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1. ⭐ 线粒体代谢与神经炎症、神经衰老及神经死亡的因果关系

• ✍️ 作者：Neuronlink
• 🏷️ 关键词：衰老、线粒体、炎症、代谢、神经
• 🔗 查看原文

2. ⭐ Cancer cell | 空间与单细胞测序解析肺腺癌演进规律：肺泡祖细胞为早期起源，IL1B-IL1R1 轴驱动前体病变进展

• ✍️ 作者：单细胞天地
• 🏷️ 关键词：cancer、测序、单细胞
• 🔗 查看原文

3. ⭐ 10月最新26+生信，多组学空间免疫谱分析确定了三级淋巴结构（TLS）的亚群并进行深入分析，建议收藏！

• ✍️ 作者：东晓生物
• 🏷️ 关键词：免疫、淋巴、生信
• 🔗 查看原文

4. ⭐ 7.7分1区生信，全文32个Figure聚焦最新热点：肿瘤神经浸润。小编认证的高质量生信文章，投稿到接收仅两个多月！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、神经、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

5. ⭐ 院士团队刚发表在Cancer Cell，结合单细胞和空转揭示肿瘤神经浸润促癌机制。大热点不容错过！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、神经、单细胞
• 📝 描述：点击查看详情
• 🔗 查看原文

6. ⭐ T细胞 | Nat.Genet. | 在原代人类T细胞中进行的遗传和表观遗传筛选将候选因果性自身免疫变异与T细胞网络关联起来

• ✍️ 作者：BioJournal Link
• 🏷️ 关键词：免疫、T细胞、表观遗传
• 🔗 查看原文

7. ⭐ 综述 | Brief.Bioinform. | 单细胞转录组细胞类型注释中计算方法的概述

• ✍️ 作者：BioJournal Link
• 🏷️ 关键词：B细胞、单细胞、转录组
• 🔗 查看原文

8. YTHDF2 通过 DUX-ZSCAN4 分子回路抑制小鼠胚胎干细胞中的 2C 样状态

• ✍️ 作者：老俊俊的生信笔记
• 🏷️ 关键词：T细胞、通路
• 🔗 查看原文

9. 48.5分，星级热点，刚发完Cancer cell又来个Nature，肿瘤神经浸润与抗 PD-1 治疗响应不佳相关！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、神经
• 📝 描述：点击查看详情
• 🔗 查看原文

10. 最新Cancer Cell重磅，胰腺癌中首次证实神经元与癌细胞间存在 “神经元-癌细胞假性突触”，并形成正反馈增强肿瘤神经浸润！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、神经
• 📝 描述：点击查看详情
• 🔗 查看原文

💡 该来源还有 20 条内容，详见 文末

详细内容（前10条）

1. GSE307834 肠道内感受功能障碍导致与年龄相关的认知能力下降 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、regex:intestin(e|al)
• 📝 描述：Contributors : Timothy Cox ; Ashwarya Devason ; Sydney Mason ; Madhav Subramanian ; Andrea Salvador ; Helene Descamps ; Alan Araujo ; Junwon Kim ; Yixuan Zhu ; Lev Litichevskiy ; Sunhee Jung ; Wondsuk Song ; Adrian Martin ; Nathan Henderson ; Kuei-Pin Huang ; Thao Nguyen ; Wisath Sae-Lee ; Iboro Umana ; Maria Sacta ; Ryan Rahman ; Stephen Wisser ; Andrew Nelson ; Ilona Golynker ; Lenka Dohnalova ; Alana McSween ; Eric Hohmann ; Shaan Patel ; Anna Bub ; Clara Sanchez ; Kevt’her Hoxha ; Lavinia Boccia ; Andrea Wong ; Klaas Bahnsen ; Jihee Kim ; Niklas Blank ; Dina Abbasian ; Clarissa Shoffler ; Christopher Petucci ; Fiona McAllister ; Amber Alhadeff ; Marc Fuccillo ; Colin Hill ; Cholsoon Jang ; Nicholas Betley ; Guillaume de Lartigue ; Virginia Lee ; Maayan Levy ; Christoph ThaissSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAging is accompanied by declining memory function, necessitating the development of effective countermeasures1. Brain- extrinsic factors influencing cognitive decline, including the intestinal microbiome, have emerged as attractive targets for peripheral interventions2-6, but the underlying mechanisms remain largely unclear. Here, by charting a high-resolution map of microbiome aging and its functional consequences throughout the lifespan of mice, we identify a mechanism whereby age- associated inhibition of gut-brain signalling results in impaired novelty-induced neuronal activation in the hippocampus and loss of memory encoding. Specifically, gut bacteria producing medium-chain fatty acids, such as Parabacteroides goldsteinii, accumulate over the lifespan and drive intestinal myeloid cell inflammation through GPR84 signalling. As a result, the function of afferent gut-innervating vagal neurons is impaired, the interoceptive signal received by the brain is weakened, and hippocampal function declines. We leverage this pathway to define interventions that restore memory in aged mice, such as phage targeting of Parabacteroides, GPR84 inhibition, and restoration of vagal activity. These findings indicate a key role for interoceptive signalling from the gastrointestinal tract in regulating brain aging and suggest that interoceptomimetics that stimulate gut-brain communication may counteract age-associated cognitive decline.
• 🔗 查看原文

2. GSE310581：通过基于CTLA-4的自调节回路改造的CAR T细胞实现空间控制的增强抗肿瘤疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatially
• 📝 描述：Contributors : Afroditi Katsarou ; George Kladis ; Thomas Baardemans ; Maria ThemeliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe widespread application of CAR T cell therapy to solid tumors is hindered by antigen expression heterogeneity, on-target off-tumor toxicity, and limited functional persistence of CAR T cells. Next generation engineering strategies aiming to overcome these hurdles rely on multiple antigen-targeting approaches that fail to simultaneously address all the limitations and/or the use of synthetic receptor transcriptional circuits, which suffer from slow activation kinetics. Here, we leveraged the unique trafficking properties of CTLA-4, regulated by a rapid internalization process, to create CTLA-4-based activation-inducible antigen receptors (CAVI-Rs). CAVI-Rs were exclusively expressed on T cells upon activation with remarkably fast on/off kinetics and self-sustainable expression. In in vitro and in vivo models of heterogeneous tumors, CAR+CAVI-R dual-engineered T cells demonstrated enhanced cytotoxicity and tumor-selective, spatially restricted functionality. Additionally, intermittent co-expression of the CAVI-R lead to improved T cell metabolic and transcriptional fitness, resulting in superior expansion, persistence and anti-tumor efficacy. The CAVI-R provides a novel, simple, safe, potent, and fully-human approach to expand CAR T cell applicability while improving anti-tumor outcomes.
• 🔗 查看原文

3. GSE282768 VEGFA 终止密码子变异加剧心肌梗死中的心脏重塑 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、scRNA
• 📝 描述：Contributors : Zhongxiang Chen ; Min ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusA sustained dosage of Vascular Endothelial Growth Factor A (VEGFA) is crucial for angiogenesis in both homeostasis and cardiovascular diseases. CUG-initiated alternative translation is a conserved mechanism for producing mature VEGFA. Genetic surveys have identified stop-gained variants predicted to prematurely terminate CUG-initiated translation without affecting ATG-initiated translation. However, the impacts of these variants on the vasculature in steady-state and disease conditions remain unknown. Here, we identified that homozygous mice carrying the stop-gained variant were viable. VEGFA dosage reduced to 70% in the Q150X homeostatic heart, with no significant alteration in cardiac function or vasculature. In the MI model, VEGFA dosage in Q150X was reduced to about 40% within the first-week post-infarction, leading to functional deterioration in the post-MI hearts. Significant changes in cellular composition were observed three days post-MI. In particular, endothelial cells in Q150X diverged into a state that showed higher level of hypoxia stress, an elevated inflammatory response, and increased extracellular matrix secretion. Additionally, we observed an increase of Nppb+ stressed cardiomyocytes in both 3 days post-MI and homeostasis. Finally, pro-inflammatory macrophages, neutrophils, and Cd8+T cells were enriched in the ischemic zone of Q150X hearts. CUG-initiated translation contributes significantly to the production of mature VEGFA in ischemic hearts. VEGFA dosage is critical in determining the cellular microenvironment during ischemic injury.
• 🔗 查看原文

4. GSE282766 VEGFA 终止密码子变异加剧心肌梗死中的心脏重塑 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、RNA-seq
• 📝 描述：Contributors : Zhongxiang Chen ; Min ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusA sustained dosage of Vascular Endothelial Growth Factor A (VEGFA) is crucial for angiogenesis in both homeostasis and cardiovascular diseases. CUG-initiated alternative translation is a conserved mechanism for producing mature VEGFA. Genetic surveys have identified stop-gained variants predicted to prematurely terminate CUG-initiated translation without affecting ATG-initiated translation. However, the impacts of these variants on the vasculature in steady-state and disease conditions remain unknown. Here, we identified that homozygous mice carrying the stop-gained variant were viable. VEGFA dosage reduced to 70% in the Q150X homeostatic heart, with no significant alteration in cardiac function or vasculature. In the MI model, VEGFA dosage in Q150X was reduced to about 40% within the first-week post-infarction, leading to functional deterioration in the post-MI hearts. Significant changes in cellular composition were observed three days post-MI. In particular, endothelial cells in Q150X diverged into a state that showed higher level of hypoxia stress, an elevated inflammatory response, and increased extracellular matrix secretion. Additionally, we observed an increase of Nppb+ stressed cardiomyocytes in both 3 days post-MI and homeostasis. Finally, pro-inflammatory macrophages, neutrophils, and Cd8+T cells were enriched in the ischemic zone of Q150X hearts. CUG-initiated translation contributes significantly to the production of mature VEGFA in ischemic hearts. VEGFA dosage is critical in determining the cellular microenvironment during ischemic injury.
• 🔗 查看原文

5. GSE282734 p38阻断逆转转移性乳腺癌中的免疫抑制微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Contributors : Priyanka Rajan ; Andrei V Bakin ; Scott I AbramsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe study investigated the role of p38α in regulating the outcome of the immune-tumor interaction in metastatic breast cancer. Single-cell transcriptomic analysis of the immune-TME showed that pharmacological p38 inhibition (p38i) or tumor-specific inactivation of p38α by CRISPR/Cas9 (p38KO) resulted in a less exhausted and more activated CD8+ T cell phenotype. Moreover, the myeloid cells in the TME exhibited reduced expression of immune-suppressive factors and chemotactic receptors. Overall, this study highlights a previously unrecognized p38α-driven pathway that promotes an immune suppressive TME and that therapeutic blockade of p38α has important implications for improving antitumor immunity and patient outcomes.
• 🔗 查看原文

6. GSE218749 尿张素 II 激活感觉皮肤通路以促进瘙痒和皮肤炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、pathway
• 📝 描述：Contributors : Hua Yang ; RenKai Zhu ; Wenhao Zhang ; Weiwei Chen ; Xinrong Yan ; Chunxu Shan ; Shanghai Xue ; Ruizhen Wang ; Xiaolong Dai ; Ciara Larkin ; Jiafu Wang ; Jianghui MengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusIn order to study the effect of UII on the transcription level regulation of itch-related genes in sensory neurons and keratinocytes, and to apply UII in mouse dorsal root ganglion neuronal cells and keratinocytes, the study showed that UII significantly upregulated the expression of various characteristics of atopic dermatitis and itch-related genes, such as Fasl, Mrgprx1, Amy2a3, INHBA, IL36G, STEAP2, etc.
• 🔗 查看原文

7. GSE307838 肠道内感受功能障碍导致与年龄相关的认知能力下降 [16S fmt]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:intestin(e|al)
• 📝 描述：Contributors : Timothy Cox ; Ashwarya Devason ; Sydney Mason ; Madhav Subramanian ; Andrea Salvador ; Helene Descamps ; Alan Araujo ; Junwon Kim ; Yixuan Zhu ; Lev Litichevskiy ; Sunhee Jung ; Wondsuk Song ; Adrian Martin ; Nathan Henderson ; Kuei-Pin Huang ; Thao Nguyen ; Wisath Sae-Lee ; Iboro Umana ; Maria Sacta ; Ryan Rahman ; Stephen Wisser ; Andrew Nelson ; Ilona Golynker ; Lenka Dohnalova ; Alana McSween ; Eric Hohmann ; Shaan Patel ; Anna Bub ; Clara Sanchez ; Kevt’her Hoxha ; Lavinia Boccia ; Andrea Wong ; Klaas Bahnsen ; Jihee Kim ; Niklas Blank ; Dina Abbasian ; Clarissa Shoffler ; Christopher Petucci ; Fiona McAllister ; Amber Alhadeff ; Marc Fuccillo ; Colin Hill ; Cholsoon Jang ; Nicholas Betley ; Guillaume de Lartigue ; Virginia Lee ; Maayan Levy ; Christoph ThaissSeries Type : OtherOrganism : Mus musculusAging is accompanied by declining memory function, necessitating the development of effective countermeasures1. Brain- extrinsic factors influencing cognitive decline, including the intestinal microbiome, have emerged as attractive targets for peripheral interventions2-6, but the underlying mechanisms remain largely unclear. Here, by charting a high-resolution map of microbiome aging and its functional consequences throughout the lifespan of mice, we identify a mechanism whereby age- associated inhibition of gut-brain signalling results in impaired novelty-induced neuronal activation in the hippocampus and loss of memory encoding. Specifically, gut bacteria producing medium-chain fatty acids, such as Parabacteroides goldsteinii, accumulate over the lifespan and drive intestinal myeloid cell inflammation through GPR84 signalling. As a result, the function of afferent gut-innervating vagal neurons is impaired, the interoceptive signal received by the brain is weakened, and hippocampal function declines. We leverage this pathway to define interventions that restore memory in aged mice, such as phage targeting of Parabacteroides, GPR84 inhibition, and restoration of vagal activity. These findings indicate a key role for interoceptive signalling from the gastrointestinal tract in regulating brain aging and suggest that interoceptomimetics that stimulate gut-brain communication may counteract age-associated cognitive decline.
• 🔗 查看原文

8. GSE307836 肠道内感受功能障碍导致与年龄相关的认知能力下降 [合住]

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:intestin(e|al)
• 📝 描述：Contributors : Timothy Cox ; Ashwarya Devason ; Sydney Mason ; Madhav Subramanian ; Andrea Salvador ; Helene Descamps ; Alan Araujo ; Junwon Kim ; Yixuan Zhu ; Lev Litichevskiy ; Sunhee Jung ; Wondsuk Song ; Adrian Martin ; Nathan Henderson ; Kuei-Pin Huang ; Thao Nguyen ; Wisath Sae-Lee ; Iboro Umana ; Maria Sacta ; Ryan Rahman ; Stephen Wisser ; Andrew Nelson ; Ilona Golynker ; Lenka Dohnalova ; Alana McSween ; Eric Hohmann ; Shaan Patel ; Anna Bub ; Clara Sanchez ; Kevt’her Hoxha ; Lavinia Boccia ; Andrea Wong ; Klaas Bahnsen ; Jihee Kim ; Niklas Blank ; Dina Abbasian ; Clarissa Shoffler ; Christopher Petucci ; Fiona McAllister ; Amber Alhadeff ; Marc Fuccillo ; Colin Hill ; Cholsoon Jang ; Nicholas Betley ; Guillaume de Lartigue ; Virginia Lee ; Maayan Levy ; Christoph ThaissSeries Type : OtherOrganism : Mus musculusAging is accompanied by declining memory function, necessitating the development of effective countermeasures1. Brain- extrinsic factors influencing cognitive decline, including the intestinal microbiome, have emerged as attractive targets for peripheral interventions2-6, but the underlying mechanisms remain largely unclear. Here, by charting a high-resolution map of microbiome aging and its functional consequences throughout the lifespan of mice, we identify a mechanism whereby age- associated inhibition of gut-brain signalling results in impaired novelty-induced neuronal activation in the hippocampus and loss of memory encoding. Specifically, gut bacteria producing medium-chain fatty acids, such as Parabacteroides goldsteinii, accumulate over the lifespan and drive intestinal myeloid cell inflammation through GPR84 signalling. As a result, the function of afferent gut-innervating vagal neurons is impaired, the interoceptive signal received by the brain is weakened, and hippocampal function declines. We leverage this pathway to define interventions that restore memory in aged mice, such as phage targeting of Parabacteroides, GPR84 inhibition, and restoration of vagal activity. These findings indicate a key role for interoceptive signalling from the gastrointestinal tract in regulating brain aging and suggest that interoceptomimetics that stimulate gut-brain communication may counteract age-associated cognitive decline.
• 🔗 查看原文

9. GSE284566 B细胞刺激改变了非活性X染色体的结构和高级组织

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell
• 📝 描述：Contributors : Isabel Sierra ; Natalie E Toothacre ; Robin H van de Weide ; Claudia D Lovell ; Son C Nguyen ; R J Varnett ; Ashley L Cook ; Han-Seul Ryu ; Sarah Pyfrom ; Harrison Wang ; Daniel Beiting ; Jennifer E Philips-Cremins ; Eric F Joyce ; Montserrat C AngueraSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusX Chromosome Inactivation (XCI) equalizes X-linked gene expression between sexes. B cells exhibit dynamic XCI, with Xist RNA/heterochromatic marks absent on the inactive X (Xi) in naive B cells but returning following mitogenic stimulation. The impact of dynamic XCI on Xi structure and maintenance was previously unknown. Here, we find dosage compensation of the Xi with state-specific XCI escape genes in naive and in vitro activated B cells. Allele-specific OligoPaints indicate similar Xi and Xa territories in B cells that are less compact than in fibroblasts. Allele-specific Hi-C reveals a lack of TAD-like structures on the Xi of naive B cells, and stimulation-induced alterations in TAD-like boundary strength independent of gene expression. Notably, Xist deletion in B cells changes TAD boundaries and large-scale Xi compaction. Altogether, our results uncover B cell-specific Xi plasticity which could underlie sex-biased biological mechanisms.
• 🔗 查看原文

10. GSE310387 甲酰肽受体2对肠上皮稳态的贡献

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:intestin(e|al)
• 📝 描述：Contributors : Shuting Yu ; Yingying LeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo elucidate the mechanisms involved in maintaining intestinal epithelial homeostasis through formyl peptide receptor 1 (FPR2), small intestinal organoids derived from Fpr2f/f mice were used as an ex vivo model. Transcriptomics were examined via RNA-seq following FPR2 activation with MMK-1.
• 🔗 查看原文

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1. 隐藏的小胶质细胞开关有助于保护大脑免受阿尔茨海默病的侵害。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists discovered that lowering a specific molecule helps microglia switch into a protective state that quiets brain inflammation in Alzheimer’s. A small group of these cells seems to have an outsized ability to keep the brain healthier. When a key signal is removed from them, Alzheimer’s symptoms worsen. This pathway may help explain why some people naturally have reduced Alzheimer’s risk.
• 🔗 查看原文

• CR：哈尔滨医科大学团队发现，PRMT3是非小细胞肺癌对放疗和免疫治疗耐受的关键！
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• Immunity重磅：曹雪涛团队揭示肿瘤免疫新机制
• 登顶top级期刊！GWAS+单细胞分析解密疾病机制，这波思路必须学！
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• 致敬时代丨从“切不完”的肿瘤，到多数患者肿瘤缩小或停止生长！新药研发为这类患者带来新生
• ANN2：用于异常检测的人工神经网络
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• 虚拟感染能触发免疫反应？《nature neuroscience》揭示大脑的神奇防御机制
• 利用生存预后模型预测癌症患者结局：从数据分析到模型解读
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• 柳叶刀：上海长海医院 CAR-NK 突破，同时医院正式揭牌成立细胞治疗中心
• 从「治病」到「治未病」：T 细胞的系统激活与超前诊断之路
• 关键代谢调节因子！同济大学附属东方医院发文：发现“最毒乳腺癌”潜在治疗靶点
• 促进耐药新机制！中南大学等单位合作发文：肺腺癌治疗潜在生物标志物或治疗靶点
• 肠道菌群如何影响疾病治疗？李华婷/陈洛南/倪岳琼/曾嵘/贾伟平团队揭示肠道菌群在抗性淀粉干预相关肝病疗效异质性中的核心作用
• 上海交大最新Cell子刊：肠道菌群影响抗性淀粉治疗脂肪肝的效果
• Carl June最新论文：IL-9信号增强CAR-T细胞治疗实体瘤效果

• GSE260742 DOT1L 通过 PRC1.1 拮抗作用提供转录记忆 [ChIP-Seq]
• GSE260456 DOT1L 通过 PRC1.1 拮抗作用提供转录记忆 [RNA-seq]
• GSE248113 TL1A 驱动 ILC 介导的粒细胞生成和结肠炎相关癌症