Quantum percolation in quantum spin Hall antidot systems

We study the influences of antidot-induced bound states on transport properties of two- dimensional quantum spin Hall insulators. The bound statesare found able to induce quantum percolation in the originally insulating bulk. At some critical antidot densities, the quantum spin Hall phase can be completely destroyed due to the maximum quantum percolation. For systems with periodic boundaries, the maximum quantum percolationbetween the bound states creates intermediate extended states in the bulk which is originally gapped and insulating. The antidot in- duced bound states plays the same role as the magnetic field inthe quantum Hall effect, both makes electrons go into cyclotron motions. We also draw an analogy between the quantum percolation phenomena in this system and that in the network models of quantum Hall effect

Surface and Edge States in Topological Semi-metals

We study the topologically non-trivial semi-metals by means of the 6-band Kane model. Existence of surface states is explicitly demonstrated by calculating the LDOS on the material surface. In the strain free condition, surface states are divided into two parts in the energy spectrum, one part is in the direct gap, the other part including the crossing point of surface state Dirac cone is submerged in the valence band. We also show how uni-axial strain induces an insulating band gap and raises the crossing point from the valence band into the band gap, making the system a true topological insulator. We predict existence of helical edge states and spin Hall effect in the thin film topological semi-metals, which could be tested with future experiment. Disorder is found to significantly enhance the spin Hall effect in the valence band of the thin films

Automatic sleep staging of single-channel EEG based on domain adversarial neural networks and domain self-attention

The diagnosis and management of sleep problems depend heavily on sleep staging. For autonomous sleep staging, many data-driven deep learning models have been presented by trying to construct a large-labeled auxiliary sleep dataset and test it by electroencephalograms on different subjects. These approaches suffer a significant setback cause it assumes the training and test data come from the same or similar distribution. However, this is almost impossible in scenario cross-dataset due to inherent domain shift between domains. Unsupervised domain adaption was recently created to address the domain shift issue. However, only a few customized UDA solutions for sleep staging due to two limitations in previous UDA methods. First, the domain classifier does not consider boundaries between classes. Second, they depend on a shared model to align the domain that could miss the information of domains when extracting features. Given those restrictions, we present a novel UDA approach that combines category decision boundaries and domain discriminator to align the distributions of source and target domains. Also, to keep the domain-specific features, we create an unshared attention method. In addition, we investigated effective data augmentation in cross-dataset sleep scenarios. The experimental results on three datasets validate the efficacy of our approach and show that the proposed method is superior to state-of-the-art UDA methods on accuracy and MF1-Score

Construction and characterization of infectious hepatitis C virus chimera containing structural proteins directly from genotype 1b clinical isolates

AbstractHCV genotype is a major determinant of clinical outcome, and GT1b HCV infection is the most difficult to treat and also the predominant genotype in East Asia and Europe. We developed 1b/JFH-1 inter-genotypic recombinants containing the structural genes (Core, E1, E2), p7 and the 1stTMD of NS2 directly from GT1b clinical isolates. Through a cloning selection strategy, we obtained 4 functional clones from 3 cases of GT1b patients' sera, which could produce infectious viruses in Huh7.5.1 cells. Sequencing analysis of recovered viruses from serial passage and reverse genetics revealed that adaptive mutations in the GT1b-originated region were enough for the enhancement of infectivity. A monoclonal antibody to E2 and original patient sera could efficiently block 3 of the viruses (26C3mt, 52B6mt and 79L9) while had little effect on 26C6mt viruses. The availability of 1b/JFH-1 chimeric viruses will be important for studies of isolate-specific neutralization and useful in evaluating antiviral therapies

Expanded CURB-65: A new score system predicts severity of community-acquired pneumonia with superior efficiency

Aim of this study was to develop a new simpler and more effective severity score for communityacquired pneumonia (CAP) patients. A total of 1640 consecutive hospitalized CAP patients in Second Affiliated Hospital of Zhejiang University were included. The effectiveness of different pneumonia severity scores to predict mortality was compared, and the performance of the new score was validated on an external cohort of 1164 patients with pneumonia admitted to a teaching hospital in Italy. Using age≥ 65 years, LDH>230u/L, albumin<3.5g/dL, platelet count<100×109/L, confusion, urea>7mmol/L, respiratory rate≥30/min, low blood pressure, we assembled a new severity score named as expanded-CURB-65. The 30-day mortality and length of stay were increased along with increased risk score. The AUCs in the prediction of 30-day mortality in the main cohort were 0.826 (95%CI, 0.807–0.844), 0.801 (95%CI, 0.781–0.820), 0.756 (95%CI, 0.735–0.777), 0.793 (95%CI, 0.773–0.813) and 0.759 (95%CI, 0.737–0.779) for the expanded-CURB-65, PSI, CURB-65, SMART-COP and A-DROP, respectively. The performance of this bedside score was confirmed in CAP patients of the validation cohort although calibration was not successful in patients with health care-associated pneumonia (HCAP). The expanded CURB-65 is objective, simpler and more accurate scoring system for evaluation of CAP severity, and the predictive efficiency was better than other score systems

Abnormal Alterations of Regional Spontaneous Neuronal Activity in Inferior Frontal Orbital Gyrus and Corresponding Brain Circuit Alterations: A Resting-State fMRI Study in Somatic Depression

Background: Major depressive disorders often involve somatic symptoms and have been found to have fundamental differences from non-somatic depression (NSD). However, the neural basis of this type of somatic depression (SD) is unclear. The aim of this study is to use the amplitude of low-frequency fluctuation (ALFF) and functional connectivity (FC) analyses to examine the abnormal, regional, spontaneous, neuronal activity and the corresponding brain circuits in SD patients.Methods: 35 SD patients, 25 NSD patients, and 27 matched healthy controls were selected to complete this study. The ALFF and seed-based FC analyses were employed, and the Pearson correlation was determined to observe possible clinical relevance.Results: Compared with NSD, the SD group showed a significant ALFF increase in the right inferior temporal gyrus; a significant ALFF decrease in left hippocampus, right inferior frontal orbital gyrus and left thalamus; and a significant decrease in the FC value between the right inferior frontal orbital gyrus and the left inferior parietal cortex (p &lt; 0.05, corrected). Within the SD group, the mean ALFF value of the right inferior frontal orbital gyrus was associated with the anxiety factor scores (r = –0.431, p = 0.010, corrected).Conclusions: Our findings suggest that abnormal differences in the regional spontaneous neuronal activity of the right inferior frontal orbital gyrus were associated with dysfunction patterns of the corresponding brain circuits during rest in SD patients, including the limbic-cortical systems and the default mode network. This may be an important aspect of the underlying mechanisms for pathogenesis of SD at the neural level

TPH-2 Gene Polymorphism in Major Depressive Disorder Patients With Early-Wakening Symptom

Background: Sleep disturbances, such as early wakening, are frequently observed in patients with major depressive disorder (MDD). The suprachiasmatic nuclei (SCN), which controls circadian rhythm, is innervated by the raphe nucleus, a region where Tryptophan hydroxylase-2 (TPH-2) gene is primarily expressed. Although TPH-2 is often implicated in the pathophysiology of depression, few studies have applied a genetic and imaging technique to investigate the mechanism of early wakening symptom in MDD. We hypothesized that TPH-2 variants could influence the function of SCN in MDD patients with early wakening symptom.Methods: One hundred and eighty five MDD patients (62 patients without early wakening and 123 patients with early wakening) and 64 healthy controls participated in this study. Blood samples were collected and genotyping of rs4290270, rs4570625, rs11178998, rs7305115, rs41317118, and rs17110747 were performed by next-generation sequencing (NGS) technology. Logistic regression model was employed for genetic data analysis using the PLINK software. Based on the allele type, rs4290270, which was significant in the early wakening MDD group, participants were categorized into two groups (A allele and T carrier). All patients underwent whole brain resting-state functional magnetic resonance imaging (rs-fMRI) scanning and a voxel-wise functional connectivity comparison was performed between the groups.Results: rs4290270 was significantly linked to MDD patients who exhibited early wakening symptom. The functional connectivities of the right SCN with the right fusiform gyrus and right middle frontal gyrus were increased in the T carrier group compared to the A allele group. In addition, the functional connectivities of the left SCN with the right lingual gyrus and left calcarine sulcus were decreased in the T carrier group compared to the A allele group.Conclusion: These findings suggested that the TPH-2 gene variant, rs4290270, affected the circadian regulating function of SCN. The altered functional connectivities, observed between the SCN and right fusiform gyrus, right middle frontal gyrus, the right lingual gyrus and left calcarine sulcus, could highlight the neural mechanism by which SCN induces sleep-related circadian disruption in T carrier MDD patients. Hence, rs4290270 could potentially serve as a reliable biomarker to identify MDD patients with early wakening symptom

Contra-Directional Expression of Serum Homocysteine and Uric Acid as Important Biomarkers of Multiple System Atrophy Severity: A Cross-Sectional Study

Aims. There is evidence suggesting that inflammatory responses play a critical role in the pathogenesis of multiple system atrophy (MSA). Whether inflammatory mediators can be used as reliable biomarkers to detect the severity and progression of MSA remains largely unknown. Methods. We performed a cross-sectional study that included 47 patients with MSA and 50 healthy age-matched controls. Serum levels of homocysteine (Hcy), uric acid (UA) and C-reactive protein (CRP) were measured. These levels positively correlated with the severity of MSA, based on both motor and non-motor symptoms (NMS). Several scales were used to rate the severity of MSA, including the Unified multiple system atrophy rating scale (UMSARS), Parkinson’s disease sleep scale (PDSS), Non-motor Symptoms Scale (NMSS), the Schwab & England Activities of Daily Living Scale (ADL), Webster Scale, modified Hoehn and Yahr staging scale (H&Y), and the Mini-Mental State Examination (MMSE). Receiver Operating Characteristic (ROC) curves was applied to map the diagnostic accuracy of MSA against healthy subjects. Results. Compared with healthy subjects, we found that serum Hcy was higher, UA was lower, and CRP levels were unchanged in MSA patients. These findings were especially prominent in male patients. No significant differences of serum Hcy and UA were observed between patients of MSA and PD. Interestingly, there was a significant correlation between Hcy levels and MSA severity such as movement dysfunction, declined cognition, and cardiovascular symptoms. Additionally, the ROC curve for the combination of Hcy and UA (AUC 0.736) showed potential diagnostic value in discriminating MSA from healthy subjects. Conclusions. Our findings suggest that the inflammatory mediators Hcy and UA may play important roles in the pathogenesis of MSA. The measurement of serum Hcy and UA levels could then be a useful tool to accurately distinguish MSA from healthy subjects