科研日报 2025-12-25

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📅 Daily Report - 2025-12-25

今日筛选出 34 条内容,来自 2 个来源

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🤖 今日AI智能总结

🧬 数据前沿

今日焦点: 揭示了小鼠巨噬细胞IFNγ信号通路中的新型JAK1/2-STAT3分支,并利用单细胞多组学技术绘制了唐氏综合征人类皮层发育图谱。

主要方向

  • 脑衰老表观遗传学研究:通过单核甲基化测序解析不同年龄小鼠大脑的表观遗传特征。
  • 唐氏综合征皮层发育:构建人类皮层发育的单细胞多组学图谱,包括胎儿期和体外诱导神经元。
  • 炎症与免疫调控:研究Luspatercept抑制单核细胞焦亡在再生障碍性贫血中的作用,以及微生物代谢物马尿酸对巨噬细胞促炎反应的影响。

技术亮点

  • 单细胞甲基化测序(scNMT-seq)和单细胞多组学技术在脑衰老和发育研究中的应用。
  • 双RNA-seq技术鉴定致病菌的效应分子。

🧪 博客更新

今日焦点: 新型纳米粒子成像技术能通过检测超弱光信号,更早地识别并区分癌变组织;MIT科学家开发新策略,帮助免疫系统更有效地识别并攻击癌细胞。

主要方向

  • 肠道微生物组研究:揭示社会伙伴基因对宿主肠道菌群的影响。
  • 癌症诊断与治疗:开发早期癌症检测成像技术;利用纳米粒子靶向杀伤癌细胞并增强免疫系统抗癌能力。
  • 基因组学:推出基于深度学习的长读RNA测序变异检测工具。

技术亮点

  • 深度学习:Clair3-RNA工具提升长读RNA测序变异检测精度。
  • 纳米技术:开发能特异性结合肿瘤标记物或增强细胞内应激的纳米粒子,实现癌症早期成像与选择性杀伤。

📚 分类浏览

🧬 数据前沿 (29条)

详细内容(前10条)

1.GSE169384 通过单核甲基化测序研究大脑衰老的表观遗传特征 [FC-8wk-m-018]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:aging、sequencing、epigenetic、methylation
  • 📝 描述:Contributors : Wei Tian ; Anna Bartlett ; Jordan Altshul ; Rosa Gomez Castanon ; Joseph R Nery ; Jacinta D Lucero ; Julia K Osteen ; Huaming Chen ; M M Behrens ; Joseph R EckerSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusIllustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.
  • 🔗 查看原文

2.GSE181116 通过单核甲基化测序研究大脑衰老的表观遗传特征 [FC-18mo]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:aging、sequencing、epigenetic、methylation
  • 📝 描述:Contributors : Wei Tian ; Anna Bartlett ; Jordan Altshul ; Rosa Gomez Castanon ; Joseph R Nery ; Jacinta D Lucero ; Julia K Osteen ; Huaming Chen ; M M Behrens ; Joseph R EckerSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusIllustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of both male and female mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.
  • 🔗 查看原文

3.GSE169467 通过单核甲基化测序研究大脑衰老的表观遗传特征 [NACB-9mo-m-012]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:aging、sequencing、epigenetic、methylation
  • 📝 描述:Contributors : Wei Tian ; Anna Bartlett ; Jordan Altshul ; Rosa Gomez Castanon ; Joseph R Nery ; Jacinta D Lucero ; Julia K Osteen ; Huaming Chen ; M M Behrens ; Joseph R EckerSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusIllustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.
  • 🔗 查看原文

4.GSE314453 Luspatercept 联合免疫抑制剂通过抑制单核细胞焦亡来减轻重型再生障碍性贫血患者的炎症 [scRNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:monocyte、inflammation、regex:immuno(logy|therapy|suppression)、scRNA
  • 📝 描述:Contributors : Zining Wang ; Jiaming Hu ; Yiyu Guo ; Xinrui Zhang ; Yu Gao ; Nan Song ; Rong FuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAplastic anemia (AA) is a bone marrow failure disorder caused by diverse etiologies. AA pathogenesis involves aberrant immune activation and an imbalanced inflammatory bone marrow microenvironment. Previous studies have shown that inhibition of transforming growth factor-β (TGF-β) signaling in patients with AA can improve multilineage hematopoietic recovery and immune balance. This study is the first to demonstrate the synergistic mechanisms of TGF-β inhibitor luspatercept in combination with Cyclosporine and Eltrombopag for the treatment of severe aplastic anemia (SAA) by acting on monocytes. Single-cell RNA sequencing revealed increased inflammatory cytokine levels and elevated expression of pyroptosis-related genes in monocytes after luspatercept withdrawal. Mechanistic investigations further showed luspatercept suppressed pyroptosis in monocytes, reshaping the immune microenvironment, and attenuating pro-inflammatory cytokine secretion and cytotoxic molecule expression in CD8+T cells. This groundbreaking study uncovers that Luspatercept can reduce inflammation and pyroptosis through multi-target immune modulation, which provides a novel therapeutic strategy for AA.
  • 🔗 查看原文

5.GSE314452 Luspatercept 联合免疫抑制剂通过抑制单核细胞焦亡来减轻重型再生障碍性贫血患者的炎症 [RNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:monocyte、inflammation、regex:immuno(logy|therapy|suppression)、RNA-seq
  • 📝 描述:Contributors : Zining Wang ; Jiaming Hu ; Yiyu Guo ; Xinrui Zhang ; Yu Gao ; Nan Song ; Rong FuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAplastic anemia (AA) is a bone marrow failure disorder caused by diverse etiologies. AA pathogenesis involves aberrant immune activation and an imbalanced inflammatory bone marrow microenvironment. Previous studies have shown that inhibition of transforming growth factor-β (TGF-β) signaling in patients with AA can improve multilineage hematopoietic recovery and immune balance. This study is the first to demonstrate the synergistic mechanisms of TGF-β inhibitor luspatercept in combination with Cyclosporine and Eltrombopag for the treatment of severe aplastic anemia (SAA) by acting on monocytes. The aim was to explore the effects of the drug Luspatercept on monocyte cell lines by performing RNA-seq after treating the THP-1 cell line. Mechanistic investigations further showed luspatercept suppressed pyroptosis in monocytes, reshaping the immune microenvironment, and attenuating pro-inflammatory cytokine secretion and cytotoxic molecule expression in CD8+T cells. This groundbreaking study uncovers that Luspatercept can reduce inflammation and pyroptosis through multi-target immune modulation, which provides a novel therapeutic strategy for AA.
  • 🔗 查看原文

6. GSE307919 芳香族微生物代谢产物马尿酸通过 TLR-MyD88 信号通路和脂质重塑增强巨噬细胞的促炎反应

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:TLR、regex:micro(b|be|bial|organism)
  • 📝 描述:Contributors : Gauri Mirji ; Rahul S ShindeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe gut microbiome generates a diverse array of metabolites that actively shape host immunity, yet the pro-inflammatory potential of microbial metabolites remains incompletely understood. Using a non-targeted, liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based metabolomics, we identified hippuric acid, an aromatic gut microbe-derived metabolite, as a potent enhancer of pro-inflammatory responses in Escherichia coli infection model. Intraperitoneal administration of hippuric acid significantly heightened pro-inflammatory responses, promoted innate immune cell activation, and reduced survival in infected mice. Similar pro-inflammatory effects were observed in an LPS-induced inflammation model. In vitro, hippuric acid selectively potentiated M1-like macrophage polarization (LPS + IFNγ) but had no effect on M2-like polarization (IL-4). Hippuric acid further augmented responses to multiple myeloid differentiation primary response 88 (MyD88)-dependent toll-like receptor (TLR) ligands, but not to TRIF-dependent TLR3, or to cytosolic innate immune stimuli such as STING and NOD2 agonists, implicating TLR-MyD88 signaling as a likely mechanism of action. Genetic deletion of MyD88 abrogated the pro-inflammatory effects of hippuric acid both in vitro and in vivo, confirming its dependence on the MyD88 pathway. Transcriptomic and lipidomic analyses revealed that hippuric acid upregulated cholesterol biosynthesis and induced lipid accumulation. Pharmacological reduction of cellular cholesterol using fluvastatin or 25-hydroxycholesterol attenuated its pro-inflammatory effects. Notably, hippuric acid also enhanced pro-inflammatory responses in human macrophages, and its elevated levels correlated with increased sepsis mortality, underscoring its clinical relevance. Together, these findings identify hippuric acid as a previously unrecognized microbial-derived pro-inflammatory modulator that links gut microbial metabolism, lipid remodeling, and innate immune signaling, and offer new insights into its role in infection and inflammation.
  • 🔗 查看原文

7. GSE305139 唐氏综合征人类皮层发育的单细胞多组学图谱 - 胎儿皮层批量 RNA 测序数据集

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNA-seq、single-cell
  • 📝 描述:Contributors : Michael Lattke ; Vincenzo De PaolaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDown syndrome, caused by an extra copy of chromosome 21, is the most common genetic form of intellectual disability, which affects up to 1 in 700 live births. Yet, how increased dosage of the ~200 protein-coding genes on human chromosome 21 affects cortical development and function remains unclear. Here we generated a single-cell transcriptome and chromatin accessibility atlas of the human foetal cortex at mid gestation (11-20 weeks after conception), a critical period of cortical development. We uncovered an early global transcriptional network disruption, subtly altering ~1000 genes involved in neural development and function primarily in excitatory neurons. These changes reflected clinical phenotypes like intellectual disability and epilepsy, were accompanied by a significant reduction in layer 4 neurons, and were driven by a network of transcription factors including chromosome 21 genes BACH1, PKNOX1, and GABPA. Finally, a xenograft model replicates key molecular features, offering an experimental platform for validating new therapeutic targets. This resource defines the gene-regulatory landscape of the developing human cortex in Down syndrome, revealing the earliest known molecular and cellular signatures of its neurological manifestations and novel candidate targets for therapeutic interventions.
  • 🔗 查看原文

8. GSE305135 唐氏综合征人类皮层发育的单细胞多组学图谱 - 体外神经细胞基础表征批量RNA测序数据集

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNA-seq、single-cell
  • 📝 描述:Contributors : Michael Lattke ; Vincenzo De PaolaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDown syndrome, caused by an extra copy of chromosome 21, is the most common genetic form of intellectual disability, which affects up to 1 in 700 live births. Yet, how increased dosage of the ~200 protein-coding genes on human chromosome 21 affects cortical development and function remains unclear. Here we generated a single-cell transcriptome and chromatin accessibility atlas of the human foetal cortex at mid gestation (11-20 weeks after conception), a critical period of cortical development. We uncovered an early global transcriptional network disruption, subtly altering ~1000 genes involved in neural development and function primarily in excitatory neurons. These changes reflected clinical phenotypes like intellectual disability and epilepsy, were accompanied by a significant reduction in layer 4 neurons, and were driven by a network of transcription factors including chromosome 21 genes BACH1, PKNOX1, and GABPA. Finally, a xenograft model replicates key molecular features, offering an experimental platform for validating new therapeutic targets. This resource defines the gene-regulatory landscape of the developing human cortex in Down syndrome, revealing the earliest known molecular and cellular signatures of its neurological manifestations and novel candidate targets for therapeutic interventions.
  • 🔗 查看原文

9. GSE305132 唐氏综合征人类皮质发育的单细胞多组学图谱 - 体外神经祖细胞 - PKNOX1、BACH1 和 GABPA 反义寡核苷酸治疗(批量 RNA-seq 数据集)

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNA-seq、single-cell
  • 📝 描述:Contributors : Michael Lattke ; Vincenzo De PaolaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDown syndrome, caused by an extra copy of chromosome 21, is the most common genetic form of intellectual disability, which affects up to 1 in 700 live births. Yet, how increased dosage of the ~200 protein-coding genes on human chromosome 21 affects cortical development and function remains unclear. Here we generated a single-cell transcriptome and chromatin accessibility atlas of the human foetal cortex at mid gestation (11-20 weeks after conception), a critical period of cortical development. We uncovered an early global transcriptional network disruption, subtly altering ~1000 genes involved in neural development and function primarily in excitatory neurons. These changes reflected clinical phenotypes like intellectual disability and epilepsy, were accompanied by a significant reduction in layer 4 neurons, and were driven by a network of transcription factors including chromosome 21 genes BACH1, PKNOX1, and GABPA. Finally, a xenograft model replicates key molecular features, offering an experimental platform for validating new therapeutic targets. This resource defines the gene-regulatory landscape of the developing human cortex in Down syndrome, revealing the earliest known molecular and cellular signatures of its neurological manifestations and novel candidate targets for therapeutic interventions.
  • 🔗 查看原文

10. GSE304589 揭示巨噬细胞 IFNγ 信号传导中非传统的 JAK1/2-STAT3 分支 [ChIP-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:macrophage、ChIP-seq
  • 📝 描述:Contributors : Mees Botman ; Josje Huisman ; Marten A HoeksemaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusInterferon-γ (IFNγ) is a key cytokine in immune activation and anti-viral responses that classically signals via JAK1/2-mediated STAT1 homodimers to drive macrophage activation. Here, we identify a non-canonical signaling component in which IFNγ also activates STAT3. Our results show that IFNγ activates STAT3 rapidly and directly through JAK1 and JAK2. We provide the first evidence that STAT3 can form heterodimers with STAT1 in this context and demonstrate that STAT3 is co-recruited to a subset of IFNγ-induced, STAT1-bound regulatory elements. While IFNγ directly activates STAT3, our results reveal that its contribution to gene regulation is limited, indicating that STAT1 easily substitutes the STAT1–STAT3 heterodimer for STAT1 homodimers when STAT3 is absent. These findings uncover STAT3 as a new unconventional player in macrophage IFNγ signaling, underscoring the complex and context-dependent nature of cytokine signaling networks.
  • 🔗 查看原文

💡 该来源还有 19 条内容,详见 文末

🧪 博客更新 (5条)

详细内容(全部5条)

1.你室友的基因可能正在影响你的肠道菌群。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
  • 📝 描述:Scientists studying thousands of rats discovered that gut bacteria are shaped by both personal genetics and the genetics of social partners. Some genes promote certain microbes that can spread between individuals living together. When researchers accounted for this social sharing, genetic influence on the microbiome turned out to be much stronger than previously thought. The study suggests genes can affect others indirectly, without DNA ever being exchanged.
  • 🔗 查看原文

2. Clair3-RNA——一款基于深度学习的长读长RNA测序数据小变异检测工具

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:sequencing
  • 📝 描述:A new deep learning tool improves RNA sequencing variant detection from long reads, enabling accurate analysis of full-length isoforms and RNA editing across PacBio and Nanopore platforms…
  • 🔗 查看原文

3. 这种超灵敏成像系统可以更早地发现癌症。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:A new imaging technology can distinguish cancerous tissue from healthy cells by detecting ultra-weak light signals. It relies on nanoparticles that bind to tumor markers, making cancerous areas easier to identify. The system is far more sensitive than existing tools and could speed up cancer screening. Scientists believe it may help detect tumors earlier and reduce delays in diagnosis.
  • 🔗 查看原文

4. 麻省理工学院科学家剥离癌细胞的糖蛋白外壳

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:Scientists at MIT and Stanford have unveiled a promising new way to help the immune system recognize and attack cancer cells more effectively. Their strategy targets a hidden “off switch” that tumors use to stay invisible to immune defenses—special sugar molecules on the cancer cell surface that suppress immune activity. Early tests show it can supercharge immune responses and outperform current antibody therapies.
  • 🔗 查看原文

5. 这些纳米颗粒能杀死癌细胞,同时不伤及健康细胞。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:Researchers have created tiny metal-based particles that push cancer cells over the edge while leaving healthy cells mostly unharmed. The particles work by increasing internal stress in cancer cells until they trigger their own shutdown process. In lab tests, they killed cancer cells far more effectively than healthy ones. The technology is still early-stage, but it opens the door to more precise and gentler cancer treatments.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
RNA-seq8
single-cell7
sequencing4
aging3
epigenetic3
methylation3
cancer3
monocyte3
inflammation3
resistance2
macrophage2
ChIP-seq2
metabolism2
scRNA2
regex:immuno(logytherapy
TLR1
regex:micro(bbe
transcriptomics1
pathway1
transcriptome1

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🧬 数据前沿 其他内容 (19条)

📅 报告生成时间:2025-12-24 21:37
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