatalytic hydrogen evolution reaction (HER) is one of the most promising and clean strategies to prepare hydrogen on a large scale. Nevertheless, the efficiency of HER is greatly restricted by the large overpotential at the anode, and it is necessary to develop low cost electrocatalysts with excellent performance and stability. Molybdenum carbide has shown great potential in the field of HER due to its unique electronic structure and physical and chemical properties. In this paper, the current progress of molybdenum carbide-based catalysts for HER is summarized. The influence of phase structure, nanostructure, heterostructure and heteroatoms doping on its catalytic performance is discussed in detail. Especially, the catalytic mechanisms are analyzed according to structural characterization and theoretical calculation results. Finally, the challenges and prospects for the further development of molybdenum carbide-based catalysts for HER are put forward to guide the progress of this field.
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P2X receptors are cation channels that sense extracellular ATP. Many therapeutic candidates targeting P2X receptors have begun clinical trials or acquired approval for the treatment of refractory chronic cough (RCC) and other disorders. However, the present negative allosteric modulation of P2X receptors is primarily limited to the central pocket or the site below the left flipper domain. Here, we uncover a mechanism of allosteric regulation of P2X3 in the inner pocket of the head domain (IP-HD), and show that the antitussive effects of quercetin and PSFL2915 (our nM-affinity P2X3 inhibitor optimized based on quercetin) on male mice and guinea pigs were achieved by preventing allosteric changes of IP-HD in P2X3. While being therapeutically comparable to the newly licensed P2X3 RCC drug gefapixant, quercetin and PSFL2915 do not have an adverse effect on taste as gefapixant does. Thus, allosteric modulation of P2X3 via IP-HD may be a druggable strategy to alleviate RCC.
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Carcinoma de Células Renais , Neoplasias Renais , Masculino , Animais , Cobaias , Camundongos , Tosse/tratamento farmacológico , Quercetina/farmacologia , Quercetina/uso terapêutico , PaladarRESUMO
Microalgae has been widely used in aquaculture to improve both the water environment and fish growth; however, the current understanding of the effects of microalgae addition on the key players involved in regulating the water environment and fish health, such as microorganisms, remains limited. Here, a 50-day mesocosm experiment was set up to simulate the culture of Genetic Improvement of Farmed Tilapia (GIFT, Oreochromis niloticus) with an average weight of 14.18 ± 0.93 g and an average length of 82.77 ± 2.80 mm. Different amounts of Chlorella pyrenoidosa were added into these artificial systems to investigate dynamics of bacterial communities in aquaculture water, fish gill, and gut using amplicon-based high-throughput sequencing technology. Our results showed that Chlorella pyrenoidosa addition increased diversity and network complexity of gill-associated bacterial communities rather than those of the water and gut. Furthermore, more biomarkers in the gill-associated bacterial communities were detected in response to Chlorella pyrenoidosa addition than the water and fish gut samples. These findings highlighted the high sensitivity of gill-associated bacterial communities in response to the Chlorella pyrenoidosa addition, implying Chlorella pyrenoidosa addition could play important roles in regulating the fish mucosal immunity by altering the gill-associated microbiota.
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To assess the effectiveness and molecular mechanisms of mild hypothermia and remote ischemic postconditioning (RIPC) in patients with acute ischemic stroke (AIS) who have undergone thrombolysis therapy. A total of 58 AIS patients who received recombinant tissue plasmin activator (rt-PA) intravenous thrombolysis were included in this prospective study. Participants were randomly allocated to the experimental group (rt-PA intravenous thrombolysis plus mild hypothermic ice cap plus remote ischemic brain protection, n = 30) and the control group (rt-PA intravenous thrombolysis plus 0.9% saline, n = 28). The RIPC was performed for 14 consecutive days on both upper limb arteries spaced 2 minutes apart. Five cycles of ischemia-reperfusion were performed sequentially (2-2, 3-3, 4-4, 5-5, 5-0 minutes, respectively). The outcome measures of the National Institute of Health stroke scale (NIHSS) score, volume of cerebral infarction, serum levels of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1ß, tumor necrosis factor α, nuclear factors kappa B (NF-κB), and NOD-1ike receptor pyrin 3 (NLRP3) were evaluated at different time points after treatment. Similarly, the 90-day modified Rankin Scale (mRS) scores were compared between the two groups. After treatment, the NIHSS score, MDA, NF-κB, and NLRP3 levels in the experimental group were significantly lower than those in the control group (p < 0.05). While the SOD in the experimental group was significantly higher than in the control group (p < 0.05), the NIHSS scores decreased within groups (all p < 0.05) in both experimental and control groups. The 90-day mRS score (0-2 points) in the experimental group was significantly higher than that in the control group (73.33% vs. 53.57%, p < 0.05) and no significant differences were observed in the safety indices between the two groups (all p > 0.05). Our study shows that combining mild hypothermia and RIPC has a positive effect on brain protection and can significantly reduce the oxidative stress and associated outburst of inflammatory response. The Clinical Trial Registration number is ChiCTR2300073136.
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Seeds establish dormancy to delay germination until the arrival of a favorable growth season. Here, we identify a fate switch constituted by the MKK3-MPK7 kinase cascade and the ethylene response factor ERF4 responsible for the seed state transition from dormancy to germination. We show that dormancy-breaking factors activate the MKK3-MPK7 module, which affects and relies on the expression of some EXPAs to control seed dormancy. Furthermore, we identify a direct downstream substrate of this module, ERF4, which suppresses the expression of these EXPAs by directly binding to the GCC boxes in their exon regions. The activated MKK3-MPK7 module phosphorylates ERF4, leading to its rapid degradation, thereby releasing its inhibitory effect on the expression of these EXPAs. Overall, our work identifies a signaling chain consisting of protein phosphorylation, degradation, and gene transcription, dependent on which the germination promoters within the embryo are sensing and activated by the germination signals from ambient conditions.
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AIMS: The clinical correlates and outcomes of asymptomatic atrial fibrillation (AF) in hospitalized patients are largely unknown. We aimed to investigate the clinical correlates and in-hospital outcomes of asymptomatic AF in hospitalized Chinese patients. METHODS AND RESULTS: We conducted a cross-sectional registry study of inpatients with AF enrolled in the Improving Care for Cardiovascular Disease in China-Atrial Fibrillation Project between February 2015 and December 2019. We investigated the clinical characteristics of asymptomatic AF and the association between the clinical correlates and in-hospital outcomes of asymptomatic AF. Asymptomatic and symptomatic AF were defined according to the European Heart Rhythm Association score.Asymptomatic patients were more commonly male (56.3%) and had more comorbidities such as hypertension (57.4%), diabetes mellitus (18.6%), peripheral artery disease (PAD) (2.3%), coronary artery disease (CAD) (55.5%), previous history of stroke/transient ischemic attack (TIA) (17.9%), and myocardial infarction (MI) (5.4%); however, they had less prevalent heart failure (9.6%) or left ventricular ejection fractions ≤40% (7.3%). Asymptomatic patients were more often hospitalized with a non-AF diagnosis as the main diagnosis and were more commonly first diagnosed with AF (23.9%) and long-standing persistent/permanent AF (17.0%). The independent determinants of asymptomatic presentation were male sex, long-standing persistent AF/permanent AF, previous history of stroke/TIA, MI, PAD, and previous treatment with antiplatelet drugs. The incidence of in-hospital clinical events, including all-cause death, ischemic stroke/TIA, and acute coronary syndrome (ACS), was higher in asymptomatic patients than in symptomatic patients, and asymptomatic clinical status was an independent risk factor for in-hospital all-cause death, ischemic stroke/TIA, and ACS. CONCLUSIONS: Asymptomatic atrial fibrillation is common among hospitalized patients with AF. Asymptomatic clinical status is associated with male sex, comorbidities, and a higher risk of in-hospital outcomes. The adoption of effective management strategies for patients with AF should not be solely based on clinical symptoms.
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Purpose: Deficits in voluntary activation of the core stabilizing muscles are consistently observed in patients with chronic low back pain (CLBP); however, the underlying neural mechanism remains unclear. This cross-sectional study aimed at testing the hypothesis that the impaired voluntary activation of core stabilizing muscles is associated with structural and functional alterations in the basal ganglia, thalamus, and cortex in patients with CLBP. Methods: We obtained structural and resting-state functional magnetic resonance imaging (rs-fMRI) data from 53 patients with CLBP and 67 healthy controls and estimated the alterations in grey matter volume (GMV) and functional and effective connectivity (EC) of regions with altered GMV via whole brain analysis. The voluntary activation of the multifidus (MF) and transversus abdominis (TrA) was evaluated by ultrasound imaging in these patients. Results: Compared with the HCs, they displayed a significant decrease in GMV in the bilateral thalamus and caudate nucleus, a significant increase in GMV in the left middle frontal gyrus, and increased resting-state functional connectivity between the right caudate nucleus and the bilateral precuneus (voxel-level p < 0.005, Gaussian random field-corrected p < 0.05). The patients also showed increased EC from the right caudate nucleus to the bilateral precuneus, which was significantly correlated with voluntary activation of the bilateral MF and TrA (all p < 0.050). Conclusions: Grey matter alterations may be confined to regions responsible for perception, motor control, and emotion regulation in patients with CLBP. The interrupted EC from the basal ganglia to the default mode network might be involved in the impairment of voluntary activation of the core stabilizing muscles.
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Dor Lombar , Humanos , Dor Lombar/diagnóstico por imagem , Estudos Transversais , Gânglios da Base/diagnóstico por imagem , Músculos Abdominais/diagnóstico por imagem , EncéfaloRESUMO
Series compensation grids connected with type-3 wind turbine generator (WTG)-based wind farms have suffered numerous subsynchronous oscillation (SSO) events worldwide. For early alerting of SSO and effective development of protection and control strategies, it is critical to monitor and identify SSO accurately and quickly. Ambient data is continuously available, which is useful for online monitoring. This paper proposes an ambient data-driven SSO online monitoring method based on the Kalman filter (KF) combined with the multi-model partitioning filter (MMPF). The KF is utilized to fit the measured ambient data with an auto regressive (AR) model. Then, the damping factor (or damping ratio) and frequency in the SSO mode can be acquired by solving the roots of the characteristic polynomial corresponding to the AR model. Moreover, the MMPF is an effective model order selection method applied to the KF for better identification. The performance of the MMPF-KF method is demonstrated by simulations and real-time experiments. The results of case studies validate the effectiveness of the proposed method under various conditions.