Abnormal surface morphology of the central sulcus in children with attention-deficit/hyperactivity disorder

The central sulcus (CS) divides the primary motor and somatosensory areas, and its three-dimensional (3D) anatomy reveals the structural changes of the sensorimotor regions. Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that is associated with sensorimotor and executive function deficits. However, it is largely unknown whether the morphology of the CS alters due to inappropriate development in the ADHD brain. Here, we employed the sulcus-based morphometry approach to investigate the 3D morphology of the CS in 42 children whose ages spanned from 8.8 to 13.5 years (21 with ADHD and 21 controls). After automatic labeling of each CS, we computed 7 regional shape metrics for each CS, including the global average length, average depth, maximum depth, average span, surface area, average cortical thickness and local sulcal profile. We found that the average depth and maximum depth of the left CS as well as the average cortical thickness of bilateral CS in the ADHD group were significantly larger than those in the healthy children. Moreover, significant between-group differences in the sulcal profile had been found in middle sections of the CSs bilaterally, and these changes were positively correlated with the hyperactivity-impulsivity scores in the children with ADHD. Altogether, our results provide evidence for the abnormity of the CS anatomical morphology in children with ADHD due to the structural changes in the motor cortex, which significantly contribute to the clinical symptomatology of the disorder

Profibrotic, Electrical, and Calcium-Handling Remodeling of the Atria in Heart Failure Patients With and Without Atrial Fibrillation

Atrial fibrillation (AF) and heart failure (HF) are common cardiovascular diseases that often co-exist. Animal models have suggested complex AF-promoting atrial structural, electrical, and Ca2+-handling remodeling in the setting of HF, but data in human samples are scarce, particularly regarding Ca2+-handling remodeling. Here, we evaluated atrial remodeling in patients with severe left ventricular (LV) dysfunction (HFrEF), long-standing persistent (‘chronic’) AF (cAF) or both (HFrEF-cAF), and sinus rhythm controls with normal LV function (Ctl) using western blot in right-atrial tissue, sharp-electrode action potential (AP) measurements in atrial trabeculae and voltage-clamp experiments in isolated right-atrial cardiomyocytes. Compared to Ctl, expression of profibrotic markers (collagen-1a, fibronectin, periostin) was higher in HFrEF and HFrEF-cAF patients, indicative of structural remodeling. Connexin-43 expression was reduced in HFrEF patients, but not HFrEF-cAF patients. AP characteristics were unchanged in HFrEF, but showed classical indices of electrical remodeling in cAF and HFrEF-cAF (prolonged AP duration at 20% and shorter AP duration at 50% and 90% repolarization). L-type Ca2+ current (ICa,L) was significantly reduced in HFrEF, cAF and HFrEF-cAF, without changes in voltage-dependence. Potentially proarrhythmic spontaneous transient-inward currents were significantly more frequent in HFrEF and HFrEF-cAF compared to Ctl, likely resulting from increased sarcoplasmic reticulum (SR) Ca2+ load (integrated caffeine-induced current) in HFrEF and increased ryanodine-receptor (RyR2) single-channel open probability in HFrEF and HFrEF-cAF. Although expression and phosphorylation of the SR Ca2+-ATPase type-2a (SERCA2a) regulator phospholamban were unchanged in HFrEF and HFrEF-cAF patients, protein levels of SERCA2a were increased in HFrEF-cAF and sarcolipin expression was decreased in both HFrEF and HFrEF-cAF, likely increasing SR Ca2+ uptake and load. RyR2 protein levels were decreased in HFrEF and HFrEF-cAF patients, but junctin levels were higher in HFrEF and relative Ser2814-RyR2 phosphorylation levels were increased in HFrEF-cAF, both potentially contributing to the greater RyR2 open probability. These novel insights into the molecular substrate for atrial arrhythmias in HF-patients position Ca2+-handling abnormalities as a likely trigger of AF in HF patients, which subsequently produces electrical remodeling that promotes the maintenance of the arrhythmia. Our new findings may have important implications for the development of novel treatment options for AF in the context of HF

Design of Embedded Network Voice Communication Terminal Based on STM32 and μCOSIII

Aiming at the application demand of voice communication between user terminals in the simulated training environment, a design and implementation method of embedded network voice communication terminal based on STM32 and μCOSIII is proposed. The hardware module of communication terminal is based on STM32 microcontroller, voice communication module, LCD display module and SD card storage module. The embedded real-time operating system μCOSIII is transplanted in order to enhance the real time and stability of the control system, and the user interface management system STemWin is used to manage LCD module. The signal exchange protocol of speech communication is designed, and the realization of the communication function software based on TCP/IP protocol is completed. In order to detect the voice communication function of communication terminal, a communication server software based on .NET Framework platform is designed, which is responsible for managing the communication terminal and forwarding the communication data. The experimental results show that the user interface of the communication terminal is good, the data transmission is stable and the communication function is reliable

Differential Age-Related Changes in Structural Covariance Networks of Human Anterior and Posterior Hippocampus

The hippocampus plays an important role in memory function relying on information interaction between distributed brain areas. The hippocampus can be divided into the anterior and posterior sections with different structure and function along its long axis. The aim of this study is to investigate the effects of normal aging on the structural covariance of the anterior hippocampus (aHPC) and the posterior hippocampus (pHPC). In this study, 240 healthy subjects aged 18–89 years were selected and subdivided into young (18–23 years), middle-aged (30–58 years), and older (61–89 years) groups. The aHPC and pHPC was divided based on the location of uncal apex in the MNI space. Then, the structural covariance networks were constructed by examining their covariance in gray matter volumes with other brain regions. Finally, the influence of age on the structural covariance of these hippocampal sections was explored. We found that the aHPC and pHPC had different structural covariance patterns, but both of them were associated with the medial temporal lobe and insula. Moreover, both increased and decreased covariances were found with the aHPC but only increased covariance was found with the pHPC with age (p < 0.05, family-wise error corrected). These decreased connections occurred within the default mode network, while the increased connectivity mainly occurred in other memory systems that differ from the hippocampus. This study reveals different age-related influence on the structural networks of the aHPC and pHPC, providing an essential insight into the mechanisms of the hippocampus in normal aging

Table2_Association of oxidative stress, programmed cell death, GSTM1 gene polymorphisms, smoking and the risk of lung carcinogenesis: A two-step Mendelian randomization study.DOCX

Aim: We aimed to examine the association of oxidative stress, programmed cell death, smoking, and the GSTM1 gene in the risk of lung carcinogenesis. The two-step Mendelian randomization will reveal evidence supporting the association of the exposure and mediators with the resulting outcome.Methods: In step 1, we estimated the impact of smoking exposure on lung carcinogenesis and programmed cell death. Our study involved a total of 500,000 patients of European ancestry, from whom we obtained genotype imputation information. Specifically, we genotyped two arrays: the UK Biobank Axiom (UKBB) which accounted for 95% of marker content, and the UK BiLIEVE Axiom (UKBL). This allowed us to unmask the association between smoking exposure and the incidence of lung carcinogenesis. In step 2, we further examined the effects of smoking on oxidative stress, programmed cell death, and the incidence of lung carcinogenesis.Results: Different outcomes emerged from the two-step Mendelian randomization. The GSTM1 gene variant was found to be critical in the development of lung carcinogenesis, as its deletion or deficiency can induce the condition. A GWAS study on participant information obtained from the UK Biobank revealed that smoking interferes with the GSTM1 gene, causing programmed cell death in the lungs and ultimately leading to lung carcinogenesis. The relative risk of developing lung carcinogenesis associated with oxidative stress was significantly high among current smokers (a hazard ratio of 17.8, 95% confidence interval of 12.2–26.0) and heavy smokers (a hazard ratio of 16.6 and a 95% confidence interval of 13.6–20.3) compared to individuals who never smoked. The GSTM1 gene polymorphism was found to be 0.006 among participants who have never smoked, We compared the effect of smoking within two particular time frames, 6 years and 55 years, and found that smoking’s impact on the GSTM1 gene was highest among participants who were 55 years old. The genetic risk peaked among individuals aged 50 years and above (PRS of at least 80%).Conclusion: Exposure to smoking is a significant factor in developing lung carcinogenesis, as it is associated with programmed cell death and other mediators involved in the condition. Oxidative stress caused by smoking is also a key mechanism in lung carcinogenesis. The results of the present study highlight the association between oxidative stress, programmed cell death, and the GSTM1 gene in the development of lung carcinogenesis.</p

Effect of Continuous Planting on Tree Growth Traits and Growth Stress in Plantation Forests of <i>Eucalyptus urophylla × E. grandis</i>

Continuous planting is the primary method for managing Eucalyptus plantations. The “space-replacing time” approach assesses growth parameters of Eucalyptus trees in China across generations, including height, diameter at breast height (DBH), slenderness ratio, trunk oblateness, and longitudinal growth strain. The findings reveal: (1) significant variations in growth strain occur among generations, with average strain increasing noticeably; and (2) growth-linked traits of Eucalyptus urophylla × E. grandis are impacted, with negative correlation between slenderness ratio and growth strain, and positive correlation between height and trunk oblateness. Factors influencing growth strain include height, slenderness, and surface longitudinal growth strain at breast height, with strong correlations observed. These parameters serve as growth strain indicators. Continuous planting affects growth traits and strain in Eucalyptus plantations. It is advisable to select trees with stable or slow growth rates and to avoid continuous planting without limits

Table3_Association of oxidative stress, programmed cell death, GSTM1 gene polymorphisms, smoking and the risk of lung carcinogenesis: A two-step Mendelian randomization study.DOCX

Aim: We aimed to examine the association of oxidative stress, programmed cell death, smoking, and the GSTM1 gene in the risk of lung carcinogenesis. The two-step Mendelian randomization will reveal evidence supporting the association of the exposure and mediators with the resulting outcome.Methods: In step 1, we estimated the impact of smoking exposure on lung carcinogenesis and programmed cell death. Our study involved a total of 500,000 patients of European ancestry, from whom we obtained genotype imputation information. Specifically, we genotyped two arrays: the UK Biobank Axiom (UKBB) which accounted for 95% of marker content, and the UK BiLIEVE Axiom (UKBL). This allowed us to unmask the association between smoking exposure and the incidence of lung carcinogenesis. In step 2, we further examined the effects of smoking on oxidative stress, programmed cell death, and the incidence of lung carcinogenesis.Results: Different outcomes emerged from the two-step Mendelian randomization. The GSTM1 gene variant was found to be critical in the development of lung carcinogenesis, as its deletion or deficiency can induce the condition. A GWAS study on participant information obtained from the UK Biobank revealed that smoking interferes with the GSTM1 gene, causing programmed cell death in the lungs and ultimately leading to lung carcinogenesis. The relative risk of developing lung carcinogenesis associated with oxidative stress was significantly high among current smokers (a hazard ratio of 17.8, 95% confidence interval of 12.2–26.0) and heavy smokers (a hazard ratio of 16.6 and a 95% confidence interval of 13.6–20.3) compared to individuals who never smoked. The GSTM1 gene polymorphism was found to be 0.006 among participants who have never smoked, We compared the effect of smoking within two particular time frames, 6 years and 55 years, and found that smoking’s impact on the GSTM1 gene was highest among participants who were 55 years old. The genetic risk peaked among individuals aged 50 years and above (PRS of at least 80%).Conclusion: Exposure to smoking is a significant factor in developing lung carcinogenesis, as it is associated with programmed cell death and other mediators involved in the condition. Oxidative stress caused by smoking is also a key mechanism in lung carcinogenesis. The results of the present study highlight the association between oxidative stress, programmed cell death, and the GSTM1 gene in the development of lung carcinogenesis.</p

Adsorption of Indium(III) Ions from an Acidic Solution by Using UiO-66

Considering environmental friendliness and economic factors, the separation and extraction of indium under acidic conditions are of great significance. In this research, metal-organic frameworks (MOFs) of UiO-66 were successfully prepared and used for the separation and adsorption of indium. The properties of UiO-66 were structurally characterized using powder X-ray diffraction (XRD), Fourier-Transform Infrared Spectroscopy (FTIR), Brunauer-Emmett-Teller surface area analyzer (BET), thermogravimetric analysers (TGA) and Scanning Electron Microscope (SEM). The results show that UiO-66 can resist acid and keep its structure unchanged, even at a strong acidity of pH 1. The adsorption performance of UiO-66 to indium (III) was also evaluated. The results show that the adsorption process of indium ions was by the Langmuir adsorption isotherm, with a maximum adsorption capacity of 11.75 mg&middot;g&minus;1 being recorded. The adsorption kinetics experiment preferably fits the second-order kinetic model. A possible mechanism for the adsorption of In(III) by UiO-66 was explored through X-ray photoelectron spectroscopy (XPS) and Fourier transform infrared analysis(FT-IR). It was concluded that the C=O of free &ndash;COOH of UiO-66 was involved in the adsorption of In(III) by cation exchange. This study indicates, for the first time, that UiO-66 can be applied as an acid-resistant adsorbent to recover indium (III)

Table1_Association of oxidative stress, programmed cell death, GSTM1 gene polymorphisms, smoking and the risk of lung carcinogenesis: A two-step Mendelian randomization study.DOCX

Aim: We aimed to examine the association of oxidative stress, programmed cell death, smoking, and the GSTM1 gene in the risk of lung carcinogenesis. The two-step Mendelian randomization will reveal evidence supporting the association of the exposure and mediators with the resulting outcome.Methods: In step 1, we estimated the impact of smoking exposure on lung carcinogenesis and programmed cell death. Our study involved a total of 500,000 patients of European ancestry, from whom we obtained genotype imputation information. Specifically, we genotyped two arrays: the UK Biobank Axiom (UKBB) which accounted for 95% of marker content, and the UK BiLIEVE Axiom (UKBL). This allowed us to unmask the association between smoking exposure and the incidence of lung carcinogenesis. In step 2, we further examined the effects of smoking on oxidative stress, programmed cell death, and the incidence of lung carcinogenesis.Results: Different outcomes emerged from the two-step Mendelian randomization. The GSTM1 gene variant was found to be critical in the development of lung carcinogenesis, as its deletion or deficiency can induce the condition. A GWAS study on participant information obtained from the UK Biobank revealed that smoking interferes with the GSTM1 gene, causing programmed cell death in the lungs and ultimately leading to lung carcinogenesis. The relative risk of developing lung carcinogenesis associated with oxidative stress was significantly high among current smokers (a hazard ratio of 17.8, 95% confidence interval of 12.2–26.0) and heavy smokers (a hazard ratio of 16.6 and a 95% confidence interval of 13.6–20.3) compared to individuals who never smoked. The GSTM1 gene polymorphism was found to be 0.006 among participants who have never smoked, We compared the effect of smoking within two particular time frames, 6 years and 55 years, and found that smoking’s impact on the GSTM1 gene was highest among participants who were 55 years old. The genetic risk peaked among individuals aged 50 years and above (PRS of at least 80%).Conclusion: Exposure to smoking is a significant factor in developing lung carcinogenesis, as it is associated with programmed cell death and other mediators involved in the condition. Oxidative stress caused by smoking is also a key mechanism in lung carcinogenesis. The results of the present study highlight the association between oxidative stress, programmed cell death, and the GSTM1 gene in the development of lung carcinogenesis.</p

Individual Morphological Brain Network Construction Based on Multivariate Euclidean Distances Between Brain Regions

Morphological brain network plays a key role in investigating abnormalities in neurological diseases such as mild cognitive impairment (MCI) and Alzheimer's disease (AD). However, most of the morphological brain network construction methods only considered a single morphological feature. Each type of morphological feature has specific neurological and genetic underpinnings. A combination of morphological features has been proven to have better diagnostic performance compared with a single feature, which suggests that an individual morphological brain network based on multiple morphological features would be beneficial in disease diagnosis. Here, we proposed a novel method to construct individual morphological brain networks for two datasets by calculating the exponential function of multivariate Euclidean distance as the evaluation of similarity between two regions. The first dataset included 24 healthy subjects who were scanned twice within a 3-month period. The topological properties of these brain networks were analyzed and compared with previous studies that used different methods and modalities. Small world property was observed in all of the subjects, and the high reproducibility indicated the robustness of our method. The second dataset included 170 patients with MCI (86 stable MCI and 84 progressive MCI cases) and 169 normal controls (NC). The edge features extracted from the individual morphological brain networks were used to distinguish MCI from NC and separate MCI subgroups (progressive vs. stable) through the support vector machine in order to validate our method. The results showed that our method achieved an accuracy of 79.65% (MCI vs. NC) and 70.59% (stable MCI vs. progressive MCI) in a one-dimension situation. In a multiple-dimension situation, our method improved the classification performance with an accuracy of 80.53% (MCI vs. NC) and 77.06% (stable MCI vs. progressive MCI) compared with the method using a single feature. The results indicated that our method could effectively construct an individual morphological brain network based on multiple morphological features and could accurately discriminate MCI from NC and stable MCI from progressive MCI, and may provide a valuable tool for the investigation of individual morphological brain networks