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Thermoelectric technology can be another direct way to convert solar radiation into electricity, using the Seebeck effect. Herein, a prototype concentration solar thermoelectric generator (CTG) and a discrete numerical model for the evaluation of the whole system are presented. The model takes into account the temperature dependence of the thermoelectric material properties by dividing the thermoelectric leg into finite elements and is proved to be more accurate for calculation of the conversion efficiency of the thermoelectric modules when large temperature gradients occur in the CTG system. Based on the best available properties of various bulk thermoelectric materials reported in the literature, the best possible performance of the CTG system is predicted, and the CTG system design, including the selection of the concentration ratio and the cooling method for different thermoelectric materials, are discussed in detail. [ABSTRACT FROM AUTHOR]

CD4+ T cells that lack surface expression of the CD28 co-stimulatory molecule (CD4+CD28- T cells) were expanded in peripheral blood of patients with multiple sclerosis (MS) [5.20 ± 1.67% vs 13.00 ± 2.68% (healthy controls (HC) versus patients with MS)]. Both the CD4+CD28+ and CD4+CD28- T-cell populations of patients with MS produced higher levels of interferon (IFN)-γ compared with those in HC. In particular, the proportion of IFN-γ+ cells among CD4+CD28- T cells from patients with MS was considerably high. However, expression of co-stimulatory molecules including inducible costimulator (ICOS), activating natural killer receptors, or members of tumor necrosis factor receptor family that replace CD28 in CD4+CD28- T cells of patients with MS could not be identified. A unique subpopulation bearing the CD45RAhighCCR7- phenotype was identified among the CD4+CD28- T cells of some patients with MS. Because only MS samples contained this CD45RAhighCCR7- population attributed to terminally differentiated effector memory cells and lacked naive CD45RAhighCCR7+ cells, we suggest that CD4+CD28- T cells of patients with MS represent a cell population which is in more differentiated state than healthy subjects. In patients treated with IFN-β-1b, IFN-γ production from CD4+CD28+ T cells was suppressed compared with that in untreated patients. On the contrary, in the CD4+CD28- population, production of IFN-γ in IFN-β-1b-treated patients was not significantly suppressed compared with that in untreated patients with MS. Thus, an additional treatment strategy that specifically targets this cell population may enhance the beneficial effect of IFN-β on MS. [ABSTRACT FROM AUTHOR]

In multiple sclerosis (MS), β-adrenergic receptor densities on peripheral blood mononuclear cells are enhanced, while the astrocytes present in plaques lack β[sub 2] adrenergic receptor (β[sub 2]AR) expression. This differentially altered expression suggests that β[sub 2]ARs may influence the pathogenesis of MS. In the present study, we investigated the association of polymorphisms of the β[sub 2]AR gene with the occurrence of MS. Our results showed no significant differences in the distribution of the polymorphisms between MS patients overall and control subjects. Furthermore, no association was observed between the presence of β[sub 2]AR gene polymorphisms and clinical characteristics, such as age at disease onset and disease severity. While a trend towards an increase of the Gly allele frequency in codon 16 was observed in the secondary–progressive MS, this result was not significantly different from that observed in relapsing–remitting MS patients or control subjects. Together, our findings suggest that the presence of β[sub 2]AR gene polymorphisms may be inconclusive in the susceptibility to MS or in the clinical characteristics of Japanese patients with MS and, therefore, need further studies. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses a case study involving a 79-year-old woman with neuromyelitis optica (NMO) spectrum disorder, who exhibited seroconversion of AQP4 antibody and hyperCKemia at the onset of myelitis.

Incomplete Freund's adjuvant (IFA) has long been used to trigger autoimmune diseases in animal models, such as experimental autoimmune encephalitis and collagen-induced arthritis. However, the molecular mechanisms that control CD4 T cell effector functions and lead to the development of autoimmune diseases are not well understood. A self-antigen and heat-killed Mycobacterium tuberculosis emulsified in IFA augmented the activation of CD4 T cells, leading to the differentiation of pathogenic CD4 T cells in the draining lymph nodes. In contrast, IFA emulsification did not elicit Foxp3 + regulatory T cell expansion. We found that pathogenic Th1 cells expressed miR-147-3p, which targets multiple genes to affect T cell function. Finally, miR-147-3p expressed in CXCR6 + SLAMF6 - Th1 cells was required for the onset of neurological symptoms through the control of CXCR3 expression. Our findings demonstrate that miR-147-3p expressed in pathogenic CD4 T cells regulates the migratory potential in peripheral tissues and impacts the development of autoimmune diseases., Competing Interests: Declaration of competing interest The authors declare no competing financial interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)