46 research outputs found

    Causal connectivity abnormalities of regional homogeneity in children with attention deficit hyperactivity disorder: a rest-state fMRI study

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    The present study aimed to investigate individual differences of causal connectivity between brain regions in attention deficit hyperactivity disorder (ADHD) which was a psychiatric disorder. Resting-state functional magnetic resonance imaging (R-fMRI) data of typically-developing controls (TDC) children group and combined ADHD (ADHD-C) children group were distinguished by the support vector machine (SVM) with linear kernel function, based on regional homogeneity (ReHo), amplitude of low frequency fluctuation (ALFF) and fractional ALFF (FALFF). The highest classification accuracy yielded by ReHo was 90.91 %. Furthermore, the granger causality analysis (GCA) method based on the classified weight map of regions of interesting (ROIs) showed that five causal flows existed significant difference between TDC and ADHD-C. That is, the averaged GCA values of three causal connections (i.e. left VLPFC left CC1, right PoCG left CC1, and right PoCG right CC2) for ADHD-C were separately stronger than those for TDC. And the other two connections (i.e. right FEF right SOG and right CC1 right SOG) were weaker for ADHD-C than those for TDC. In addition, only two causality flows (i.e. left VLPFC left CC1 and right PoCG right CC2) presented that their GCA values were positively correlation with ADHD index scores, respectively. Our findings revealed that ADHD children represented widespread abnormalities in the causality connectivity, especially involved in the attention and memory related regions. And further provided evidence that the potential neural causality flows could play a key role in characterizing individual’s ADHD

    Role of Epicardial Adipose Tissue in Triggering and Maintaining Atrial Fibrillation

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    Atrial fibrillation is the most common arrhythmia leading to cardiogenic stroke. Without membranous sructure between epicardial adipose tissue and atrial myocardium, epicardial adipose tissue directly covers the surface of the atrial myocardium. The formation of an epicardial adipose tissue inflammatory microenvironment, fibrosis, infiltration by epicardial adipose tissue, autonomic dysfunction and oxidative stress are important mechanisms that trigger and maintain atrial fibrillation. Those mechanisms are reviewed herein

    Termination of Recurrent Atrial Fibrillation by Superior Vena Cava Isolation: A Case Report

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    Background: Paroxysmal atrial fibrillation can be triggered by non-pulmonary vein foci, such as the superior vena cava. Here, we report the case of a patient with a 6-year history of paroxysmal atrial fibrillation who received cryoballoon ablation in 2012 but relapsed in 2014. He then received cardiac radiofrequency ablation, which successfully isolated the left pulmonary vein and superior vena cava, but the arrhythmia recently relapsed again. The tachycardia was finally successfully terminated by ablation on the free wall without recurrence during a 2-year following up. Conclusion: Superior vena cava isolation may not require ablation isolation with a full circle way and can be accomplished by ablating several connection points between the superior vena cava and the right atrium

    Explore postgraduate biomedical engineering course integration between medical signal processing and drug development: example for drug development in brain disease

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    Medical signal processing is a compulsory course in our university’s undergraduate biomedical engineering programme. Recently, application of medical signal processing in supporting new drug development has emerged as a promising strategy in neurosciences. Here, we discuss the curriculum reformation in biomedical signal processing course in the context of drug development and application in central nervous system, with a particular emphasis in knowledge integration

    Sex‐specific activation of SK current by isoproterenol facilitates action potential triangulation and arrhythmogenesis in rabbit ventricles

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    Sex has a large influence on cardiac electrophysiological properties. Whether sex differences exist in apamin‐sensitive small conductance Ca2+‐activated K+ (SK) current (IKAS) remains unknown. We performed optical mapping, transmembrane potential, patch clamp, western blot and immunostaining in 62 normal rabbit ventricles, including 32 females and 30 males. IKAS blockade by apamin only minimally prolonged action potential (AP) duration (APD) in the basal condition for both sexes, but significantly prolonged APD in the presence of isoproterenol in females. Apamin prolonged APD at the level of 25% repolarization (APD25) more prominently than APD at the level of 80% repolarization (APD80), consequently reversing isoproterenol‐induced AP triangulation in females. In comparison, apamin prolonged APD to a significantly lesser extent in males and failed to restore the AP plateau during isoproterenol infusion. IKAS in males did not respond to the L‐type calcium current agonist BayK8644, but was amplified by the casein kinase 2 (CK2) inhibitor 4,5,6,7‐tetrabromobenzotriazole. In addition, whole‐cell outward IKAS densities in ventricular cardiomyocytes were significantly larger in females than in males. SK channel subtype 2 (SK2) protein expression was higher and the CK2/SK2 ratio was lower in females than in males. IKAS activation in females induced negative intracellular Ca2+–voltage coupling, promoted electromechanically discordant phase 2 repolarization alternans and facilitated ventricular fibrillation (VF). Apamin eliminated the negative Ca2+–voltage coupling, attenuated alternans and reduced VF inducibility, phase singularities and dominant frequencies in females, but not in males. We conclude that β‐adrenergic stimulation activates ventricular IKAS in females to a much greater extent than in males. IKAS activation plays an important role in ventricular arrhythmogenesis in females during sympathetic stimulation

    SoybeanNet: Transformer-Based Convolutional Neural Network for Soybean Pod Counting from Unmanned Aerial Vehicle (UAV) Images

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    Soybeans are a critical source of food, protein and oil, and thus have received extensive research aimed at enhancing their yield, refining cultivation practices, and advancing soybean breeding techniques. Within this context, soybean pod counting plays an essential role in understanding and optimizing production. Despite recent advancements, the development of a robust pod-counting algorithm capable of performing effectively in real-field conditions remains a significant challenge This paper presents a pioneering work of accurate soybean pod counting utilizing unmanned aerial vehicle (UAV) images captured from actual soybean fields in Michigan, USA. Specifically, this paper presents SoybeanNet, a novel point-based counting network that harnesses powerful transformer backbones for simultaneous soybean pod counting and localization with high accuracy. In addition, a new dataset of UAV-acquired images for soybean pod counting was created and open-sourced, consisting of 113 drone images with more than 260k manually annotated soybean pods captured under natural lighting conditions. Through comprehensive evaluations, SoybeanNet demonstrated superior performance over five state-of-the-art approaches when tested on the collected images. Remarkably, SoybeanNet achieved a counting accuracy of 84.51%84.51\% when tested on the testing dataset, attesting to its efficacy in real-world scenarios. The publication also provides both the source code (\url{https://github.com/JiajiaLi04/Soybean-Pod-Counting-from-UAV-Images}) and the labeled soybean dataset (\url{https://www.kaggle.com/datasets/jiajiali/uav-based-soybean-pod-images}), offering a valuable resource for future research endeavors in soybean pod counting and related fields.Comment: 12 pages, 5 figure

    Specific frequency bands of amplitude low-frequency fluctuations in memory-related cognitive impairment: predicting Alzheimer’s disease

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    Resting-state functional magnetic resonance imaging was utilized to measure the amplitude low frequency fluctuations (ALFF) in human subjects with Alzheimer’s disease (AD) and normal control (NC). Two specific frequency bands (Slow5: 0.01-0.027Hz and Slow4: 0.027-0.073Hz) were analysed in the main cognitive control related four subregions of the right ventral lateral prefrontal cortex (VLPFC), i.e. IFJ, posterior-VLPFC, mid-VLPFC, and anterior-VLPFC. Differences in ALFF values between the AD and the NC group were found throughout the subregions of the right VLPFC. Compared to normal control group, decreased ALFF values were observed in AD patients in the IFJ (in two given frequency bands), and the mid-VLPFC (in Slow5). In contrast, increased ALFF valued were observed in AD patients in the posterior- and anterior-VLPFC (in both Slow5 and Slow4), and also in the mid-VLPFC in Slow4. Moreover, significant ALFF differences between the IFJ and three other subregions of the right VLPFC were found. Furthermore, ALFF values in the right VLPFC showed significant correlations with the time course of disease. Taken together, our findings suggest that AD patients have largely abnormalities in intrinsic neural oscillations which are in line with the AD pathophysiology, and further reveal that the abnormalities are dependent on specific frequency bands. Thus, frequency-domain analyses of the ALFF may provide a useful tool to investigate the AD pathophysiology

    Interleukin-22 Ameliorates Cerulein-Induced Pancreatitis in Mice by Inhibiting the Autophagic Pathway

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    Pancreatitis occurs when digestive enzymes are activated in the pancreas. Severe pancreatitis has a 10-30% mortality rate. No specific treatments for pancreatitis exist now. Here, we discovered that interleukin-22 (IL-22) may have therapeutic potential in treating acute and chronic pancreatitis. Wild-type and IL-22 knockout mice were equally susceptible to cerulein-induced acute and chronic pancreatitis, whereas liver-specific IL-22 transgenic mice were completely resistant to cerulein-induced elevation of serum digestive enzymes, pancreatic necrosis and apoptosis, and inflammatory cell infiltration. Treatment of wild-type mice with recombinant IL-22 or adenovirus IL-22 markedly attenuated the severity of cerulein-induced acute and chronic pancreatitis. Mechanistically, we show that the protective effect of IL-22 on pancreatitis was mediated via the induction of Bcl-2 and Bcl-XL, which bind to Beclin-1 and subsequently inhibit autophagosome formation to ameliorate pancreatitis. In conclusion, IL-22 ameliorates cerulein-induced pancreatitis by inhibiting the autophagic pathway. IL-22 could be a promising therapeutic drug to treat pancreatitis

    Single-cell sequencing combined with machine learning reveals the mechanism of interaction between epilepsy and stress cardiomyopathy

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    BackgroundEpilepsy is a disorder that can manifest as abnormalities in neurological or physical function. Stress cardiomyopathy is closely associated with neurological stimulation. However, the mechanisms underlying the interrelationship between epilepsy and stress cardiomyopathy are unclear. This paper aims to explore the genetic features and potential molecular mechanisms shared in epilepsy and stress cardiomyopathy.MethodsBy analyzing the epilepsy dataset and stress cardiomyopathy dataset separately, the intersection of the two disease co-expressed differential genes is obtained, the co-expressed differential genes reveal the biological functions, the network is constructed, and the core modules are identified to reveal the interaction mechanism, the co-expressed genes with diagnostic validity are screened by machine learning algorithms, and the co-expressed genes are validated in parallel on the epilepsy single-cell data and the stress cardiomyopathy rat model.ResultsEpilepsy causes stress cardiomyopathy, and its key pathways are Complement and coagulation cascades, HIF-1 signaling pathway, its key co-expressed genes include SPOCK2, CTSZ, HLA-DMB, ALDOA, SFRP1, ERBB3. The key immune cell subpopulations localized by single-cell data are the T_cells subgroup, Microglia subgroup, Macrophage subgroup, Astrocyte subgroup, and Oligodendrocytes subgroup.ConclusionWe believe epilepsy causing stress cardiomyopathy results from a multi-gene, multi-pathway combination. We identified the core co-expressed genes (SPOCK2, CTSZ, HLA-DMB, ALDOA, SFRP1, ERBB3) and the pathways that function in them (Complement and coagulation cascades, HIF-1 signaling pathway, JAK-STAT signaling pathway), and finally localized their key cellular subgroups (T_cells subgroup, Microglia subgroup, Macrophage subgroup, Astrocyte subgroup, and Oligodendrocytes subgroup). Also, combining cell subpopulations with hypercoagulability as well as sympathetic excitation further narrowed the cell subpopulations of related functions
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