Correlated disorder induced anomalous transport in magnetically doped topological insulators

We examine the transport properties of magnetically doped topological insulator (TI) thin films subject to correlated nonmagnetic disorder. For the disorder we choose a quasiperiodic potential with a random phase. We restrict the disorder to a central region, which is coupled to two leads in a clean quantum spin Hall insulator (QSHI) state and concentrate on different orientations of the quasiperiodicity in the two-dimensional central region. In the case of a diagonally oriented or purely longitudinal quasiperiodicity we find different topological Anderson insulator (TAI) phases, with a quantum anomalous Hall insulator (QAHI), a quantum spin Chern insulator (QSCI), or a QSHI phase being realized before the Anderson insulation takes over at large disorder strength. Quantized transport from extended bulk states is found for diagonal quasiperiodicity in addition to the above TAI phases that are also observed for the case of uncorrelated disorder. For a purely transverse orientation of the quasiperiodicity the emerging QSHI and QSCI phases persist to arbitrarily strong disorder potential. These topological phase transitions (except to the Anderson insulator phase) can be understood from a self consistent Born approximation

Vortex control in superconducting Corbino geometry networks

In superconductors, vortices induced by a magnetic field are nucleated where some random fluctuations determine the nucleation position, and then may be pinned by impurities or boundaries, impeding the development of vortex-based quantum devices. Here, we propose a superconducting structure, which allows to nucleate and control vortices on-demand by controlling magnetic fields and currents. Using time-dependent Ginzburg-Landau theory, we study a driven vortex motion in two-dimensional Corbino geometries of superconductor-normal metal-superconductor Josephson junctions. We remedy the randomness of nucleation by introducing normal conducting rails to the Corbino disk to guide the nucleation process and motion of vortices towards the junction. We elaborate on the consequences of rail-vortex and vortex-vortex interactions to the quantization of resistance across the junction. Finally, we simulate the nucleations and manipulations of two and four vortices in Corbino networks, and discuss its application to Majorana zero mode braiding operations. Our study provides a potential route towards quantum computation with non-Abelian anyon

Vortex control in superconducting Corbino geometry networks

In superconductors, vortices induced by a magnetic field are nucleated randomly due to some random fluctuations or pinned by impurities or boundaries, impeding the development of vortex based quantum devices. Here, we propose a superconducting structure which allows to nucleate and control vortices on-demand by controlling magnetic fields and currents. Using time-dependent Ginzburg Landau theory, we study a driven vortex motion in two-dimensional Corbino geometries of superconductor-normal metal-superconductor Josephson junctions. We remedy the randomness of nucleation by introducing normal conducting rails to the Corbino disk to guide the nucleation process and motion of vortices towards the junction. We elaborate on the consequences of rail-vortex and vortex-vortex interactions to the quantization of resistance across the junction. Finally, we simulate the nucleations and manipulations of two and four vortices in Corbino networks, and discuss its application to Majorana zero mode braiding operations. Our study provides a potential route towards quantum computation with non-Abelian anyons

Cortico-cerebellar functional connectivity and sequencing of movements in schizophrenia

<p>Abstract</p> <p>Background</p> <p>Abnormal execution of several movements in a sequence is a frequent finding in schizophrenia. Successful performance of such motor acts requires correct integration of cortico-subcortical processes, particularly those related to cerebellar functions. Abnormal connectivity between cortical and cerebellar regions with resulting cognitive dysmetria has been proposed as the core dysfunction behind many signs and symptoms of schizophrenia. The aim of the present study was to assess if these proposed abnormalities in connectivity are a unifying feature of schizophrenia, or, rather, reflect a specific symptom domain of a heterogeneous disease. We predicted that abnormal functional connectivity between the motor cortex and cerebellum would be linked with abnormal performance of movement sequencing.</p> <p>Methods</p> <p>We examined 24 schizophrenia patients (SCH) and 24 age-, sex-, and handedness-matched healthy controls (HC) using fMRI during a modified finger-tapping task. The ability to perform movement sequencing was tested using the Neurological Evaluation Scale (NES). The subjects were categorized into two groups, with (SQ+) and without (SQ-) movement sequencing abnormalities, according to the NES-SQ score. The effects of diagnosis and movement sequencing abnormalities on the functional connectivity parameters between the motor cortex and cerebellum (MC-CRBL) and the supplementary motor cortex and cerebellum (SMA-CRBL) activated during the motor task were analyzed.</p> <p>Results</p> <p>We found no effect of diagnosis on the functional connectivity measures. There was, however, a significant effect on the SQ group: SQ + patients showed a lower level of MC-CRBL connectivity than SQ- patients and healthy controls. Moreover, the level of MC-CRBL and SMA-CRBL negatively correlated with the magnitude of NES-SQ abnormalities, but with no other NES domain.</p> <p>Conclusions</p> <p>Abnormal cortico-cerebellar functional connectivity during the execution of a motor task is linked with movement sequencing abnormalities in schizophrenia, but not with the diagnosis of schizophrenia per se. It seems that specific patterns of inter-regional connectivity are linked with corresponding signs and symptoms of clinically heterogeneous conditions such as schizophrenia.</p

Cimetidine modulates the antigen presenting capacity of dendritic cells from colorectal cancer patients

Cimetidine, a H2 receptor antagonist, has been reported to improve survival in gastrointestinal cancer patients. These effects have largely been attributed to the enhancing effects of cimetidine on the host's antitumour cell-mediated immune response, such as inhibition of suppressor T lymphocyte activity, stimulation of natural killer cell activity and increase of interleukin-2 production from helper T lymphocytes. We conducted an in vitro study on the effects of cimetidine on differentiation and antigen presenting capacity of monocyte-derived dendritic cells from advanced colorectal cancer patients and normal controls. As a result, an investigation of expression of surface molecules associated with dendritic cells by flow cytometric analyses showed that cimetidine had no enhancing effect on differentiation of dendritic cells from cancer patients and normal controls. An investigation of [3H]thymidine incorporation by allogeneic mixed lymphocyte reactions revealed that cimetidine increased the antigen presenting capacity of dendritic cells from both materials. Moreover, a higher antigen presenting capacity was observed in advanced cancer patients compared to normal controls. These effects might be mediated via specific action of cimetidine and not via H2 receptors because famotidine did not show similar effects. Our results suggest that cimetidine may enhance the host's antitumour cell-mediated immunity by improving the suppressed dendritic cells function of advanced cancer patients

Update on HER-2 as a target for cancer therapy: HER2/neu peptides as tumour vaccines for T cell recognition

During the past decade there has been renewed interest in the use of vaccine immunotherapy for the treatment of cancer. This review focuses on HER2/neu, a tumour-associated antigen that is overexpressed in 10–40% of breast cancers and other carcinomata. Several immunogenic HER2/neu peptides recognized by T lymphocytes have been identified to be included in cancer vaccines. Some of these peptides have been assessed in clinical trials of patients with breast and ovarian cancer. Although it has been possible to detect immunological responses against the peptides in the immunized patients, no clinical responses have so far been described. Immunological tolerance to self-antigens like HER2/neu may limit the functional immune responses against them. It will be of interest to determine whether immune responses against HER2/neu epitopes can be of relevance to cancer treatment

Meta-analysis of diffusion tensor imaging studies shows altered fractional anisotropy occurring in distinct brain areas in association with depression

Fractional anisotropy anomalies occurring in the white matter tracts in the brains of depressed patients may reflect microstructural changes underlying the pathophysiology of this disorder. We conducted a meta-analysis of fractional anisotropy abnormalities occurring in major depressive disorder using voxel-based diffusion tensor imaging studies. Using the Embase, PubMed and Google Scholar databases, 89 relevant data sets were identified, of which 7 (including 188 patients with major depressive disorder and 221 healthy controls) met our inclusion criteria. Authors were contacted to retrieve any additional data required. Coordinates were extracted from clusters of significant white matter fractional anisotropy differences between patients and controls. Relevant demographic, clinical and methodological variables were extracted from each study or obtained directly from authors. The meta-analysis was carried out using Signed Differential Mapping. Patients with depression showed decreased white matter fractional anisotropy values in the superior longitudinal fasciculus and increased fractional anisotropy values in the fronto-occipital fasciculus compared to controls. Using quartile and jackknife sensitivity analysis, we found that reduced fractional anisotropy in the left superior longitudinal fasciculus was very stable, with increases in the right fronto-occipital fasciculus driven by just one study. In conclusion, our meta-analysis revealed a significant reduction in fractional anisotropy values in the left superior longitudinal fasciculus, which may ultimately play an important role in the pathology of depression

Anthrax Lethal Toxin Disrupts Intestinal Barrier Function and Causes Systemic Infections with Enteric Bacteria

A variety of intestinal pathogens have virulence factors that target mitogen activated protein kinase (MAPK) signaling pathways, including Bacillus anthracis. Anthrax lethal toxin (LT) has specific proteolytic activity against the upstream regulators of MAPKs, the MAPK kinases (MKKs). Using a murine model of intoxication, we show that LT causes the dose-dependent disruption of intestinal epithelial integrity, characterized by mucosal erosion, ulceration, and bleeding. This pathology correlates with an LT-dependent blockade of intestinal crypt cell proliferation, accompanied by marked apoptosis in the villus tips. C57BL/6J mice treated with intravenous LT nearly uniformly develop systemic infections with commensal enteric organisms within 72 hours of administration. LT-dependent intestinal pathology depends upon its proteolytic activity and is partially attenuated by co-administration of broad spectrum antibiotics, indicating that it is both a cause and an effect of infection. These findings indicate that targeting of MAPK signaling pathways by anthrax LT compromises the structural integrity of the mucosal layer, serving to undermine the effectiveness of the intestinal barrier. Combined with the well-described immunosuppressive effects of LT, this disruption of the intestinal barrier provides a potential mechanism for host invasion via the enteric route, a common portal of entry during the natural infection cycle of Bacillus anthracis