论文推荐-11-神经炎症 · Jun 12 11:09

{"success": true, "name": "paper-recommender", "description": "每日定时推送高质量论文推荐 — PubMed检索 → Hermes+Claude双重评估 → 仅推最优1篇 → HTML深度解读", "tags": ["PubMed", "论文推荐", "Claude评估", "文献解读", "科研"], "related_skills": [], "content": "---\nname: paper-recommender\ndescription: \"每日定时推送高质量论文推荐 — PubMed检索 → Hermes+Claude双重评估 → 仅推最优1篇 → HTML深度解读\"\nversion: 2.2.0\nauthor: Hermes\ntags: [PubMed, 论文推荐, Claude评估, 文献解读, 科研]\n---\n\n# 📚 每日论文推荐工作流 (Paper Recommender)\n\n## 职责\n根据用户的6个研究兴趣方向，每日定时从PubMed检索近期高质量论文，经过Hermes+Claude双重评估后，**只选最优的1篇**，下载PDF+提取原图，制作公众号风格的HTML深度解读文件并推送。\n\n## 用户研究方向\n1. 帕金森病(PD) / GZR18 / α-synuclein\n2. 神经炎症 / 小胶质细胞 / 星形胶质细胞\n3. 细胞死亡方式 (Mitoxyperiosis / 铁死亡 / 焦亡 / 泛素化降解)\n4. 外泌体 / 细胞外囊泡 / 神经退行性疾病\n5. 脑缺血 / 脑卒中 / 神经保护\n6. 生信分析 / 单细胞测序 / 多组学\n\n## 定时推送安排\n\n| 时间 | 主题 | 关键词 |\n|:----:|------|--------|\n| 08:00 | PD/帕金森病 | Parkinson's disease, α-synuclein, MPTP, dopamine neuron |\n| 11:00 | 神经炎症/胶质细胞 | neuroinflammation, microglia, astrocyte, NLRP3 |\n| 13:00 | 细胞死亡/信号通路 | cell death, mitoxyperiosis, ferroptosis, ubiquitination |\n| 15:00 | 外泌体/细胞通讯 | exosome, extracellular vesicle, neural, brain |\n| 17:00 | 脑缺血/神经保护 | cerebral ischemia, stroke, neuroprotection, MCAO |\n| 19:00 | 生信/前沿技术 | single-cell, multi-omics, bioinformatics, spatial transcriptomics |\n\n## ⚠️ 已知工具陷阱\n\n### 文件系统隔离（重要！）\n`execute_code` 运行在沙箱环境中，**不能直接访问** `terminal` 工具写入 `/tmp/` 或 `$HOME/` 的文件。反之亦然。\n- ❌ 错误做法：terminal写入`/tmp/fig1_b64.txt`，然后用execute_code的`open()`读取 → 文件不存在\n- ✅ 正确做法1：所有数据处理在terminal中完成（Python脚本通过`python script.py`执行）\n- ✅ 正确做法2：将数据处理写成`.py`文件写入磁盘，再用terminal(`python path/to/script.py`)执行\n\n### 大文件HTML生成\n当HTML嵌入base64图片时（5张Nature原图 ≈ 4MB），`write_file`会因大小限制失败。\n- ❌ 不要直接用write_file写4MB+的HTML\n- ✅ 策略：写一个Python builder脚本到磁盘（`write_file → build_html.py`），然后`terminal(\"python build_html.py\")`执行它\n\n### Windows Python路径陷阱\n在 Windows git-bash 中，Python 脚本不识别 MSYS 路径格式（`/c/Users/...`）：\n- ❌ `open(\"/c/Users/forgase/fig1_b64.txt\")` → FileNotFoundError\n- ✅ `open(\"C:/Users/forgase/fig1_b64.txt\")` — 正斜杠在 Windows Python 中可识别\n- 同理，`python3` 命令在 Windows 上可能被应用执行别名拦截 → 始终使用 `python`\n\n## 执行流程（完整版）\n\n### Step 1: PubMed检索 — 两阶段策略\n\n**方式：Python urllib**（推荐，避免curl的SSL/编码问题）\n```python\nimport urllib.request, urllib.parse, json\nparams = {\n 'db': 'pubmed', 'term': query,\n 'mindate': '<3个月前>', 'maxdate': '<今天>',\n 'datetype': 'pdat', 'retmax': 15, 'retmode': 'json'\n}\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?' + urllib.parse.urlencode(params)\n```\n\n**阶段A — 主题搜索**：用关键词搜该方向近期论文\n**阶段B — 高IF期刊过滤**：用主题词 + `(\"Nature\"[Journal] OR \"Cell\"[Journal] OR ...)` 格式搜\n\n⚠️ 关键陷阱：\n- `sort=date` 被PubMed忽略（返回warning），不要用\n- 期刊名必须用 `\"全称\"[Journal]` 格式，裸词会被翻译为MeSH词条\n- 复杂查询在curl中容易URL编码失败，优先用Python\n\n### Step 2: 获取论文详情并初筛\n\n```python\n# 获取元数据\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&id=<PMIDs>&retmode=json'\n# 获取摘要\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMIDs>&retmode=xml'\n```\n\n**初筛硬性门槛**（必须同时满足）：\n1. IF > 10 或领域顶刊\n2. 2026年3月后发表\n3. 与用户研究方向直接相关\n4. 原创研究（pubtype不含Review）\n5. 非 News & Views / Letter / 编辑评论\n\n### Step 3: Claude Code深度评估（Hermes + Claude 双重评判）\n\n将经过初筛的候选论文交给 Claude Code 严格评估：\n```\nclaude -p \"严格评估以下论文，从5个维度各评1-10分...\"\n```\n\n**5维度评分**：\n1. **逻辑完整性** (1-10)：完整正反验证（gain+loss of function）、KO/KI模型\n2. **方法学水平** (1-10)：前沿技术（单细胞测序、冷冻电镜、活细胞成像、TurboID等）\n3. **创新性** (1-10)：新概念/新机制/新方法，首次报道\n4. **可借鉴性** (1-10)：实验设计是否值得用户在自己的课题中参考 **← 这是最关键的维度**\n5. **临床转化潜力** (1-10)：体内验证或治疗意义\n\n### Step 4: 唯一推荐（核心规则）\n\n- Claude评分 < 30分（平均<6分）或任何单维度 < 5分 → **不推荐**，跳过\n- 多个候选都达标 → **只选最优的1篇**，不要让用户选\n- Hermes再次确认质量 + 相关性 + 可借鉴性 → 只有双方都确认才通过\n- **如果这篇研究方向不匹配（如planarian flatworm研究），即使评分高也不能推**\n\n### Step 5: 下载PDF + 提取Figure图片\n\n**PDF下载**：\n- Nature: `https://www.nature.com/articles/{article_id}.pdf`\n- Cell Press/Elsevier: PDF有ScienceDirect防护，通常无法通过curl下载\n- 所有期刊的Figure图片可通过CDN下载（详见`references/figure-download-patterns.md`）\n- 注意：部分期刊有付费墙，PDF可能无法下载，此时跳过PDF但继续下载Figure图片\n\n**Figure提取（Nature系列通用模式 — 已验证 Nature & Nat Neurosci）**：\n```bash\n# 1. 从HTML中提取所有figure图片URL（通用模式，匹配所有s415XX系列期刊）\ncurl -s -L -H \"User-Agent: Mozilla/5.0\" \"https://www.nature.com/articles/{article_id}\" \\\n | grep -oP 'https://media\\.springernature\\.com/[^\"'\"'\"'<>]+s415\\d\\d[^\"'\"'\"'<>]*\\.(?:png|jpg|webp)' \\\n | sort -u\n\n# 2. 下载每个figure为base64（用于HTML嵌入）\n# 先用grep确定实际的journal_id/year/article_num，然后：\nFIG_URL=\"https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F{s415XX-...}/MediaObjects/{journal_id}_{year}_{article_num}_Fig{N}_HTML.png\"\ncurl -s \"$FIG_URL\" -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt\n```\n\n**分辨率选择**：\n- `/full/` — 最高分辨率（推荐用于Fig1）\n- `/lw1200/` — 宽1200px（其余Figures用此即可）\n- `/m685/` — 宽685px（小尺寸）\n\n**已验证的图片URL模式**：\n| 期刊 | article_id 示例 | journal_id | URL模式 |\n|------|----------------|------------|---------|\n| Nature | s41586-026-10597-2 | 41586 | `41586_{year}_{article_num}_Fig{N}_HTML.png` |\n| Nat Neurosci | s41593-026-02317-w | 41593 | `41593_{year}_{article_num}_Fig{N}_HTML.png` |\n\n- 参考 `references/figure-download-patterns.md` 获取各期刊的详细URL模式\n\n### Step 6: 制作公众号风格HTML深度解读 — Python Builder模式\n\nHTML文件要求：\n1. 所有图片用JS变量(base64)嵌入，不使用file://协议\n2. 仿公众号排版（简洁卡片风格）\n3. 每条结果配\"复现建议\"（🔬 复现建议：...）\n4. 包含论文原图 + 逐图解读 + 文章小结\n5. 保存到桌面，文件命名规范：`{主题关键词}_文献解读.html`\n\n**实现方法**（大文件HTML必须用此方式）：\n由于HTML含5张base64图片（~4MB），不能直接用`write_file`写入。\n```python\n# 1. 先读取base64数据（terminal工具写入的文件）\n# ⚠️ 重要：Windows Python不识别 MSYS 路径 /c/Users/，必须用 C:/Users/ 格式\nfig_b64 = {}\nfor i in range(1, 7):\n with open(f\"C:/Users/<user>/fig{i}_b64.txt\", \"r\") as f:\n fig_b64[f\"fig{i}\"] = f.read().strip()\n\n# 2. 构建HTML字符串（用f-string嵌入base64）\nhtml = f'''...<img src=\"data:image/png;base64,{fig_b64['fig1']}\">...'''\n\n# 3. 写入文件（使用正斜杠路径，Windows Python可识别）\nwith open(\"C:/Users/<user>/Desktop/外泌体_文献解读.html\", \"w\", encoding=\"utf-8\") as f:\n f.write(html)\n```\n\n**流程总结**（6步）：\n1. terminal中`curl | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt` 下载所有图片（保存到用户目录，/tmp/在沙箱中不可用）\n2. 用`write_file`将HTML builder脚本写入磁盘（不含base64数据，仅模板）\n3. terminal中执行该Python脚本（读取base64文件 + 构建完整HTML + 写入桌面）\n4. 验证HTML和PDF文件存在：`ls -la /c/Users/<user>/Desktop/`\n\n**HTML模板风格指南**：\n- 头部：渐变深蓝背景 + 白色文字 + 标签徽章\n- 评分卡片：flex网格布局，5维度评分条\n- 图文解读：Fig依次排列，每个配canvas+caption+复现建议\n- 文章小结：渐变紫色卡片\n- 参考 `references/html-template-structure.md` 获取模板框架\n\n### Step 7: 微信推送\n\n**格式要求**：\n```\n🔥 {时间} {主题} 论文推荐\n\n🏆 标题...\n📅 日期 | 📰 期刊\n⭐ Claude评分：X/50\n💡 推荐理由：...\n\n（解读HTML已生成，请查收）\n```\n\n**如果当天没有好论文**：\n```\n📭 {时间} {主题}\n今天这个方向没有找到特别适合你的论文，下次继续关注。\n```\n\n## 核心原则\n- **只推1篇** —— 不要让用户从多个候选中选择\n- **宁缺毋滥** —— 没有好论文就不推，不强塞\n- **Hermes + Claude 双重把关** —— 都确认完美适合才推\n- **不推荐综述**（除非极高价值）\n- **不推荐与用户研究方向无关的论文**（即使评分高）\n- **推送语言用中文**，但保留英文标题和期刊名\n\n## 参考文件\n- `references/pubmed-API-patterns.md` — PubMed E-utilities API详细笔记\n- `references/figure-download-patterns.md` — Nature/Cell/Elsevier等期刊的图片URL提取模式\n", "path": "productivity\\paper-recommender\\SKILL.md", "skill_dir": "C:\\Users\\forgase\\AppData\\Local\\hermes\\skills\\productivity\\paper-recommender", "linked_files": {"references": ["references\\figure-download-patterns.md", "references\\html-template-structure.md", "references\\pubmed-API-patterns.md"]}, "usage_hint": "To view linked files, call skill_view(name, file_path) where file_path is e.g. 'references/api.md' or 'assets/config.yaml'", "required_environment_variables": [], "required_commands": [], "missing_required_environment_variables": [], "missing_credential_files": [], "missing_required_commands": [], "setup_needed": false, "setup_skipped": false, "readiness_status": "available"}

{"success": true, "name": "paper-recommender", "file": "references/pubmed-API-patterns.md", "content": "# PubMed E-utilities API 实战笔记\n\n## 搜索API (esearch)\n\n### 基础结构\n```\nbase: https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi\nparams:\n db=pubmed\n term=<查询表达式>\n mindate/maxdate — 日期范围\n datetype=pdat (publication date)\n retmax=N — 最大返回数\n retmode=json\n```\n\n### 已验证的关键查询模式\n\n**1. 主题搜索 + 高影响因子期刊过滤**\n```python\nquery = 'Parkinson AND (\"Nat Neurosci\"[Journal] OR \"Neuron\"[Journal] OR \"Nat Med\"[Journal])'\n```\n- 期刊名必须用 `\"全称\"[Journal]` 格式\n- 不加 `[Journal]` 标签时，`Neuron` 被翻译为 MeSH 的 neurons（神经元）\n- `Brain` 被翻译为 MeSH 的 brain（大脑解剖结构）\n\n**2. 细胞死亡方向搜索（已验证）**\n```python\nquery = '(ferroptosis[Title/Abstract] OR pyroptosis[Title/Abstract] OR ' + \\\n 'necroptosis[Title/Abstract] OR PANoptosis[Title/Abstract] OR ' + \\\n 'cuproptosis[Title/Abstract] OR mitophagy[Title/Abstract]) ' + \\\n 'AND (Nature[Journal] OR \"Cell\"[Journal] OR \"Nat Cell Biol\"[Journal] OR ' + \\\n '\"Cell Death Differ\"[Journal] OR \"Nat Commun\"[Journal])'\n```\n这个模式成功返回了 Nature 的精胺/铁死亡论文。\n\n**3. 已测试的有效期刊标签**\n| 期刊 | 标签 |\n|------|------|\n| Nature | `\"Nature\"[Journal]` |\n| Nature Communications | `\"Nat Commun\"[Journal]` |\n| Nature Medicine | `\"Nat Med\"[Journal]` |\n| Neuron | `\"Neuron\"[Journal]` |\n| Nature Neuroscience | `\"Nat Neurosci\"[Journal]` |\n| Science Advances | `\"Sci Adv\"[Journal]` |\n| Cell | `\"Cell\"[Journal]` |\n| Cell Reports | `\"Cell Rep\"[Journal]` |\n| Cell Death & Differentiation | `\"Cell Death Differ\"[Journal]` |\n| EMBO Journal | `\"EMBO J\"[Journal]` |\n| Molecular Neurodegeneration | `\"Mol Neurodegener\"[Journal]` |\n| EBioMedicine | `\"EBioMedicine\"[Journal]` |\n| Acta Neuropathologica | `\"Acta Neuropathol\"[Journal]` |\n| Brain | `\"Brain\"[Journal]` |\n| Lancet Neurology | `\"Lancet Neurol\"[Journal]` |\n| Developmental Cell | `\"Dev Cell\"[Journal]` |\n| Nature Structural & Molecular Biology | `\"Nat Struct Mol Biol\"[Journal]` |\n| Cell Metabolism | `\"Cell Metab\"[Journal]` |\n| Molecular Cell | `\"Mol Cell\"[Journal]` |\n\n### 已验证无用的参数\n- `sort=date` — 返回 warning \"Unknown sort schema 'date' ignored\"，无效果\n\n## 获取详情API (esummary)\n\n```python\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&id=<PMID列表>&retmode=json'\n```\n\n关键字段：\n- `pubtype` — 文章类型（含 \"Review\" 则为综述）\n- `source` — 期刊缩写名\n- `articleids[].idtype == 'doi'` — DOI\n- `attributes` — 包含 \"Has Abstract\" 则有摘要\n- `pubdate` — 发表日期\n- `title` — 标题\n\n## 获取摘要API (efetch)\n\n```python\n# XML模式（含结构化信息）\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMIDs>&retmode=xml'\n\n# 文本模式（纯文本）\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMIDs>&retmode=text&rettype=abstract'\n```\n\nXML模式返回结构化数据，适合用正则提取：\n- `<ArticleTitle>` → 标题\n- `<AbstractText>` → 摘要段落（可以有多段）\n- `<ELocationID EIdType=\"doi\">` → DOI\n- `<Journal><Title>` → 期刊全名（最后一个匹配是英文名）\n- `<PubDate><Year>` + `<Month>` → 发表日期\n\n## 获取文章元数据（XML完整模式）\n\n```python\nurl = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMIDs>&retmode=xml'\n```\n此模式返回完整XML，包含：\n- 所有作者的 `<LastName>` 和 `<ForeName>`\n- 所有 `<Keyword>`\n- 完整 `<AbstractText>`\n- `<PublicationTypeList>` 用于排除Review/Letter\n\n## 已知环境陷阱\n\n### 1. SSL连接失败（exit code 35）\n某些环境（git-bash/MSYS2）的 curl SSL 版本与 NCBI 服务器不兼容。\n- 修复1：`curl -k`（跳过证书验证）\n- 修复2：改用 Python 的 `urllib.request`（在本环境中工作可靠）\n- 修复3：更新 curl CA bundle\n\n### 2. URL编码问题\ncurl 命令行中包含 `()\"[]` 等特殊字符时容易解析失败（exit code 3）。\n- 修复：用 Python 的 `urllib.parse.urlencode(params)` 构建查询串\n\n### 3. `sort=date` 无效\nPubMed API 不支持 sort=date，搜索结果的顺序按默认相关性排序。\n\n### 4. Cell/Elsevier 付费墙\nCell Press（www.cell.com、linkinghub.elsevier.com）对脚本访问严格限制，返回403/超时。Nature系列（www.nature.com）通常可正常访问。\n\n## 搜索策略（两阶段工作流）\n\n### 阶段A：主题搜索\n```python\nquery = 'Parkinson disease AND (dopamine neuron OR synuclein OR MPTP)'\nparams = {\n 'db': 'pubmed', 'term': query,\n 'mindate': '<3月前>', 'maxdate': '<今天>',\n 'datetype': 'pdat', 'retmax': 10, 'retmode': 'json'\n}\n```\n目的：了解该时段总论文数，获取基础PMID列表。\n\n### 阶段B：高影响力期刊过滤\n```python\njournal_tags = '\"Nature\"[Journal] OR \"Cell\"[Journal] OR \"Nat Neurosci\"[Journal] OR ...'\nquery = f'({topic_keywords}) AND ({journal_tags})'\n```\n目的：直接命中IF>10的高质量论文。\n\n### 初筛要点\n1. `pubtype` 不含 \"Review\" → 原创研究\n2. `attributes` 含 \"Has Abstract\" → 有摘要\n3. 检查 DOI 是否存在\n4. 排除 \"No authors listed\" → 通常是 News & Views\n\n## 评分标准（Claude评估用，5维度各1-10分）\n\n| 维度 | 评分要点 | 满分 |\n|------|---------|------|\n| 逻辑完整性 | gain+loss of function, KO/KI, 正反验证 | 10 |\n| 方法学水平 | 单细胞测序, 冷冻电镜, 活细胞成像, TurboID等 | 10 |\n| 创新性 | 新概念/新机制/新方法 | 10 |\n| 可借鉴性 | 实验设计可迁移到神经科学 **←最重要维度** | 10 |\n| 临床转化潜力 | 体内验证, 治疗靶点, 生物标志物 | 10 |\n\n总分 >= 30 且各维度 >= 5 → 候选。再经Hermes确认相关性后，只选最优1篇。\n", "file_type": ".md"}

{"success": true, "name": "paper-recommender", "file": "references/figure-download-patterns.md", "content": "# 学术期刊Figure下载模式速查\n\n## Nature 系列\n**已验证模式（2026年6月）**\n\n### URL结构\n```\n文章页: https://www.nature.com/articles/{article_id}\nFigure URL: https://media.springernature.com/{size}/springer-static/image/\n art%3A10.1038%2F{article_id}/MediaObjects/\n {journal_id}_{year}_{article_num}_Fig{N}_HTML.png\n```\n\n### 关键参数\n- `{article_id}`: DOI中`/`后面的部分，如 `s41586-026-10597-2` 或 `s41593-026-02317-w`\n- `{journal_id}`: 期刊对应数字ID，如 Nature=41586, Nat Neurosci=41593\n- `{year}`: 4位年份\n- `{article_num}`: 文章编号（DOI中期刊ID后的数字部分，去连字符）\n- `{N}`: Figure编号（1-7）\n\n### 实例1 (Nature — 已验证 2026-06)\n```\narticle_id = s41586-026-10597-2\njournal_id = 41586\nyear = 2026\narticle_num = 10597\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41586-026-10597-2/MediaObjects/41586_2026_10597_Fig1_HTML.png\n\nFig2 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41586-026-10597-2/MediaObjects/41586_2026_10597_Fig2_HTML.png\n```\n\n### 实例2 (Nature Neuroscience — 已验证 2026-06)\n```\narticle_id = s41593-026-02317-w\njournal_id = 41593\nyear = 2026\narticle_num = 2317\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41593-026-02317-w/MediaObjects/41593_2026_2317_Fig1_HTML.png\n\nFig4 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41593-026-02317-w/MediaObjects/41593_2026_2317_Fig4_HTML.png\n```\n\n### 实例3 (Nature Medicine — 已验证 2026-06-11)\n```\narticle_id = s41591-026-04393-8\njournal_id = 41591\nyear = 2026\narticle_num = 4393\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41591-026-04393-8/MediaObjects/41591_2026_4393_Fig1_HTML.png\n\nFig2-Fig5 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41591-026-04393-8/MediaObjects/41591_2026_4393_Fig2_HTML.png\n...\nhttps://media.springernature.com/lw1200/...41591_2026_4393_Fig5_HTML.png\n\narticle_num提取: DOI \"s41591-026-04393-8\" → 取s41591后的两段 \"026\"+\"04393\" → 截取最终段的数字部分去前导零 → 4393\n```\n\n### 快速提取命令（curl + grep）\n```bash\n# 1. 从HTML提取所有Figure URL（通用模式，匹配所有s415XX系列期刊）\ncurl -s -L -H \"User-Agent: Mozilla/5.0\" \\\n \"https://www.nature.com/articles/{article_id}\" \\\n | grep -oP 'https://media\\.springernature\\.com/[^\"'\"'\"'<>]+s415\\d\\d[^\"'\"'\"'<>]*\\.(?:png|jpg|webp)' \\\n | sort -u\n\n# 2. 下载某张Figure为base64（用于HTML嵌入）\nFIG_URL=\"https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F{article_id}/MediaObjects/{journal_id}_{year}_{article_num}_Fig{N}_HTML.png\"\ncurl -s \"$FIG_URL\" -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt\n```\n\n### 分辨率控制\n| 前缀 | 尺寸 | 说明 |\n|------|------|------|\n| `/full/` | 全尺寸 | 最高分辨率，推荐用于Fig1 |\n| `/lw1200/` | 宽1200px | 中等尺寸，适用于其余Figures |\n| `/m685/` | 宽685px | 小尺寸 |\n| `/w215h120/` | 215x120px | 缩略图 |\n\n### 已测试的期刊ID\n| 期刊 | ID | DOI前缀 | 验证状态 |\n|------|----|---------|---------|\n| Nature | 41586 | s41586 | ✅ 2026-06 |\n| **Nature Medicine** | **41591** | **s41591** | **✅ 2026-06** |\n| **Nature Neuroscience** | **41593** | **s41593** | **✅ 2026-06** |\n| Nature Communications | 41467 | s41467 | 🟢 已验证 |\n| Cell Death & Differentiation | 41418 | s41418 | 🟢 已验证 |\n| Scientific Reports | 41598 | s41598 | 🟢 已验证 |\n| Cell Discovery | 41420 | s41420 | 🟢 已验证 |\n\n## Cell Press / Elsevier 系列（Cell Metabolism, Cell, Neuron, Cell Reports 等）\n**已验证模式（2026年6月）**\n\n### 关键发现：主页面有Cloudflare防护，但CDN图片可直接访问\nCell Press 主页面（www.cell.com）使用 Cloudflare 防护，curl/browser 直接访问被拦截。\n但图片通过 `ars.els-cdn.com` CDN 分发，**可以直接通过 curl 下载**。\n\n### URL结构（已成功用于 Cell Metabolism）\n```\nFigure N (大尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-gr{N}_lrg.jpg\n\nFigure N (小尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-gr{N}.jpg\n\nGraphical Abstract (大尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-fx1_lrg.jpg\n```\n\n### 关键参数\n- `{PII}`: 文章的PII（Publisher Item Identifier），可从PubMed esummary结果中获取（idtype='pii'），或从DOI对应的ScienceDirect URL中提取\n- `{N}`: Figure编号（1-7），Cell Press系列使用 `gr1, gr2, ..., gr7` 格式（非 `Fig1`）\n- `fx1`: Graphical Abstract的固定标识\n\n### 实例（Neuron — 已验证 2026-06-12）\n```bash\nPMID: 42127911\nDOI: 10.1016/j.neuron.2026.04.033\nPII: S0896-6273(26)00328-4 # 含有括号，需去除\nURL-PII: S0896627326003284 # 去除括号后的实际URL用PII\n\n# Figure URL (CDN直接访问，无防护):\n# 核心：去除PII中的括号，替换 gr{N}_lrg 和 fx1_lrg\nFig1: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr1_lrg.jpg\nFig2: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr2_lrg.jpg\nFig3: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr3_lrg.jpg\nFig4: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr4_lrg.jpg\nFig5: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr5_lrg.jpg\nFig6: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr6_lrg.jpg\nFig7: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-gr7_lrg.jpg\nGraphical Abstract: https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003284-fx1_lrg.jpg\n\n# PII括号去除规则\n# \"S0896-6273(26)00328-4\" → \"S0896627326003284\"\n# 规则：删除所有 '(' 和 ')' 字符即可\nPII_URL=$(echo \"$PII\" | tr -d '()')\necho \"$PII_URL\" # → S0896627326003284\n```\n\n### 实例（Cell Metabolism — 已验证 2026-06-11）\n```bash\nPMID: 42049021\nDOI: 10.1016/j.cmet.2026.04.001\nPII: S1550-4131(26)00139-7 # 注意：PII可能不同于全文URL中的pii\n\n# ScienceDirect URL (有Cloudflare防护，curl会失败):\n# https://www.sciencedirect.com/science/article/pii/S1550413126001397\n\n# Figure URL (CDN直接访问，无防护):\nFig1: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr1_lrg.jpg\nFig2: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr2_lrg.jpg\nFig3: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr3_lrg.jpg\nFig4: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr4_lrg.jpg\nFig5: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr5_lrg.jpg\nFig6: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr6_lrg.jpg\nFig7: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-gr7_lrg.jpg\nGraphical Abstract: https://ars.els-cdn.com/content/image/1-s2.0-S1550413126001397-fx1_lrg.jpg\n```\n\n### 快速提取命令\n```bash\n# 1. 从PubMed esummary中获取PII\n# PII字段: idtype='pii', value='S1550-4131(26)00139-7'\n# 或从DOI的ScienceDirect重定向URL中提取：/pii/{PII}\n\n# 2. 暴力枚举法：从gr1试到gr7（推荐，因为url模式固定）\nfor fig in 1 2 3 4 5 6 7; do\n url=\"https://ars.els-cdn.com/content/image/1-s2.0-${PII}-gr${fig}_lrg.jpg\"\n code=$(curl -s -o /dev/null -w \"%{http_code}\" -L \"$url\" -H \"User-Agent: Mozilla/5.0\")\n echo \"gr${fig}: HTTP ${code}\"\n if [ \"$code\" != \"404\" ]; then\n curl -s \"$url\" -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > fig${fig}_b64.txt\n fi\ndone\n\n# 3. 下载Graphical Abstract\ncurl -s \"https://ars.els-cdn.com/content/image/1-s2.0-${PII}-fx1_lrg.jpg\" \\\n -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > fig_fx1_b64.txt\n```\n\n### 已验证的Cell Press期刊\n| 期刊 | 验证状态 | 备注 |\n|------|---------|------|\n| Cell Metabolism | ✅ 已验证（2026-06） | gr1-gr7全部通过，HTTP 200 |\n| **Neuron** | **✅ 已验证（2026-06-12）** | **gr1-gr7+fx1全部通过，HTTP 200；PMID 42127911** |\n| Cell | 🟡 大概率可用 | 同属Cell Press，URL模式相同 |\n| Cell Reports | 🟡 大概率可用 | 同属Cell Press，URL模式相同 |\n| Developmental Cell | 🟡 大概率可用 | 同属Cell Press，URL模式相同 |\n| Molecular Cell | 🟡 大概率可用 | 同属Cell Press，URL模式相同 |\n\n### 已知限制\n- PDF下载：ScienceDirect有强防护，PDF无法直接通过curl下载（需订阅或机构访问）\n- 主页面HTML：Cloudflare拦截，无法直接从页面解析figure列表\n- PII格式因期刊而异，需从PubMed API或DOI重定向中获取\n\n## PMC / PubMed Central 开放获取\n```\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC{pmcid}/bin/{filename}\n```\n- 仅对开放获取文章有效\n\n## 通用最佳实践\n\n1. **先获取文章HTML页面**，从中提取Figure图片链接\n2. **优先使用全尺寸版本**（替换路径中的尺寸限定词）\n3. **base64嵌入**到HTML中，避免file://协议被浏览器拦截\n4. **文件命名**：`Figure{N}_{简短描述}.png`\n5. **注意付费墙**：3xx/4xx响应 → 放弃，不要反复重试\n6. **Nature/Nature Neuroscience/Nature Medicine PDF下载**：`https://www.nature.com/articles/{article_id}.pdf` — 已验证可下载（2026-06），Nature Medicine实例如 `s41591-026-04393-8`（7.8MB）\n\n## ⚠️ Windows 路径注意事项\n\n在 git-bash 中执行 `curl` + `base64` 保存图文件时，路径用 `/c/Users/<user>/` 形式（如 `/c/Users/forgase/fig1_b64.txt`）。但在 **Python 脚本** 中读取这些文件时，必须用 Windows 原生路径格式（`C:/Users/<user>/fig1_b64.txt`），因为 Python on Windows 不认识 MSYS 路径 `/c/Users/...`。\n\n**错误做法：**\n```python\nopen(\"/c/Users/forgase/fig1_b64.txt\", \"r\") # ❌ FileNotFoundError\n```\n\n**正确做法：**\n```python\nopen(\"C:/Users/forgase/fig1_b64.txt\", \"r\") # ✅ 正斜杠在Windows Python中可识别\n# 或\nopen(r\"C:\\Users\\forgase\\fig1_b64.txt\", \"r\") # ✅ 原始字符串\n```\n", "file_type": ".md"}

{"success": true, "name": "paper-recommender", "file": "references/html-template-structure.md", "content": "# 公众号风格HTML解读 — 模板结构\n\n## 文件架构\n\n```\n<!DOCTYPE html>\n├── <head>\n│ ├── 字符集/视口\n│ └── 样式（全部内联<style>）\n│ ├── 全局重置\n│ ├── .header — 渐变深蓝背景\n│ ├── .card — 白色圆角卡片\n│ ├── .section-title — 左边框强调标题\n│ ├── .score-bar / .score-item — 评分网格\n│ ├── .figure-box — 图片容器\n│ ├── .reproduce-tip — 蓝色复现建议\n│ ├── .highlight — 黄色高亮框\n│ └── .summary-box — 紫色渐变结论卡\n├── <body>\n│ ├── .header\n│ │ ├── 标签徽章（🔥 今日推荐 + 主题标签）\n│ │ ├── h1 中文标题\n│ │ ├── p 英文标题\n│ │ └── p 📅日期 | 📰期刊 | IF\n│ ├── .container\n│ │ ├── .card (评分) — 5维度×flex网格\n│ │ ├── .card (速览) — 摘要+高亮框\n│ │ ├── .card (团队) — 作者信息\n│ │ ├── .card (图文) — Figure×5 含canvas+caption+🔬复现建议\n│ │ ├── .card (评述) — ✅优势/⚠️缺憾/🔬借鉴\n│ │ ├── .summary-box (小结)\n│ │ └── .card (元数据) — DOI/关键词/时间\n│ └── <script>\n│ ├── const fig1_b64 = \"...\" (base64数据)\n│ └── function loadImage() → canvas渲染\n```\n\n## 评分部分（5维度flex网格）\n\n```html\n<div class=\"score-bar\">\n <div class=\"score-item\">\n <div class=\"label\">逻辑完整性</div>\n <div class=\"value\">9</div>\n <div class=\"stars\">★★★★★</div>\n </div>\n <!-- 重复 ×5 -->\n</div>\n<!-- 总分 -->\n<div style=\"text-align:center;font-size:24px;font-weight:700;color:#e94560;\">\n 总分：41 / 50 ⭐\n</div>\n```\n\n## 图文解读（每个Figure的结构）\n\n```html\n<div class=\"figure-box\">\n <canvas id=\"fig{N}-canvas\" style=\"max-width:100%\"></canvas>\n <div class=\"caption\">\n <b>Figure {N} | 标题</b><br>\n 解读文字...\n <div style=\"margin-top:8px;\">\n <b>🔬 复现建议：</b>具体建议...\n </div>\n </div>\n</div>\n<div class=\"divider\"></div>\n```\n\n## 图片嵌入方案\n\n### 期刊图片格式速查\n| 期刊系列 | 图片格式 | CDN示例 |\n|----------|---------|---------|\n| Nature系列 | PNG | `..._Fig1_HTML.png` |\n| Cell Press系列 | JPEG | `...-gr1_lrg.jpg` |\n\n### 通用加载函数（自动检测格式）\n\n```javascript\n// 1. base64数据存为JS变量（在<script>开头）\nconst fig1_b64 = \"iVBORw0KGgo...\"; // PNG格式\nconst fig2_b64 = \"/9j/4AAQSkZJRg...\"; // JPEG格式（以/9j/开头）\n\n// 2. canvas渲染（onload时自适应尺寸，自动检测PNG/JPEG）\nfunction loadImage(canvasId, b64) {\n var canvas = document.getElementById(canvasId);\n var ctx = canvas.getContext(\"2d\");\n var img = new Image();\n img.onload = function() {\n canvas.width = img.width;\n canvas.height = img.height;\n ctx.drawImage(img, 0, 0);\n };\n // 自动判断格式：PNG头部为\"iVBOR\"，JPEG头部为\"/9j/\"\n var mime = b64.startsWith(\"iVBOR\") ? \"image/png\" : \"image/jpeg\";\n img.src = \"data:\" + mime + \";base64,\" + b64;\n}\n```\n\n### 格式选择指南\n- **Nature系列** → PNG格式，使用 `data:image/png;base64,...`\n- **Cell Press系列** → JPEG格式，使用 `data:image/jpeg;base64,...`\n- **检测技巧**：base64字符串以 `iVBOR` 开头 → PNG；以 `/9j/` 开头 → JPEG\n\n## 关键样式常量\n\n| 元素 | 颜色 |\n|------|------|\n| 头部渐变 | `#1a1a2e → #0f3460` |\n| 标签徽章 | `#e94560` |\n| 卡片阴影 | `0 2px 12px rgba(0,0,0,0.08)` |\n| 评分数字 | `#e94560` |\n| 复选框背景 | `#fff8e1` + 左边框 `#ffc107` |\n| 复现建议 | `#e3f2fd` |\n| 小结卡片 | `#667eea → #764ba2` |\n| 标题左边框 | `#e94560`, 4px |\n\n## 文件命名规则\n\n```\n{主题关键词}_文献解读.html\n```\n示例：`细胞死亡_文献解读.html`、`帕金森_文献解读.html`\n\n## 注意事项\n\n1. canvas渲染：需要`onload`回调，不能直接在`<img>`上设置src（尺寸自适应问题）\n2. 所有图片必须是base64嵌入，不能用file://协议（浏览器安全策略阻止）\n3. 卡片间用`.card`统一间距（margin-bottom:20px）\n4. 长文本用`text-indent:2em`首行缩进增强可读性\n", "file_type": ".md"}

{"status": "success", "output": "Query 1 (neuroinflammation + microglia/astrocyte/NLRP3, high-IF): 20 results\r\nPMIDs: ['42268720', '42265098', '42263678', '42237024', '42215790', '42213237', '42202020', '42153336', '42129556', '42127911', '42098112', '42092136', '42087813', '42033726', '42026067', '42019491', '42014405', '41991797', '41962542', '41950930']\r\nQuery 2 (microglia/astrocyte + inflammation, high-IF): 20 results\r\nPMIDs: ['42268720', '42265098', '42263678', '42248891', '42247297', '42237401', '42237024', '42215790', '42213237', '42204590', '42202020', '42177534', '42170924', '42169139', '42153336', '42153334', '42151131', '42140967', '42129556', '42127911']\r\n\r\nTotal unique PMIDs: 30\r\nAll PMIDs: ['42268720', '42265098', '42263678', '42237024', '42215790', '42213237', '42202020', '42153336', '42129556', '42127911', '42098112', '42092136', '42087813', '42033726', '42026067', '42019491', '42014405', '41991797', '41962542', '41950930', '42248891', '42247297', '42237401', '42204590', '42177534', '42170924', '42169139', '42153334', '42151131', '42140967']\r\n", "tool_calls_made": 0, "duration_seconds": 1.42}

{"status": "success", "output": "PMID: 42268720\r\n 标题: Microglial states associate with lesion dynamics in multiple sclerosis.\r\n 期刊: Cell Rep | 日期: 2026 Jun 9\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.celrep.2026.117538\r\n PII: S2211-1247(26)00616-9\r\n 作者: van den Bosch AMR\r\n 有摘要: True\r\n---\r\nPMID: 42265098\r\n 标题: Semaglutide attenuates neuroinflammation in male mice.\r\n 期刊: Nat Commun | 日期: 2026 Jun 9\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-74038-4\r\n PII: 10.1038/s41467-026-74038-4\r\n 作者: Belmont-Rausch DM\r\n 有摘要: True\r\n---\r\nPMID: 42263678\r\n 标题: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis.\r\n 期刊: Neuron | 日期: 2026 Jun 9\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.05.015\r\n PII: S0896-6273(26)00386-7\r\n 作者: Liu Y\r\n 有摘要: True\r\n---\r\nPMID: 42237024\r\n 标题: AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction.\r\n 期刊: Acta Neuropathol | 日期: 2026 Jun 3\r\n 类型: ['Journal Article', \"Research Support, Non-U.S. Gov't\"]\r\n DOI: 10.1007/s00401-026-03033-2\r\n PII: 10.1007/s00401-026-03033-2\r\n 作者: Dunot J\r\n 有摘要: True\r\n---\r\nPMID: 42215790\r\n 标题: The C9orf72/SMCR8 complex maintains microglial homeostasis via RAB8A-ESCRT-mediated lysosomal repair.\r\n 期刊: EMBO J | 日期: 2026 May 29\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s44318-026-00817-w\r\n PII: 10.1038/s44318-026-00817-w\r\n 作者: Li S\r\n 有摘要: True\r\n---\r\nPMID: 42213237\r\n 标题: Reevaluating the role of beta2-microglobulin: new insights on selective vulnerability in ALS pathology.\r\n 期刊: Acta Neuropathol | 日期: 2026 May 29\r\n 类型: ['Journal Article', \"Research Support, Non-U.S. Gov't\"]\r\n DOI: 10.1007/s00401-026-03024-3\r\n PII: 10.1007/s00401-026-03024-3\r\n 作者: Leboeuf M\r\n 有摘要: True\r\n---\r\nPMID: 42202020\r\n 标题: TPM1 drives cytoskeleton-immunometabolism coupling and LGALS9/CD45-mediated neuroinflammatory propagation in retinitis p\r\n 期刊: Sci Adv | 日期: 2026 May 29\r\n 类型: ['Journal Article']\r\n DOI: 10.1126/sciadv.aea6467\r\n PII: \r\n 作者: Li R\r\n 有摘要: True\r\n---\r\nPMID: 42153336\r\n 标题: MIF modulates impaired astrocyte distribution in schizophrenia cortical spheroids.\r\n 期刊: Brain | 日期: 2026 May 19\r\n 类型: ['Journal Article']\r\n DOI: 10.1093/brain/awag181\r\n PII: 8687269\r\n 作者: Requena Osete J\r\n 有摘要: True\r\n---\r\nPMID: 42129556\r\n 标题: Sustaining microglial reparative function enhances stroke recovery.\r\n 期刊: Nature | 日期: 2026 May 13\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41586-026-10480-0\r\n PII: 10.1038/s41586-026-10480-0\r\n 作者: Tsuyama J\r\n 有摘要: True\r\n---\r\nPMID: 42127911\r\n 标题: Secreted GPNMB enhances uptake of fibrillar alpha-synuclein in a non-cell-autonomous process that can be blocked by anti\r\n 期刊: Neuron | 日期: 2026 May 12\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.neuron.2026.04.033\r\n PII: S0896-6273(26)00328-4\r\n 作者: Carceles-Cordon M\r\n 有摘要: True\r\n---\r\nPMID: 42098112\r\n 标题: Triose phosphate isomerase 1 remodels mitochondrial cristae ultrastructure to rewire microglial immunometabolism against\r\n 期刊: Nat Commun | 日期: 2026 May 7\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-72779-w\r\n PII: 10.1038/s41467-026-72779-w\r\n 作者: Zhang XW\r\n 有摘要: True\r\n---\r\nPMID: 42092136\r\n 标题: Androgen loss accelerates brain tumour growth via HPA axis activation.\r\n 期刊: Nature | 日期: 2026 May\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41586-026-10451-5\r\n PII: 10.1038/s41586-026-10451-5\r\n 作者: Lee J\r\n 有摘要: True\r\n---\r\nPMID: 42087813\r\n 标题: Neuroinflammation and neurodegeneration trigger a specific splice form of ribosomal protein S24.\r\n 期刊: Brain | 日期: 2026 May 6\r\n 类型: ['Journal Article']\r\n DOI: 10.1093/brain/awag166\r\n PII: 8670210\r\n 作者: Magadi SS\r\n 有摘要: True\r\n---\r\nPMID: 42033726\r\n 标题: Complement C3aR deletion does not attenuate degeneration in a tauopathy model or alter acute inflammation-induced gene e\r\n 期刊: Cell Rep | 日期: 2026 May 26\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.celrep.2026.117313\r\n PII: S2211-1247(26)00391-8\r\n 作者: Wang Y\r\n 有摘要: True\r\n---\r\nPMID: 42026067\r\n 标题: Type I interferon drives T cell responses to amyloid beta in the central nervous system.\r\n 期刊: Nat Commun | 日期: 2026 Apr 23\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-72262-6\r\n PII: 10.1038/s41467-026-72262-6\r\n 作者: Michel JJ\r\n 有摘要: True\r\n---\r\nPMID: 42019491\r\n 标题: Somatic cancer variants enriched in Alzheimer's disease microglia-like cells drive inflammatory and proliferative states\r\n 期刊: Cell | 日期: 2026 Apr 21\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.cell.2026.03.040\r\n PII: S0092-8674(26)00341-7\r\n 作者: Huang AY\r\n 有摘要: True\r\n---\r\nPMID: 42014405\r\n 标题: CK2 inhibition suppresses glial inflammation in models of neuroinflammation and neurodegeneration.\r\n 期刊: Nat Commun | 日期: 2026 Apr 22\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-71736-x\r\n PII: 10.1038/s41467-026-71736-x\r\n 作者: Da Silva IIN\r\n 有摘要: True\r\n---\r\nPMID: 41991797\r\n 标题: Consensus statement on microglial and macrophage functions in gliomas.\r\n 期刊: Acta Neuropathol | 日期: 2026 Apr 16\r\n 类型: ['Journal Article', 'Review', \"Research Support, Non-U.S. Gov't\"]\r\n DOI: 10.1007/s00401-026-02999-3\r\n PII: 10.1007/s00401-026-02999-3\r\n 作者: Zheng Y\r\n 有摘要: True\r\n---\r\nPMID: 41962542\r\n 标题: Astrocytic calcium-dependent enzyme PAD2 governs microglia activity to exacerbate amyloid pathology via citrullinated vi\r\n 期刊: Immunity | 日期: 2026 Jun 9\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.immuni.2026.03.007\r\n PII: S1074-7613(26)00118-4\r\n 作者: Zhang J\r\n 有摘要: True\r\n---\r\nPMID: 41950930\r\n 标题: Ubiquitin Ligase COP1 Suppresses Neuroinflammation by Degrading c/EBPβ in Microglia.\r\n 期刊: Cell | 日期: 2026 Apr 30\r\n 类型: ['Published Erratum']\r\n DOI: 10.1016/j.cell.2026.04.002\r\n PII: S0092-8674(26)00391-0\r\n 作者: Ndoja A\r\n 有摘要: False\r\n---\r\nPMID: 42248891\r\n 标题: Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice.\r\n 期刊: Nat Commun | 日期: 2026 Jun 5\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-74037-5\r\n PII: 10.1038/s41467-026-74037-5\r\n 作者: Zhou Q\r\n 有摘要: True\r\n---\r\nPMID: 42247297\r\n 标题: Elevated phagocytic capacity directs innate spinal cord repair.\r\n 期刊: Cell Rep | 日期: 2026 Jun 4\r\n 类型: ['Journal Article']\r\n DOI: 10.1016/j.celrep.2026.117482\r\n PII: S2211-1247(26)00560-7\r\n 作者: Klatt Shaw D\r\n 有摘要: True\r\n---\r\nPMID: 42237401\r\n 标题: Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.\r\n 期刊: Mol Neurodegener | 日期: 2026 Jun 3\r\n 类型: ['Journal Article']\r\n DOI: 10.1186/s13024-026-00946-0\r\n PII: 10.1186/s13024-026-00946-0\r\n 作者: Nicholson L\r\n 有摘要: True\r\n---\r\nPMID: 42204590\r\n 标题: Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic advances.\r\n 期刊: Mol Neurodegener | 日期: 2026 May 28\r\n 类型: ['Journal Article', 'Review']\r\n DOI: 10.1186/s13024-026-00951-3\r\n PII: 10.1186/s13024-026-00951-3\r\n 作者: Tu D\r\n 有摘要: True\r\n---\r\nPMID: 42177534\r\n 标题: In vivo profiling of astrocyte secretome reveals brain-region specific regulatory networks in a mouse model of amyloid p\r\n 期刊: Mol Neurodegener | 日期: 2026 May 23\r\n 类型: ['Journal Article']\r\n DOI: 10.1186/s13024-026-00956-y\r\n PII: 10.1186/s13024-026-00956-y\r\n 作者: Jiang Q\r\n 有摘要: True\r\n---\r\nPMID: 42170924\r\n 标题: Soluble epoxide hydrolase drives neurovascular dysfunction in a model of amyloidosis.\r\n 期刊: Brain | 日期: 2026 May 22\r\n 类型: ['Journal Article']\r\n DOI: 10.1093/brain/awag184\r\n PII: 8690502\r\n 作者: DeMeglio M\r\n 有摘要: True\r\n---\r\nPMID: 42169139\r\n 标题: Mitochondria transfer in neurological disorders: the key role of neuroglia.\r\n 期刊: Mol Neurodegener | 日期: 2026 May 21\r\n 类型: ['Journal Article', 'Review']\r\n DOI: 10.1186/s13024-026-00953-1\r\n PII: 10.1186/s13024-026-00953-1\r\n 作者: Jiao J\r\n 有摘要: True\r\n---\r\nPMID: 42153334\r\n 标题: Parkinson's disease beyond the brain: erythrocyte α-synuclein transfer across the blood-brain barrier.\r\n 期刊: Brain | 日期: 2026 May 19\r\n 类型: ['Journal Article']\r\n DOI: 10.1093/brain/awag179\r\n PII: 8687270\r\n 作者: Yang Y\r\n 有摘要: True\r\n---\r\nPMID: 42151131\r\n 标题: A comparative transcriptomic analysis of mouse demyelination models and multiple sclerosis lesions.\r\n 期刊: Nat Commun | 日期: 2026 May 18\r\n 类型: ['Journal Article', 'Comparative Study', \"Research Support, Non-U.S. Gov't\"]\r\n DOI: 10.1038/s41467-026-72383-y\r\n PII: 10.1038/s41467-026-72383-y\r\n 作者: Aboelnour EL\r\n 有摘要: True\r\n---\r\nPMID: 42140967\r\n 标题: α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.\r\n 期刊: Nat Commun | 日期: 2026 May 15\r\n 类型: ['Journal Article']\r\n DOI: 10.1038/s41467-026-73136-7\r\n PII: 10.1038/s41467-026-73136-7\r\n 作者: Chakraborty R\r\n 有摘要: True\r\n---\r\n", "tool_calls_made": 0, "duration_seconds": 4.03}

{"status": "success", "output": "=== PMID: 42129556 ===\r\n期刊: Nature | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Sustaining microglial reparative function enhances stroke recovery.\r\n摘要: Neurological symptoms after brain injury can remain as lifelong detrimental sequelae because most of the spontaneous recovery response disappears within a few months after the injury1,2. Microglia have an essential role in this process; however, the cellular and molecular mechanisms that diminish&#xa0;spontaneous functional recovery in the brain remain unclear. Here using cellular fate analysis, we show that reparative microglia persist in the brain after a stroke even after losing their benefic...\r\n\r\n=== PMID: 42263678 ===\r\n期刊: Neuron | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis.\r\n摘要: Mitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer's disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5&#xd7;FAD mice and human AD brains. Integrative...\r\n\r\n=== PMID: 42019491 ===\r\n期刊: Cell | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Somatic cancer variants enriched in Alzheimer's disease microglia-like cells drive inflammatory and proliferative states.\r\n摘要: Alzheimer's disease (AD) is a neurodegenerative condition characterized by microglia-mediated neuroinflammation. Deep (&gt;1,000&#xd7;) panel sequencing of 311 brain samples revealed enrichment of somatic single-nucleotide variants (sSNVs) in cancer driver genes in AD brains, especially in genes associated with clonal hematopoiesis (CH). These sSNVs were associated with clonal expansion and carried by both microglia-like brain macrophages (MLBMs) in multiple brain regions as well as paired blood...\r\n\r\n=== PMID: 41962542 ===\r\n期刊: Immunity | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Astrocytic calcium-dependent enzyme PAD2 governs microglia activity to exacerbate amyloid pathology via citrullinated vimentin.\r\n摘要: Glial crosstalk surrounding amyloid-&#x3b2; (A&#x3b2;) plaques establishes a self-propagating inflammatory niche fueling Alzheimer's disease (AD), yet the molecular triggers remain incompletely defined. We found that the calcium-dependent enzyme peptidyl-arginine deiminase 2 (PAD2) was selectively upregulated in plaque-associated astrocytes in human AD cortex and multiple APP AD transgenic mouse models. Astrocyte-specific deletion of Padi2 in 5&#xd7;FAD mice rescued learning and memory, lowered ...\r\n\r\n=== PMID: 42215790 ===\r\n期刊: The EMBO journal | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: The C9orf72/SMCR8 complex maintains microglial homeostasis via RAB8A-ESCRT-mediated lysosomal repair.\r\n摘要: Microglia are critical regulators of neuroinflammation and neurodegeneration. Haploinsufficiency of C9orf72, the most frequently mutated gene in&#xa0;amyotrophic lateral sclerosis and frontotemporal dementia, has been linked to autophagy-lysosomal pathway defects, but the role&#xa0;of C9orf72 in microglia remains unclear. Here, we identify the C9orf72/SMCR8 complex as a key regulator of microglial homeostasis through promoting lysosomal membrane repair. Loss of C9orf72 and SMCR8 in mice causes a...\r\n\r\n=== PMID: 42098112 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Triose phosphate isomerase 1 remodels mitochondrial cristae ultrastructure to rewire microglial immunometabolism against ischemic stroke.\r\n摘要: Mitochondrial cristae ultrastructure enables ATP synthase organization for adaptive energy production. This process is critical for regulating microglia mediated neuroinflammation in ischemic stroke pathology. However, therapeutic strategies targeting cristae remodeling remain unexplored. We identified a chemical probe, icariin II (ICS), which restores mitochondrial cristae by targeting triose phosphate isomerase 1 (TPI1). ICS-induced TPI1 conformational switching recruits ATP5MF to drive F1Fo-A...\r\n\r\n=== PMID: 42014405 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: CK2 inhibition suppresses glial inflammation in models of neuroinflammation and neurodegeneration.\r\n摘要: Neuroinflammation plays a key role in Alzheimer's disease (AD) and many other neurodegenerative disorders. Chronic activation of astrocytes and microglia fuels neuronal damage via cytokine secretion, oxidative stress, and proteolysis, yet glial inflammatory regulation remains poorly understood. Using chemoproteomics, we identified CK2, particularly the brain-enriched catalytic subunit CK2&#x3b1;2, as a key driver of astrocytic inflammation. CK2 enhances NF-&#x3ba;B activity by phosphorylating NF...\r\n\r\n=== PMID: 42268720 ===\r\n期刊: Cell reports | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Microglial states associate with lesion dynamics in multiple sclerosis.\r\n摘要: Multiple sclerosis (MS) is a neuroinflammatory disease of the CNS characterized by demyelinating lesions. Lesion expansion contributes to disability progression, whereas remyelination may restore neurological function. How these divergent outcomes relate to microglial states remains incompletely understood. Using single-cell-resolution spatial transcriptomics, we compare lesions containing foamy to those containing ramified microglia in postmortem human brain tissue. We find distinct cellular an...\r\n\r\n=== PMID: 42265098 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Semaglutide attenuates neuroinflammation in male mice.\r\n摘要: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. However, the cellular mechanisms underlying GLP-1RA effects on neuroinflammation remain poorly understood. Here we show, using a mouse model of lipopolysaccharide-induced neuroinflammation, how semaglutide coordinates cellular responses to resolve neuroinflammation. We find that semagl...\r\n\r\n=== PMID: 42248891 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Microglial CD31 suppresses A&#x3b2; clearance and promotes Alzheimer pathology in 5&#xd7;FAD mice.\r\n摘要: Microglia play crucial roles in Alzheimer's disease (AD), yet the molecular mechanisms are unclear. Here, we show that CD31, a recognized endothelial marker, is predominantly expressed in microglia but not in neurons or astrocytes, and it is significantly elevated in the brains of AD patients and mouse models. Microglia-specific CD31 knockdown in 5xFAD mice substantially attenuated the dysregulated transcription networks, suppressed microglia hyperactivation and the disease-associated microglia ...\r\n\r\n=== PMID: 42237401 ===\r\n期刊: Molecular neurodegeneration | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.\r\n摘要: Metabolic dysfunction contributes to the risk and progression of Alzheimer's disease (AD), yet the cellular mechanisms linking impaired insulin signaling and systemic metabolic stress to brain dysfunction remain incompletely defined. We examined the impact of chronic high-fat, high-sugar (HFHS)-induced insulin resistance on metabolic parameters, spatial learning and memory, and in vivo glial activation and neuropathology in Alzheimer's disease knock-in mice expressing human mutant APP and wild-t...\r\n\r\n=== PMID: 42177534 ===\r\n期刊: Molecular neurodegeneration | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: In vivo profiling of astrocyte secretome reveals brain-region specific regulatory networks in a mouse model of amyloid pathology.\r\n摘要: Coordinated cell-to-cell communications is crucial for the proper functioning and maintenance of brain activities, and its disruption contributes to neurological disorders, including Alzheimer's disease (AD). Altered astrocyte-neuron communications have been implicated in AD progression, yet the underlying regulatory networks remain poorly understood. Given that secretory proteins mediate both local and long-range intercellular signaling, we constructed a spatiotemporal profile of the astrocyte-...\r\n\r\n=== PMID: 42140967 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: &#x3b1;-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.\r\n摘要: Tunneling nanotubes (TNTs) enable direct intercellular transfer of macromolecules, organelles, and pathogenic protein aggregates. While &#x3b1;-synuclein (&#x3b1;-Syn) aggregates are known to promote TNT formation, the underlying mechanisms remain poorly defined. Here, using human neuronal and microglial cell lines, as well as iPSC-derived dopaminergic neurons and microglia, we show that &#x3b1;-Syn aggregates induce severe mitochondrial damage, leading to cytosolic release of mitochondrial DNA ...\r\n\r\n=== PMID: 42247297 ===\r\n期刊: Cell reports | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Elevated phagocytic capacity directs innate spinal cord repair.\r\n摘要: Immune cells elicit a continuum of transcriptional states after spinal cord injury (SCI). In mammals, inefficient debris clearance and chronic inflammation impede recovery and overshadow pro-regenerative immune functions. We found that zebrafish SCI elicits transient immune activation and efficient debris clearance. Transcriptomics and genetic ablation showed zebrafish macrophages are highly phagocytic and required for regeneration. Comparisons between zebrafish and mammalian macrophages identif...\r\n\r\n=== PMID: 42087813 ===\r\n期刊: Brain : a journal of neurology | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Neuroinflammation and neurodegeneration trigger a specific splice form of ribosomal protein S24.\r\n摘要: Neuroinflammation, particularly that involving reactive microglia, the brain's resident immune cells, is implicated in the pathogenesis of major neurodegenerative diseases (NDs). Multiple studies have reported changes in ribosomal protein (RP) expression during neurodegeneration, but the significance of these changes remains unclear. Ribosomes are evolutionarily conserved protein-synthesizing machines, and although commonly viewed as invariant, accumulating evidence suggests functional ribosome ...\r\n\r\n=== PMID: 42153336 ===\r\n期刊: Brain : a journal of neurology | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: MIF modulates impaired astrocyte distribution in schizophrenia cortical spheroids.\r\n摘要: Neuroinflammation and astrocyte dysfunction are associated with schizophrenia. To elucidate the molecular mechanisms involved, we generated induced pluripotent stem cells from 14 schizophrenia patients and 14 healthy controls and differentiated them to human cortical spheroids. Transcriptional profiling revealed overexpression of cilia-related genes in schizophrenia spheroids which was mainly driven by astrocytes. We identified baseline abnormal astrocyte distribution in schizophrenia and show t...\r\n\r\n=== PMID: 42026067 ===\r\n期刊: Nature communications | 年度: 2026\r\n类型: ['<PublicationType UI=\"D016428\">Journal Article']\r\n标题: Type I interferon drives T cell responses to amyloid beta in the central nervous system.\r\n摘要: Amyloid beta (A&#x3b2;) plaque deposition in the central nervous system (CNS) is a hallmark of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), triggering robust innate immune responses. However, the role of the adaptive immune system remains less well understood. Here we show the immune microenvironment dynamics in APP23 transgenic (APP23-tg) mice modelling CNS amyloid pathology, using single-cell transcriptomics. We observed a marked increase in T-cell populations during late di...\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.83}

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{"status": "success", "output": "\r\n================================================================================\r\nPMID: 42129556\r\nTitle: Sustaining microglial reparative function enhances stroke recovery.\r\nJournal: Nature | Year: 2026\r\nDOI: 10.1038/s41586-026-10480-0\r\nAuthors: Tsuyama Jun; Sakai Seiichiro; Kurabayashi Kumiko; Nakamura Ayaka; Tanaka Eri...\r\nKeywords: \r\n\r\nFull Abstract:\r\nNeurological symptoms after brain injury can remain as lifelong detrimental sequelae because most of the spontaneous recovery response disappears within a few months after the injury1,2. Microglia have an essential role in this process; however, the cellular and molecular mechanisms that diminish spontaneous functional recovery in the brain remain unclear. Here using cellular fate analysis, we show that reparative microglia persist in the brain after a stroke even after losing their beneficial functions. In these cells, ZFP384 is identified as a pivotal transcriptional regulator that diminishes the expression of genes associated with the recovery phase, turning them into dysfunctional microglia that lose their reparative functions. Mechanistically, ZFP384 diminishes the YY1-mediated chromatin interaction necessary to induce the expression of these genes in microglia. The use of antisense oligonucleotides that target Zfp384 can sustain the broad range of neural repair effects of microglia and enhance recovery after stroke, even in the chronic phase of ischaemic stroke. Thus, therapeutics that prevent the loss of reparative immunity-the beneficial restorative functions of immune cells-can prolong functional recovery in the brain.\r\n================================================================================\r\n\r\n================================================================================\r\nPMID: 41962542\r\nTitle: Astrocytic calcium-dependent enzyme PAD2 governs microglia activity to exacerbate amyloid pathology via citrullinated vimentin.\r\nJournal: Immunity | Year: 2026\r\nDOI: 10.1016/j.immuni.2026.03.007\r\nAuthors: Zhang Jingyan; Huang Yufei; Chen Yanbing; Zhang Yusi; Chen Jianmin...\r\nKeywords: <Keyword MajorTopicYN=\"N\">Alzheimer&#x2019;s disease, PAD2, TLR4, astrocyte, citrullination, glial crosstalk, microglia, neuroinflammation, vimentin\r\n\r\nFull Abstract:\r\nGlial crosstalk surrounding amyloid-β (Aβ) plaques establishes a self-propagating inflammatory niche fueling Alzheimer's disease (AD), yet the molecular triggers remain incompletely defined. We found that the calcium-dependent enzyme peptidyl-arginine deiminase 2 (PAD2) was selectively upregulated in plaque-associated astrocytes in human AD cortex and multiple APP AD transgenic mouse models. Astrocyte-specific deletion of Padi2 in 5&#xd7;FAD mice rescued learning and memory, lowered Aβ load, restrained pro-inflammatory microglial activation, and restored microglial phagocytosis. Multi-omics profiling tied these benefits to rewiring of the astrocytic proteome and the microglial transcriptome toward homeostasis. PAD2 converted astrocytic vimentin to citrullinated Cit-Vim175/184. The released Cit-vimentin drove a proinflammatory phenotype while dampening Aβ clearance in microglia-a process dependent on TLR4 signaling. Pharmacological PAD2 inhibition mimicked the genetic rescue, normalizing glial signatures and cognition. These findings identify PAD2-dependent vimentin citrullination as a key inter-glial signaling hub that worsens AD pathology and highlight PAD2 as a promising therapeutic target.\r\n================================================================================\r\n\r\n================================================================================\r\nPMID: 42019491\r\nTitle: Somatic cancer variants enriched in Alzheimer's disease microglia-like cells drive inflammatory and proliferative states.\r\nJournal: Cell | Year: 2026\r\nDOI: 10.1016/j.cell.2026.03.040\r\nAuthors: Huang August Yue; Zhou Zinan; Talukdar Maya; Enyenihi Liz; Miller Michael B...\r\nKeywords: <Keyword MajorTopicYN=\"N\">Alzheimer&#x2019;s disease, brain macrophage, clonal expansion, microglia, somatic variant\r\n\r\nFull Abstract:\r\nAlzheimer's disease (AD) is a neurodegenerative condition characterized by microglia-mediated neuroinflammation. Deep (&gt;1,000&#xd7;) panel sequencing of 311 brain samples revealed enrichment of somatic single-nucleotide variants (sSNVs) in cancer driver genes in AD brains, especially in genes associated with clonal hematopoiesis (CH). These sSNVs were associated with clonal expansion and carried by both microglia-like brain macrophages (MLBMs) in multiple brain regions as well as paired blood, suggesting a likely hematopoietic origin. Single-nucleus RNA sequencing data from 62 additional AD and control brains revealed increased somatic copy number variants (sCNVs) associated with CH in AD MLBMs, whereas single-cell multi-omic analyses demonstrated that sSNV- and sCNV-carrying MLBMs exhibited inflammatory and proliferative transcriptional signatures characteristic of disease-associated microglia. These signatures were recapitulated in induced pluripotent stem cell-derived microglia-like cells with TET2, ASXL1, and DNMT3A variants. These findings suggest that clonal somatic driver variants in MLBMs are enriched in AD, potentially promoting neuroinflammation and neurodegeneration.\r\n================================================================================\r\n\r\n================================================================================\r\nPMID: 42263678\r\nTitle: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis.\r\nJournal: Neuron | Year: 2026\r\nDOI: 10.1016/j.neuron.2026.05.015\r\nAuthors: Liu Yongqing; Ye Yingzhi; Fan Minghua; Cheng Henry Yi; Sun Shuying...\r\nKeywords: <Keyword MajorTopicYN=\"N\">Alzheimer&#x2019;s disease, CMPK2, KAT7, cGAS-STING, microglia, mitochondrial DNA, neuroinflammation\r\n\r\nFull Abstract:\r\nMitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer's disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5&#xd7;FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of cytidine/uridine monophosphate kinase 2 (Cmpk2), a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cyclic guanosine monophosphate-AMP synthase (cGAS)-stimulator of interferon genes (STING) and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease β-amyloid burden, restore synaptic plasticity, and improve cognitive function in 5&#xd7;FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a potential therapeutic target for AD.\r\n================================================================================\r\n", "tool_calls_made": 0, "duration_seconds": 1.02}

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{"output": "# Neuroinflammation Research Paper Evaluation\n\n---\n\n**Paper1: 38/50** `[8, 8, 7, 7, 8]`\n\nStroke recovery via the ZFP384-YY1 chromatin axis sustaining reparative microglial function. Gain+loss-of-function and cellular fate analysis provide strong causal evidence at the transcriptional level. ASO therapy is a genuine translational asset (approved modality class). However, the chromatin axis is a single regulatory node — generalizability to other injury contexts is unproven, and ASO delivery specifically to microglia remains a translational bottleneck. Strong clinical unmet need in stroke, but mechanistic depth is narrower than the neurodegeneration papers.\n\n**Paper2: 41/50** `[9, 9, 8, 8, 7]`\n\nAstrocytic PAD2 → citrullinated vimentin → microglial TLR4 → AD pathology is an elegant intercellular signaling cascade. Astrocyte-specific KO resolves cell-type origin cleanly. Pharmacological inhibition + multi-omics gives both translational and discovery depth. The citrullinated vimentin as a novel TLR4 ligand is mechanistically fresh. Clinical potential is tempered by TLR4's historical difficulty as a drug target and CNS delivery challenges for PAD2 inhibitors, but the astrocyte entry point may prove more tractable.\n\n**Paper3: 37/50** `[7, 9, 10, 6, 5]`\n\nDeep sequencing 311 brains for somatic cancer-driver variants (TET2/ASXL1/DNMT3A) enriched in AD microglia is conceptually the most innovative paper here — somatic mosaicism as a driver of neuroinflammation is a frontier insight. iPSC-microglia validation is commendable. But the causal chain is incomplete: do mutations drive pathology, or does the AD microenvironment select for mutant clones? Low-frequency somatic events strain statistical power. Clinical translation is decades away with no obvious intervention point for somatic variants in brain. Groundbreaking science, but furthest from application.\n\n**Paper4: 43/50** `[9, 9, 8, 8, 9]`\n\nKAT7 (epigenetic) → Cmpk2 (mitochondrial metabolism) → mtDNA release → cGAS-STING/NLRP3 (innate immune) → AD pathology. This is the most *complete* mechanistic chain — epigenetics through metabolism through innate immunity converging on pathology. Microglia-specific KO establishes cell-type causality. Both cGAS-STING and NLRP3 inhibitors are in active clinical pipelines for peripheral inflammatory diseases, giving this work a near-term translational runway. KAT7 inhibition adds an orthogonal intervention node. The 5xFAD model is standard and comparable. Minor weakness: Cmpk2-mtDNA-STING is a recognized axis; the KAT7 connection is the true novelty here.\n\n---\n\n## Best: **Paper 4 (Neuron)** — 43/50\n\n**Recommendation rationale:** Paper 4 offers the optimal balance of mechanistic completeness, methodological rigor, and clinical translatability. The KAT7→Cmpk2→mtDNA→cGAS-STING/NLRP3 pathway is mapped from epigenetics to innate immune output, cell-type validated, and converges on *druggable targets already in clinical development* (cGAS-STING and NLRP3 inhibitors). For a neuroinflammation researcher, this paper provides both a mechanistic framework and immediate translational hypotheses — the rare combination that justifies top recommendation over Paper 2's elegant intercellular signaling axis, Paper 3's bold innovation (too distant from application), and Paper 1's focused stroke mechanism (narrower scope).", "exit_code": 0, "error": null}

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