The Harang reversal and the interchange stability of the magnetotail

The present study addresses steady convection in the plasma sheet in terms of the interchange stability with special attention to the Harang reversal. The closure of the tail current with a field-aligned current (FAC) results from the divergence/convergence of the pressure gradient current. If the magnetotail is in a steady state, the associated change of local plasma pressure p has to balance with its advective change. Accordingly, for adiabatic transport, the flux tube entropy parameter pVγ increases and decreases along the convection path in regions corresponding to downward and upward FACs, respectively. This requirement, along with the condition for the interchange stability imposes an important constraint on the direction of convection especially in the regions of downward FACs. It is deduced that for the dusk cell, the convection in the downward R2 current has to be directed azimuthally duskward, which follows the sunward, possibly dawnward deflected, convection in the region of the premidnight upward R1 current. This duskward turn of convection takes place in the vicinity of the R1-R2 demarcation, and it presumably corresponds to the Harang reversal. For the dawn cell the convection in the postmidnight downward R1 current has to deflect dawnward, and then it proceeds sunward in the upward R2 current. The continuity of the associated ionospheric currents consistently reproduces the assumed FAC distribution. The proposed interrelationships between the convection and FACs are also verified with a quasi-steady plasma sheet configuration and convection reproduced by a modified Rice Convection Model with force balance

Modulatory Function of Invariant Natural Killer T Cells in Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease with complex immunological and clinical manifestations. Multiple organ failure in SLE can be caused by immune dysfunction and deposition of autoantibodies. Studies of SLE-susceptible loci and the cellular and humoral immune responses reveal variable aberrations associated with this systemic disease. Invariant natural killer T (iNKT) cells are a unique subset of lymphocytes that control peripheral tolerance. Mounting evidence showing reductions in the proportion and activity of iNKT cells in SLE patients suggests the suppressive role of iNKT cells. Studies using murine lupus models demonstrate that iNKT cells participate in SLE progression by sensing apoptotic cells, regulating immunoglobulin production, and altering the cytokine profile upon activation. However, the dichotomy of iNKT cell actions in murine models implies complicated interactions within the body's milieu. Therefore, application of potential therapy for SLE using glycolipids to regulate iNKT cells should be undertaken cautiously

Homogeneous point mutation detection by quantum dot-mediated two-color fluorescence coincidence analysis

This report describes a new genotyping method capable of detecting low-abundant point mutations in a homogeneous, separation-free format. The method is based on integration of oligonucleotide ligation with a semiconductor quantum dot (QD)-mediated two-color fluorescence coincidence detection scheme. Surface-functionalized QDs are used to capture fluorophore-labeled ligation products, forming QD-oligonucleotide nanoassemblies. The presence of such nanoassemblies and thereby the genotype of the sample is determined by detecting the simultaneous emissions of QDs and fluorophores that occurs whenever a single nanoassembly flows through the femtoliter measurement volume of a confocal fluorescence detection system. The ability of this method to detect single events enables analysis of target signals with a multiple-parameter (intensities and count rates of the digitized target signals) approach to enhance assay sensitivity and specificity. We demonstrate that this new method is capable of detecting zeptomoles of targets and achieve an allele discrimination selectivity factor >10(5)

Continuous epidermal growth factor receptor-tyrosine kinase inhibitor administration in primary lung adenocarcinoma patients harboring favorable mutations with controlled target lung tumors dose not hinder survival benefit despite small new lesions

AbstractBackgroundIn this study, we investigated the efficacy of continuous epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) administration in lung adenocarcinoma patients harboring favorable mutations regarding the progressive disease (PD) status with appearance of indolent new lesions.MethodsFrom June 2010 to October 2012, 102 patients with lung adenocarcinoma, harboring favorable EGFR mutations and treated with EGFR-TKI were analyzed. Definite new lesions were detected during EGFR-TKI therapy, even though the primary target tumors were controlled.ResultsOf the 102 patients, 57 continued and 45 discontinued EGFR-TKI therapy. The median overall survival was 529 days for the discontinuation group and 791 days for the continuation group (p = 0.0197). Median survival time after the discontinuation of EGFR-TKI was 181 days and 115 days in the discontinuation and continuation groups, respectively (p = 0.1776), whereas median survival time after the appearance of indolent new lesions was 204 days and 262 days, respectively (p = 0.0237).ConclusionContinuous EGFR-TKI administration in favorable EGFR-mutative lung adenocarcinoma patients with controlled primary tumors did not hinder the survival benefit, despite the appearance of new lesions