Presentation_1_Orally Administered Brain Protein Combined With Probiotics Increases Treg Differentiation to Reduce Secondary Inflammatory Damage Following Craniocerebral Trauma.pdf

Craniocerebral trauma is caused by external forces that can have detrimental effects on the vasculature and adjacent nerve cells at the site. After the mechanical and structural primary injury, a complex series of secondary cascades of injury exacerbates brain damage and cognitive dysfunction following mechanical and structural primary injury. Disruption of the blood-brain barrier and exposure of brain proteins following craniocerebral trauma, recognition by the immune system triggering autoimmune attack, and excessive secondary inflammatory responses causing malignant brain swelling, cerebral edema, and subsequent brain cell apoptosis provide a new direction for the suppression of brain inflammatory responses in the treatment of craniocerebral trauma. We observed that CD4+T/CD8+T in peripheral blood T cells of craniocerebral trauma rats were significantly higher than those of normal rats, and the ratio of CD4+CD25+Foxp3 (Foxp3)+Regulatory T cell (Treg) was significantly lower than that of normal rats and caused increased secondary inflammation. We constructed a rat model of post-surgical brain injury and orally administered brain protein combined with probiotics, which was observed to significantly reduce CD4+T/CD8+T and induce T-cell differentiation into CD4+CD25+Foxp3+Treg, thus, reducing secondary inflammatory responses following craniocerebral trauma. However, collecting intestinal stool and small intestinal tissues for broad target metabolomics, 16s rRNA bacteriomics, and the combined analysis of intestinal tissue proteomics revealed that oral administration of brain protein combined with probiotics activates glycerophospholipid and vitamin B6 metabolic pathways to promote the production of CD4+CD25+Foxp3+Treg. Therefore, we propose the novel idea that oral administration of brain protein combined with probiotics can induce immune tolerance by increasing Treg differentiation, thus, reducing secondary inflammatory injury following craniocerebral trauma.</p

DataSheet_1_Orally Administered Brain Protein Combined With Probiotics Increases Treg Differentiation to Reduce Secondary Inflammatory Damage Following Craniocerebral Trauma.docx

Craniocerebral trauma is caused by external forces that can have detrimental effects on the vasculature and adjacent nerve cells at the site. After the mechanical and structural primary injury, a complex series of secondary cascades of injury exacerbates brain damage and cognitive dysfunction following mechanical and structural primary injury. Disruption of the blood-brain barrier and exposure of brain proteins following craniocerebral trauma, recognition by the immune system triggering autoimmune attack, and excessive secondary inflammatory responses causing malignant brain swelling, cerebral edema, and subsequent brain cell apoptosis provide a new direction for the suppression of brain inflammatory responses in the treatment of craniocerebral trauma. We observed that CD4+T/CD8+T in peripheral blood T cells of craniocerebral trauma rats were significantly higher than those of normal rats, and the ratio of CD4+CD25+Foxp3 (Foxp3)+Regulatory T cell (Treg) was significantly lower than that of normal rats and caused increased secondary inflammation. We constructed a rat model of post-surgical brain injury and orally administered brain protein combined with probiotics, which was observed to significantly reduce CD4+T/CD8+T and induce T-cell differentiation into CD4+CD25+Foxp3+Treg, thus, reducing secondary inflammatory responses following craniocerebral trauma. However, collecting intestinal stool and small intestinal tissues for broad target metabolomics, 16s rRNA bacteriomics, and the combined analysis of intestinal tissue proteomics revealed that oral administration of brain protein combined with probiotics activates glycerophospholipid and vitamin B6 metabolic pathways to promote the production of CD4+CD25+Foxp3+Treg. Therefore, we propose the novel idea that oral administration of brain protein combined with probiotics can induce immune tolerance by increasing Treg differentiation, thus, reducing secondary inflammatory injury following craniocerebral trauma.</p

Rolling Up Gold Nanoparticle-Dressed DNA Origami into Three-Dimensional Plasmonic Chiral Nanostructures

Construction of three-dimensional (3D) plasmonic architectures using structural DNA nanotechnology is an emerging multidisciplinary area of research. This technology excels in controlling spatial addressability at sub-10 nm resolution, which has thus far been beyond the reach of traditional top-down techniques. In this paper, we demonstrate the realization of 3D plasmonic chiral nanostructures through programmable transformation of gold nanoparticle (AuNP)-dressed DNA origami. AuNPs were assembled along two linear chains on a two-dimensional rectangular DNA origami sheet with well-controlled positions and particle spacing. By rational rolling of the 2D origami template, the AuNPs can be automatically arranged in a helical geometry, suggesting the possibility of achieving engineerable chiral nanomaterials in the visible range

Data from: Increased connections among soil microbes and microfauna enhances soil multifunctionality along a long-term restoration chronosequence

1. 土壤微生物在退化土地恢复中的功能作用受到微生物群落内部和之间的相互作用以及高营养级土壤生物（微型动物）的极大影响。然而，对于土壤微生物及其共存的微生物之间连接模式的变化如何导致生态系统恢复过程中土壤功能的相关变化知之甚少。2. 本研究以黄土高原原前耕地为研究对象，沿50年恢复时间序列，评估了植树造林和自然再生方式对土壤微生物与其共存微生物之间连接模式的影响。定量评估了土壤网络连接、微生物功能关联和多种土壤功能（如多功能性）之间的关系。3. 尽管与最近被遗弃的地点相比，植树造林和自然再生方法都增强了土壤微生物与其共存的微生物之间的联系，但在整个恢复时间序列中，这两种方法之间的联系趋势是相反的。植树造林导致土壤微生物和微型动物物种数量增加，具有单峰连接模式，而自然更新导致土壤网络连接在演替过程中不断增加。土壤网络连接的增加，特别是土壤微生物与微生物和微生物界间连接的增加，与微生物功能关联的增强相对应。编码不同中枢功能途径的微生物功能基因之间存在显著相关性，而微生物功能基因又与土壤多功能性呈正相关。4. 合成与应用。 土壤微生物与其共存的微生物之间连接的变化与土壤多功能性的变化呈正相关，由微生物功能关联介导。在早期恢复阶段，植树造林后的土壤网络比自然再生后的土壤网络包含更多的连接，而在后期的恢复阶段，植树造林网络的连接数量下降，最终被自然再生后的土壤网络所超越。这些发现引发了人们对黄土高原历史草地植树造林措施生态可持续性的关注，表明自然再生是实现长期生态恢复成功的首选方法。</p

Comparison of clinical manifestations between smokers and nonsmokers in SLE patients.

<p>F, female; M, male</p><p>Comparison of clinical manifestations between smokers and nonsmokers in SLE patients.</p

Comparison of clinical manifestations between smokers and nonsmoker systemic lupus erythematosus patients in the case-control study.

<p>Comparison of clinical manifestations between smokers and nonsmoker systemic lupus erythematosus patients in the case-control study.</p

Comparison of laboratory findings and SLEDAI scores between smokers and nonsmoker SLE patients in the case-control study.

<p>SLE, systemic lupus erythematosus; SLEDAI, SLE disease activity index; ANA, antinuclear antibody; Sm, Smith; RNP, ribonucleoprotein; rRNP, ribosomal RNP; APL antiphospholipid.</p><p>Comparison of laboratory findings and SLEDAI scores between smokers and nonsmoker SLE patients in the case-control study.</p

Comparison of clinical manifestations between smokers and nonsmokers in SLE patients.

<p>F, female; M, male</p><p>Comparison of clinical manifestations between smokers and nonsmokers in SLE patients.</p

Comparison of laboratory findings and SLEDAI scores between smokers and nonsmoker SLE patients.

<p>SLE: systemic lupus erythematosus; SLEDAI: SLE disease activity index; ANA: antinuclear antibody; Sm: Smith; RNP: ribonucleoprotein; rRNP: ribosomal RNP; APL: antiphospholipid.</p><p>Comparison of laboratory findings and SLEDAI scores between smokers and nonsmoker SLE patients.</p