Density Functional Theory Study on the Electrical Properties of α-CsPbX3 (X=I, Cl, Br)

All-inorganic perovskite solar cells have become more important in the commercialization of the photovoltaic devices. In this study the structural, electronic properties of inorganic metal halide cubic perovskites CsPbX3 (X = I, Br, Cl) for perovskite solar cells are simulated using first-principles Density Functional Theory (DFT). The newly adjusted parameters make the calculations more accurate. These compounds are semiconductors with direct band gap energy. Results suggest that the α-CsPbX3 (X=I, Cl, Br) have a wide bandgap adjustment range with potential application in solar cells and other optoelectronic energy devices. On the basis of the electronic properties, one can expect that the α-CsPbI3 would be a better used to perovskite solar cell. α -CsPbCl3 and α-CsPbBr3 better suitable for others photovoltaic device

Controllable Text Generation with Residual Memory Transformer

Large-scale Causal Language Models (CLMs), e.g., GPT3 and ChatGPT, have brought great success in text generation. However, it is still an open challenge to control the generation process of CLM while balancing flexibility, control granularity, and generation efficiency. In this paper, we provide a new alternative for controllable text generation (CTG), by designing a non-intrusive, lightweight control plugin to accompany the generation of CLM at arbitrary time steps. The proposed control plugin, namely Residual Memory Transformer (RMT), has an encoder-decoder setup, which can accept any types of control conditions and cooperate with CLM through a residual learning paradigm, to achieve a more flexible, general, and efficient CTG. Extensive experiments are carried out on various control tasks, in the form of both automatic and human evaluations. The results show the superiority of RMT over a range of state-of-the-art approaches, proving the effectiveness and versatility of our approach.Comment: github:https://github.com/littlehacker26/Residual_Memory_Transforme

Development of Murine Hepatic NK Cells during Ontogeny: Comparison with Spleen NK Cells

The phenotype of developing liver NK cells (CD3−NK1.1+) was investigated during mouse ontogeny comparing with spleen NK cells. The highest percentage of hepatic CD27−CD11b− NK cells occurred at the fetal stage. After birth, the percentage of CD27−CD11b−NK cells in both the liver and spleen gradually decreased to their lowest level at 6 weeks. More CD27+CD11b−NK cells were detected in the liver than that in spleen from week 1 to 6. Expression of NKG2A on liver NK cells was decreased but still much higher than that of spleen NK cells after 1 week. The NKG2D expression on liver NK cells increased to its highest level and was significantly higher than on spleen NK cells till 4 weeks. During mouse ontogeny, weaker expression of NKp46 and CD2 and stronger expression of CD69, CD11c, 2B4, and CD73 were observed on liver NK cells. Furthermore, neonatal liver NK cells express higher IFN-γ and perforin than adult .These results suggest that the maturation process of NK cells is unique in the livers, and liver microenvironments might play critical roles to keep NK cells in an immature status

Involvement of HAND1 and CBS in maintenance of cardiac micro-architecture following obesity-induced heart failure

Purpose: To study the role of heart and neural crest derivatives expressed 1 (HAND1) and cystathionine-beta-synthase (CBS) in the maintenance of cardiac architecture following high fat dietinduced obesity. Methods: Mouse models of initial and critical heart disease were established by continuous feeding of high fat diet for 7 and 12 months, respectively. The expression of HAND1 and CBS were assayed using immunohistochemistry and Western blotting. Results: Obesity led to mild and severe forms of heart disease which were confirmed through histological imaging. Initial obesity resulted in cardiac tissue remodeling along with initial degeneration, while critical obesity resulted in tissue hardening. The expression of HAND1 was upregulated 4.3 folds in the mild form of cardiac failure, relative to marginal expression pattern of HAND1 in control tissue. However, as the disease progressed, the expression of HAND1 was limited in serve form of cardiac failure. Moreover, the expression of cystathionine beta-synthase (CBS) was upregulated 3.7-fold in the initial form of heart failure, but was subsequently reduced in serve form of heart disease. Conclusion: These results reveal that in high fat diet-induced cardiac stress, the over-expressions of HAND1 and CBS at the initial stages induce extensive alterations in cardiac architecture

SR-OOD: Out-of-Distribution Detection via Sample Repairing

It is widely reported that deep generative models can classify out-of-distribution (OOD) samples as in-distribution with high confidence. In this work, we propose a hypothesis that this phenomenon is due to the reconstruction task, which can cause the generative model to focus too much on low-level features and not enough on semantic information. To address this issue, we introduce SR-OOD, an OOD detection framework that utilizes sample repairing to encourage the generative model to learn more than just an identity map. By focusing on semantics, our framework improves OOD detection performance without external data and label information. Our experimental results demonstrate the competitiveness of our approach in detecting OOD samples

CD4+CD62L+ Central Memory T Cells Can Be Converted to Foxp3+ T Cells

The peripheral Foxp3+ Treg pool consists of naturally arising Treg (nTreg) and adaptive Treg cells (iTreg). It is well known that naive CD4+ T cells can be readily converted to Foxp3+ iTreg in vitro, and memory CD4+ T cells are resistant to conversion. In this study, we investigated the induction of Foxp3+ T cells from various CD4+ T-cell subsets in human peripheral blood. Though naive CD4+ T cells were readily converted to Foxp3+ T cells with TGF-β and IL-2 treatment in vitro, such Foxp3+ T cells did not express the memory marker CD45RO as do Foxp3+ T cells induced in the peripheral blood of Hepatitis B Virus (HBV) patients. Interestingly, a subset of human memory CD4+ T cells, defined as CD62L+ central memory T cells, could be induced by TGF-β to differentiate into Foxp3+ T cells. It is well known that Foxp3+ T cells derived from human CD4+CD25- T cells in vitro are lack suppressive functions. Our data about the suppressive functions of CD4+CD62L+ central memory T cell-derived Foxp3+ T cells support this conception, and an epigenetic analysis of these cells showed a similar methylation pattern in the FOXP3 Treg-specific demethylated region as the naive CD4+ T cell-derived Foxp3+ T cells. But further research showed that mouse CD4+ central memory T cells also could be induced to differentiate into Foxp3+ T cells, such Foxp3+ T cells could suppress the proliferation of effector T cells. Thus, our study identified CD4+CD62L+ central memory T cells as a novel potential source of iTreg

Cytotoxic effects of ZnO hierarchical architectures on RSC96 Schwann cells

The alteration in intracellular Zn(2+) homeostasis is attributed to the generation of intracellular reactive oxygen species, which subsequently results in oxidative damage of organelles and cell apoptosis. In this work, the neurotoxic effects of ZnO hierarchical architectures (nanoparticles and microspheres, the prism-like and flower-like structures) were evaluated through the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay using RSC96 Schwann cells as the model. Cell apoptosis and cell cycle were detected using flow cytometry. The concentration of Zn(2+) in the culture media was monitored using atomic absorption spectrometry. The results show that ZnO nanoparticles and microspheres displayed significant cytotoxic effects on RSC96 Schwann cells in dose- and time-dependent manners, whereas no or low cytotoxic effect was observed when the cells were treated with the prism-like and flower-like ZnO. A remarkable cell apoptosis and G2/M cell cycle arrest were observed when RSC96 Schwann cells were exposed to ZnO nanoparticles and microspheres at a dose of 80 μg/mL for 12 h. The time-dependent increase of Zn(2+) concentration in the culture media suggests that the cytotoxic effects were associated with the decomposition of ZnO hierarchical architecture and the subsequent release of Zn(2+). These results provide new insights into the cytotoxic effects of complex ZnO architectures, which could be prominently dominated by nanoscale building blocks

Activation of TLR Signaling in Sensitization-Recruited Inflammatory Monocytes Attenuates OVA-Induced Allergic Asthma

The activation of Toll-like receptor (TLR) signaling is widely reported to be involved in preventing the development of allergic asthma. However, the mechanism of the protective function of TLR signaling remains limited. Here, we studied the mouse model of ovalbumin (OVA)-induced allergic asthma and found that deficiency of TLR signaling or activating TLR signaling with agonist would aggravate or attenuate OVA-induced allergic asthma, respectively, and TLR signaling-mediated protective effect mainly affected the sensitization phase. After OVA/alum sensitization, neutrophils and inflammatory monocytes were recruited into peritoneal cavity and up-regulated TLRs expression. However, adoptive transfer of inflammatory monocytes but not peritoneal macrophages or neutrophils induced allergic symptoms in recipient mice after OVA challenge even without OVA/alum sensitization, and treating the inflammatory monocytes with TLR agonist in vitro before transfer could abolish this effect, indicating that recruited inflammatory monocytes played a determinant role in OVA-induced allergic asthma, and activation of TLR signaling in them could attenuate allergic symptoms. Finally, we found that activation of TLR signaling could increase the expression of T-helper (Th) 1-associated cytokines in inflammatory monocytes. Our results suggest that activation of TLR signaling in sensitization-recruited inflammatory monocytes attenuates OVA-induced allergic asthma by promoting the expression of Th1-associated cytokines

CD4+ T Cells Play a Critical Role in Microbiota-Maintained Anti-HBV Immunity in a Mouse Model

The ability of the host to clear hepatitis B virus (HBV) is closely correlated to the establishment of commensal microbiota. However, how microbiota affects anti-HBV immunity is still unclear. Using a well-known hydrodynamical HBV transfection mouse model and treatment with antibiotics (Atb), we explored the change in adaptive immunity (CD4+ cells, germinal center B cells and anti-HBs Ab). In our setting, normal mice exhibited complete clearance of HBV within 6 weeks post-hydrodynamic injection (HDI) of HBV-containing plasmid, whereas Atb-treated mice lost this capacity, showing high serum level of hepatitis B surface antigen (HBsAg) without hepatitis B surface antibodies (anti-HBs), similar as what happened in Rag1−/− mice or CD4−/− mice, suggesting that microbiota may influence the function of CD4+ T cells. Furthermore, the numbers of splenic and hepatic effector CD4+ T cells (CD44hiCD62L−CD4+ T cells) both decreased with impaired function (IFN-γ synthesis), resulting in lower frequency of germinal center B cells and CD4+ follicular helper T cells, and impaired anti-HBs production. We further tried to find the bacterial species responsible for maintaining anti-HBV immunity, and found that each antibiotic alone could not significantly influence HBV clearance compared to antibiotic combination, suggesting that global commensal microbial load is critical for promoting HBV clearance. We also confirmed that TLRs (e.g., TLR2, 4, 9) are not major players in immune clearance of HBV using their agonists and knock-out mice. These results suggest that commensal microbiota play an important role in maintaining CD4+ T cell immunity against HBV infection