论文推荐-17-脑缺血 · Jun 11 17:08

{"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### 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 |\n|------|----|\n| Nature | 41586 |\n| **Nature Neuroscience** | **41593** |\n| Nature Communications | 41467 |\n| Cell Death & Differentiation | 41418 |\n| Scientific Reports | 41598 |\n| Cell Discovery | 41420 |\n\n## Cell Press / Elsevier 系列\n**注意：Cell Press有强付费墙，以下模式仅供参考**\n\n### 典型URL模式\n```\nhttps://www.cell.com/cms/10.1016/j.{journal_abbr}.{year}.{article_id}/asset/\n{hash}/main.assets/gr{N}_large.jpg\n```\n\n### 备选CDN路径\n```\nhttps://els-jbs-prod-cdn.jbs.elsevierhealth.com/journals/{journal_abbr}/\n...\n```\n- Cell Press 2025年起对脚本访问限制严格（403）\n- 建议通过 PubMed Central OA 获取，或使用付费订阅机构的访问\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 PDF下载**：`https://www.nature.com/articles/{article_id}.pdf` — 已验证可下载（2026-06）\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```javascript\n// 1. base64数据存为JS变量（在<script>开头）\nconst fig1_b64 = \"iVBORw0KGgo...\";\n\n// 2. canvas渲染（onload时自适应尺寸）\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 img.src = \"data:image/png;base64,\" + b64;\n}\n```\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": "阶段A (主题搜索): 共 2186 篇论文，获取 20 个PMID\r\nPMIDs: 42268517, 42268470, 42268366, 42267436, 42267329, 42267103, 42267063, 42266798, 42266622, 42266620...\r\n\r\n阶段B (高IF期刊过滤): 共 24 篇论文，获取 15 个PMID\r\nPMIDs: 42265101, 42201999, 42139356, 42129556, 42119560, 42091041, 42049021, 42048184, 41997149, 41995880, 41962540, 41928509, 41916277, 41894504, 41887219\r\n\r\n合并共计: 34 个不重复PMID\r\n", "tool_calls_made": 0, "duration_seconds": 5.83}

{"status": "success", "output": "获取到 35 篇论文元数据\r\n\r\nPMID: 42268517\r\n 标题: Ischemic Stroke Induces Ferroptosis and Neuroinflammation via Activation of the Microglial Tbp-Lpl Transcriptional Axis.\r\n 期刊: Neurochem Res | 日期: 2026 Jun 10\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1007/s11064-026-04812-9\r\n\r\nPMID: 42268470\r\n 标题: Effects of Sphingosine 1-phosphate Modulators on Central Remyelination: A Systematic Review of Animal Models.\r\n 期刊: Cell Mol Neurobiol | 日期: 2026 Jun 10\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1007/s10571-026-01748-0\r\n\r\nPMID: 42268366\r\n 标题: Unlocking Neuroprotection: Exercise-Induced Muscle Secretome (Myokines) as a Therapeutic Avenue Against Alzheimer's Dise\r\n 期刊: J Mol Neurosci | 日期: 2026 Jun 10\r\n 类型: ['Journal Article', 'Review'] | 有摘要: True\r\n DOI: 10.1007/s12031-026-02556-3\r\n\r\nPMID: 42267436\r\n 标题: Remote Ischemic Postconditioning in Endovascular Thrombectomy for Stroke: The EnTRIPS Randomized Clinical Trial.\r\n 期刊: Stroke | 日期: 2026 Jun 10\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1161/STROKEAHA.126.054857\r\n\r\nPMID: 42267329\r\n 标题: Heat Stroke Encephalopathy Without the Presence of Distinct Imaging Findings: Case Report and Review of Literature.\r\n 期刊: Case Rep Crit Care | 日期: 2026\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1155/crcc/6609879\r\n\r\nPMID: 42267103\r\n 标题: Combined heat and exercise stress disrupt gut microbiota and promote microbial translocation.\r\n 期刊: Front Microbiol | 日期: 2026\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.3389/fmicb.2026.1779295\r\n\r\nPMID: 42267063\r\n 标题: Assessment of Enteral Baclofen Prescribing Practices for Infants With Hypertonia.\r\n 期刊: J Pediatr Pharmacol Ther | 日期: 2026 Jun\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.5863/JPPT-25-00052\r\n\r\nPMID: 42266798\r\n 标题: Elucidating the Neural Basis of Bipolar Disorder - Secondary Publication.\r\n 期刊: JMA J | 日期: 2026 May 15\r\n 类型: ['Journal Article', 'Review'] | 有摘要: True\r\n DOI: 10.31662/jmaj.2026-0004\r\n\r\nPMID: 42266622\r\n 标题: Vitamin D and sudden sensorineural hearing loss: emerging associations, mechanistic insights, and prospects for precisio\r\n 期刊: Front Nutr | 日期: 2026\r\n 类型: ['Journal Article', 'Review'] | 有摘要: True\r\n DOI: 10.3389/fnut.2026.1844126\r\n\r\nPMID: 42266620\r\n 标题: Intermittent fasting and neuroprotection in Alzheimer's disease: metabolic mechanisms, cellular signaling, and brain-per\r\n 期刊: Front Nutr | 日期: 2026\r\n 类型: ['Journal Article', 'Review'] | 有摘要: True\r\n DOI: 10.3389/fnut.2026.1839995\r\n\r\nPMID: 42266431\r\n 标题: Beyond 20/20: How Laser Eye Surgery Boosts Quality of Life (SMILE vs. FS-LASIK).\r\n 期刊: J Ophthalmol | 日期: 2026\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1155/joph/7225757\r\n\r\nPMID: 42266398\r\n 标题: Distal Renal Tubular Acidosis in Pregnancy: A Case Report and Systematic Literature Review.\r\n 期刊: Eur J Case Rep Intern Med | 日期: 2026\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.12890/2026_006821\r\n\r\nPMID: 42265806\r\n 标题: Development and application of a simple LC-MS/MS method for therapeutic drug monitoring to guide colistin dosing in crit\r\n 期刊: BMC Pharmacol Toxicol | 日期: 2026 Jun 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1186/s40360-026-01162-8\r\n\r\nPMID: 42265746\r\n 标题: A method utilizing chemical carcinogens and a Western diet to reliably induce advanced hepatocellular carcinoma in male \r\n 期刊: Cancer Metab | 日期: 2026 Jun 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1186/s40170-026-00441-6\r\n\r\nPMID: 42265728\r\n 标题: The impact of emergency intubation on surgical outcomes in patients with acute aortic dissection AADA (DeBakey I). Is a \r\n 期刊: J Cardiothorac Surg | 日期: 2026 Jun 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1186/s13019-026-04349-6\r\n\r\nPMID: 42265487\r\n 标题: Dead-Space Microdomains as Explicit Barriers to Extracellular Drug Transport in Alzheimer's Disease.\r\n 期刊: Pharm Res | 日期: 2026 Jun 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1007/s11095-026-04129-w\r\n\r\nPMID: 42265044\r\n 标题: Comment on \"optimizing radical cystectomy recovery: The role of modified ERAS in improving postoperative outcomes\".\r\n 期刊: Urol Oncol | 日期: 2026 Jun 9\r\n 类型: ['Letter'] | 有摘要: False\r\n DOI: 10.1016/j.urolonc.2026.05.020\r\n\r\nPMID: 42264818\r\n 标题: Development and validation of a semi-structured interview guide to explore patient perspectives on physiotherapy advance\r\n 期刊: J Bodyw Mov Ther | 日期: 2026 Jul\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.jbmt.2026.04.025\r\n\r\nPMID: 42264813\r\n 标题: Effectiveness of diathermy in reducing subcutaneous adipose tissue affected by lipedema: a pilot study.\r\n 期刊: J Bodyw Mov Ther | 日期: 2026 Jul\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.jbmt.2026.04.009\r\n\r\nPMID: 42264569\r\n 标题: Lung Cancer Screening Guidelines: Moving Beyond Pack-Years for Equity and Efficiency.\r\n 期刊: Chest | 日期: 2026 Jun\r\n 类型: ['Editorial'] | 有摘要: False\r\n DOI: 10.1016/j.chest.2026.02.029\r\n\r\nPMID: 42265101\r\n 标题: Scg2 drives corticospinal circuit reorganization with spinal premotor interneurons and astrocytes for motor recovery aft\r\n 期刊: Nat Commun | 日期: 2026 Jun 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1038/s41467-026-73518-x\r\n\r\nPMID: 42201999\r\n 标题: State-specific inhibition of NMDA receptors by memantine provides insight into NMDAR channel blocker tolerability.\r\n 期刊: Sci Adv | 日期: 2026 May 29\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1126/sciadv.aec3154\r\n\r\nPMID: 42139356\r\n 标题: An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling.\r\n 期刊: Sci Adv | 日期: 2026 May 15\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1126/sciadv.aeb7558\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'] | 有摘要: True\r\n DOI: 10.1038/s41586-026-10480-0\r\n\r\nPMID: 42119560\r\n 标题: Intrinsic endothelial remodeling drives brain capillary repair.\r\n 期刊: Neuron | 日期: 2026 May 11\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.neuron.2026.04.020\r\n\r\nPMID: 42091041\r\n 标题: Exerkine GPLD1 bridges liver and brain.\r\n 期刊: Cell Metab | 日期: 2026 May 5\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.cmet.2026.04.002\r\n\r\nPMID: 42049021\r\n 标题: Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic \r\n 期刊: Cell Metab | 日期: 2026 Apr 27\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.cmet.2026.04.001\r\n\r\nPMID: 42048184\r\n 标题: Heat shock protein 90β lactylation acts as a metabolic switch to drive cerebrovascular apoptosis under heat stress.\r\n 期刊: Cell Rep | 日期: 2026 May 26\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.celrep.2026.117317\r\n\r\nPMID: 41997149\r\n 标题: SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\n 期刊: Neuron | 日期: 2026 Apr 16\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.neuron.2026.03.027\r\n\r\nPMID: 41995880\r\n 标题: A model-based prion vaccine protects a transgenic mouse line carrying a Gerstmann-Sträussler-Scheinker disease mutation.\r\n 期刊: Acta Neuropathol | 日期: 2026 Apr 17\r\n 类型: ['Journal Article', \"Research Support, Non-U.S. Gov't\", 'Research Support, N.I.H., Extramural'] | 有摘要: True\r\n DOI: 10.1007/s00401-026-03015-4\r\n\r\nPMID: 41962540\r\n 标题: A genome-wide in vivo CRISPR screen identifies neuroprotective strategies in the mouse and human retina.\r\n 期刊: Neuron | 日期: 2026 Apr 9\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.neuron.2026.03.022\r\n\r\nPMID: 41928509\r\n 标题: Noninvasive tactile stimulation engaging a thalamic-amygdala circuit ameliorates mood dysfunction in mouse models of dep\r\n 期刊: Neuron | 日期: 2026 Apr 1\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.neuron.2026.03.012\r\n\r\nPMID: 41916277\r\n 标题: Cell-type-focused compound screen in human organoids reveals CK1 inhibition protects cone photoreceptors from death.\r\n 期刊: Neuron | 日期: 2026 Mar 30\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.neuron.2026.02.024\r\n\r\nPMID: 41894504\r\n 标题: Clinically relevant stereochemistry reprograms amyloid proteome for aggregation cross-talk-conferred neuroprotection.\r\n 期刊: Sci Adv | 日期: 2026 Mar 27\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1126/sciadv.aeb2729\r\n\r\nPMID: 41887219\r\n 标题: Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chr\r\n 期刊: Cell Rep | 日期: 2026 Mar 25\r\n 类型: ['Journal Article'] | 有摘要: True\r\n DOI: 10.1016/j.celrep.2026.117135\r\n\r\n=== 初筛通过: 29 篇 ===\r\n PMID 42268517: [Neurochem Res] Ischemic Stroke Induces Ferroptosis and Neuroinflammation via Activation of the Microglial Tbp-Lpl T\r\n PMID 42268470: [Cell Mol Neurobiol] Effects of Sphingosine 1-phosphate Modulators on Central Remyelination: A Systematic Review of Anima\r\n PMID 42267436: [Stroke] Remote Ischemic Postconditioning in Endovascular Thrombectomy for Stroke: The EnTRIPS Randomized Cli\r\n PMID 42267329: [Case Rep Crit Care] Heat Stroke Encephalopathy Without the Presence of Distinct Imaging Findings: Case Report and Review\r\n PMID 42267103: [Front Microbiol] Combined heat and exercise stress disrupt gut microbiota and promote microbial translocation.\r\n PMID 42267063: [J Pediatr Pharmacol Ther] Assessment of Enteral Baclofen Prescribing Practices for Infants With Hypertonia.\r\n PMID 42266431: [J Ophthalmol] Beyond 20/20: How Laser Eye Surgery Boosts Quality of Life (SMILE vs. FS-LASIK).\r\n PMID 42266398: [Eur J Case Rep Intern Med] Distal Renal Tubular Acidosis in Pregnancy: A Case Report and Systematic Literature Review.\r\n PMID 42265806: [BMC Pharmacol Toxicol] Development and application of a simple LC-MS/MS method for therapeutic drug monitoring to guide col\r\n PMID 42265746: [Cancer Metab] A method utilizing chemical carcinogens and a Western diet to reliably induce advanced hepatocellula\r\n PMID 42265728: [J Cardiothorac Surg] The impact of emergency intubation on surgical outcomes in patients with acute aortic dissection AAD\r\n PMID 42265487: [Pharm Res] Dead-Space Microdomains as Explicit Barriers to Extracellular Drug Transport in Alzheimer's Disease.\r\n PMID 42264818: [J Bodyw Mov Ther] Development and validation of a semi-structured interview guide to explore patient perspectives on p\r\n PMID 42264813: [J Bodyw Mov Ther] Effectiveness of diathermy in reducing subcutaneous adipose tissue affected by lipedema: a pilot stu\r\n PMID 42265101: [Nat Commun] Scg2 drives corticospinal circuit reorganization with spinal premotor interneurons and astrocytes fo\r\n PMID 42201999: [Sci Adv] State-specific inhibition of NMDA receptors by memantine provides insight into NMDAR channel blocker\r\n PMID 42139356: [Sci Adv] An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling.\r\n PMID 42129556: [Nature] Sustaining microglial reparative function enhances stroke recovery.\r\n PMID 42119560: [Neuron] Intrinsic endothelial remodeling drives brain capillary repair.\r\n PMID 42091041: [Cell Metab] Exerkine GPLD1 bridges liver and brain.\r\n PMID 42049021: [Cell Metab] Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neurona\r\n PMID 42048184: [Cell Rep] Heat shock protein 90β lactylation acts as a metabolic switch to drive cerebrovascular apoptosis und\r\n PMID 41997149: [Neuron] SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\n PMID 41995880: [Acta Neuropathol] A model-based prion vaccine protects a transgenic mouse line carrying a Gerstmann-Sträussler-Scheink\r\n PMID 41962540: [Neuron] A genome-wide in vivo CRISPR screen identifies neuroprotective strategies in the mouse and human ret\r\n PMID 41928509: [Neuron] Noninvasive tactile stimulation engaging a thalamic-amygdala circuit ameliorates mood dysfunction in\r\n PMID 41916277: [Neuron] Cell-type-focused compound screen in human organoids reveals CK1 inhibition protects cone photorecep\r\n PMID 41894504: [Sci Adv] Clinically relevant stereochemistry reprograms amyloid proteome for aggregation cross-talk-conferred\r\n PMID 41887219: [Cell Rep] Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, w\r\n", "tool_calls_made": 0, "duration_seconds": 3.44}

{"status": "success", "output": "=== PMID: 42129556 ===\r\n标题: Sustaining microglial reparative function enhances stroke recovery.\r\n提示: Nature — Sustaining microglial reparative function enhances stroke recovery\r\n摘要(前500字): 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 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 f\r\n\r\n=== PMID: 42049021 ===\r\n标题: Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic stroke.\r\n提示: Cell Metab — Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic\r\n摘要(前500字): Astrocytes regulate brain metabolism and homeostasis, but how oxidative stress reshapes astrocytic metabolism to drive neuronal damage remains unclear. Here, we demonstrate that oxidative stress turns on astrocytic type I collagen (COL1) production via a redox-glycosylation coupling mechanism. Hydrogen peroxide (H2O2) suppresses miR-29 and enhances fucosyltransferase 8 (FUT8)-mediated core fucosylation, integrating post-transcriptional and glycosylation-dependent regulation of COL1. Astrocyte-de\r\n\r\n=== PMID: 41997149 ===\r\n标题: SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\n提示: Neuron — SARM1 executes neuronal parthanatos and promotes excitotoxic cell death\r\n摘要(前500字): The nicotinamide adenine dinucleotide (NAD+) hydrolase sterile alpha and Toll/interleukin-1 receptor motif-containing 1 (SARM1) is the central executioner of pathological axon degeneration and is allosterically activated by an increased nicotinamide mononucleotide (NMN)/NAD+ ratio. DNA damage induces NAD+ loss and an increased NMN/NAD+ ratio by hyperactivating poly(ADP-ribose) polymerase 1 (PARP1), which triggers the parthanatos cell death pathway. Multiple mechanistically distinct DNA-damaging \r\n\r\n=== PMID: 42119560 ===\r\n标题: Intrinsic endothelial remodeling drives brain capillary repair.\r\n提示: Neuron — Intrinsic endothelial remodeling drives brain capillary repair\r\n摘要(前500字): The brain's microvasculature is essential for oxygen and nutrient delivery; however, the mechanisms underlying cerebral capillary repair following injury remain largely elusive. Here, we identify an unrecognized mechanism through which brain capillary endothelial cells (ECs) autonomously promote capillary remodeling. Using longitudinal two-photon imaging in mice, we demonstrate that following focal endothelial injury and selective loss of a single EC, neighboring ECs extend their plasma membrane\r\n\r\n=== PMID: 42265101 ===\r\n标题: Scg2 drives corticospinal circuit reorganization with spinal premotor interneurons and astrocytes for motor recovery after stroke in mice.\r\n提示: Nat Commun — Scg2 drives corticospinal circuit reorganization for motor recovery\r\n摘要(前500字): Brain injuries such as stroke damage neural circuitry and lead to functional deficits. Spared motor pathways are often reorganized for recovery; however, the connectivity and mechanisms that drive the reorganization are largely unknown. Here, we demonstrate structural and functional connectivity reformed by corticospinal axons after stroke in male mice and determine a secretory protein that drives the reorganization. We first find that corticospinal axons innervate the denervated cervical cord a\r\n\r\n=== PMID: 42201999 ===\r\n标题: State-specific inhibition of NMDA receptors by memantine provides insight into NMDAR channel blocker tolerability.\r\n提示: Sci Adv — State-specific inhibition of NMDA receptors by memantine\r\n摘要(前500字): N-methyl-d-aspartate (NMDA) receptors (NMDARs) are key mediators of calcium ion (Ca2+) influx required for proper neuronal function. Excessive NMDAR-mediated Ca2+ influx is neurotoxic and associated with neurological disease. Memantine and ketamine, two NMDAR antagonists with overlapping binding sites in the NMDAR channel, are of high clinical interest. Whereas memantine is a well-tolerated Alzheimer's disease medication, ketamine is a fast-acting antidepressant with abuse potential and psychoto\r\n\r\n=== PMID: 42267436 ===\r\n标题: Remote Ischemic Postconditioning in Endovascular Thrombectomy for Stroke: The EnTRIPS Randomized Clinical Trial.\r\n提示: Stroke — Remote Ischemic Postconditioning in Endovascular Thrombectomy\r\n摘要(前500字): Although the neuroprotective potential of remote ischemic postconditioning (RIPC) has been reported, the efficacy and safety of ultra-early RIPC administered after endovascular treatment (EVT) in patients with acute ischemic stroke remain unclear. This study evaluated the efficacy and safety of ultra-early RIPC in patients with acute ischemic stroke undergoing EVT. The EnTRIPS trial (Endovascular Treatment Combined with Remote Ischemic Postconditioning in Patients with Acute Ischemic Stroke) was\r\n\r\n=== PMID: 42048184 ===\r\n标题: Heat shock protein 90β lactylation acts as a metabolic switch to drive cerebrovascular apoptosis under heat stress.\r\n提示: Cell Rep — HSP90β lactylation drives cerebrovascular apoptosis under heat stress\r\n摘要(前500字): Lysine lactylation (Kla) is a metabolite-sensing post-translational modification that bridges cellular metabolism to protein function. Here, we discover that heat stress triggers anaerobic glycolysis and lactate accumulation in brain microvascular endothelial cells. We find that plasma lactate inversely correlates with Glasgow Coma Scale scores in heat stroke patients and predicts poor outcomes. Mechanistically, AARS1 catalyzes the transfer of lactate to HSP90β at lysine 275 (K275). Critically, \r\n\r\n=== PMID: 41887219 ===\r\n标题: Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.\r\n提示: Cell Rep — EPA reprograms cerebrovascular metabolism impairs repair after brain injury\r\n摘要(前500字): Repetitive mild traumatic brain injury (rmTBI) precedes chronic traumatic encephalopathy (CTE) and involves neurovascular dysfunction. Omega-3 polyunsaturated fatty acids (PUFA) are promoted as neuroprotective but their long-term effects after brain injury remain uncertain. We uncover a metabolic vulnerability associated with cerebral accumulation of eicosapentaenoic acid (EPA), a major PUFA derived from fish oil. In a fish oil diet model, EPA accumulates at baseline yet is selectively depleted \r\n\r\n=== PMID: 42091041 ===\r\n标题: Exerkine GPLD1 bridges liver and brain.\r\n提示: Cell Metab — Exerkine GPLD1 bridges liver and brain\r\n摘要(前500字): A recent study by Bieri et al. shows that exercise elevates hepatic glycosylphosphatidylinositol-specific phospholipase D1 (GPLD1), which cleaves endothelial tissue-nonspecific alkaline phosphatase (TNAP) to rejuvenate cerebrovascular signaling, enhance cognition in aging, and attenuate Alzheimer's-related pathology. This liver-to-brain enzymatic axis positions hepatokines as potent mediators of exercise-induced neuroprotection, which redefines systemic metabolism as a driver of brain resilience\r\n\r\n=== PMID: 41962540 ===\r\n标题: A genome-wide in vivo CRISPR screen identifies neuroprotective strategies in the mouse and human retina.\r\n提示: Neuron — Genome-wide in vivo CRISPR screen identifies neuroprotective strategies\r\n摘要(前500字): Retinitis pigmentosa (RP) is a genetically diverse blinding disorder lacking broadly effective therapies. We performed a genome-wide in vivo CRISPR knockout screen in mice carrying the P23H rhodopsin mutation, the most common cause of autosomal dominant RP in the United States, to systematically identify neuroprotective genes. We discovered multiple knockouts that accelerated rod photoreceptor loss, validated top candidates, and showed that overexpressing two genes-ubiquitin fusion degradation 1\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.42}

{"status": "success", "output": "=== PMID: 42129556 ===\r\n标题: Sustaining microglial reparative function enhances stroke recovery.\r\n期刊: Nature | 日期: 2026 May 13\r\nDOI: 10.1038/s41586-026-10480-0\r\n第一作者: Tsuyama Jun\r\n关键词: \r\n\r\n完整摘要:\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 microgl\r\n\r\n============================================================\r\n\r\n=== PMID: 42049021 ===\r\n标题: Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic stroke.\r\n期刊: Cell metabolism | 日期: 2026 Apr 27\r\nDOI: 10.1016/j.cmet.2026.04.001\r\n第一作者: Lee Jae-Hun\r\n关键词: extracellular matrix, fucosylation, glial barrier, hydrogen peroxide, ischemic stroke, neuronal death, oxidative stress, photothrombosis\r\n\r\n完整摘要:\r\nAstrocytes regulate brain metabolism and homeostasis, but how oxidative stress reshapes astrocytic metabolism to drive neuronal damage remains unclear. Here, we demonstrate that oxidative stress turns on astrocytic type I collagen (COL1) production via a redox-glycosylation coupling mechanism. Hydrogen peroxide (H2O2) suppresses miR-29 and enhances fucosyltransferase 8 (FUT8)-mediated core fucosylation, integrating post-transcriptional and glycosylation-dependent regulation of COL1. Astrocyte-derived COL1 activates integrin signaling and promotes neuronal death. In a photothrombotic stroke model, an H2O2 surge induces astrogliosis, glycosylation remodeling, and COL1 expression, leading to glial barrier formation, neuronal loss, and neurological deficits. These pathological cascades are mitigated by astrocyte-specific silencing of COL1 or FUT8 or by KDS12025, a peroxidase enhancer that reduces H2O2 burden. Notably, KDS12025 exerts potent neuroprotection in a non-human primate stroke mod\r\n\r\n============================================================\r\n\r\n=== PMID: 41997149 ===\r\n标题: SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\n期刊: Neuron | 日期: 2026 Apr 16\r\nDOI: 10.1016/j.neuron.2026.03.027\r\n第一作者: Wu Tong\r\n关键词: ALS, NAD⁺ metabolism, Parkinson’s disease, SARM1, dopaminergic neurons, excitotoxicity, iPSC, neurodegeneration\r\n\r\n完整摘要:\r\nThe nicotinamide adenine dinucleotide (NAD+) hydrolase sterile alpha and Toll/interleukin-1 receptor motif-containing 1 (SARM1) is the central executioner of pathological axon degeneration and is allosterically activated by an increased nicotinamide mononucleotide (NMN)/NAD+ ratio. DNA damage induces NAD+ loss and an increased NMN/NAD+ ratio by hyperactivating poly(ADP-ribose) polymerase 1 (PARP1), which triggers the parthanatos cell death pathway. Multiple mechanistically distinct DNA-damaging agents activate SARM1 and induce axon degeneration following PARP1 activation. Remarkably, SARM1 is required for key steps downstream of hyperactivated PARP1, which are pathognomonic of parthanatos, including mitochondrial depolarization, nuclear translocation of apoptosis-inducing factor (AIF), and cell death. Hence, SARM1 is an essential component of neuronal parthanatos. Moreover, complex neurodegenerative stimuli whose mechanisms include activation of parthanatos, such as 1-methyl-4-phenyl-p\r\n\r\n============================================================\r\n\r\n=== PMID: 42265101 ===\r\n标题: Scg2 drives corticospinal circuit reorganization with spinal premotor interneurons and astrocytes for motor recovery after stroke in mice.\r\n期刊: Nature communications | 日期: 2026 Jun 09\r\nDOI: 10.1038/s41467-026-73518-x\r\n第一作者: Sato Tokiharu\r\n关键词: \r\n\r\n完整摘要:\r\nBrain injuries such as stroke damage neural circuitry and lead to functional deficits. Spared motor pathways are often reorganized for recovery; however, the connectivity and mechanisms that drive the reorganization are largely unknown. Here, we demonstrate structural and functional connectivity reformed by corticospinal axons after stroke in male mice and determine a secretory protein that drives the reorganization. We first find that corticospinal axons innervate the denervated cervical cord and reconnect to premotor V2a interneurons after stroke. Kinematic analyses and chemogenetic silencing reveal their contribution to motor recovery. Translated mRNA expression analyses identify a secretory protein secretogranin II (Scg2), which is upregulated in astrocytes by injury-induced ATP and in V2a neurons by rehabilitation-induced neural activity. Scg2 promotes axon growth via cAMP and S6 and enhances axon rewiring, while its knockdown attenuates it. Our data reveal the neural substrate an\r\n\r\n============================================================\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.02}

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{"output": "# 神经科学论文严格评审报告\n\n---\n\n## 📄 候选论文 1: Nature — Microglial reparative function in stroke\n\n### 评分表格\n\n| 维度 | 得分 | 理由 |\n|------|------|------|\n| 逻辑完整性 | **8/10** | 因果链清晰（ZFP384 → YY1-染色质互作 → 修复基因沉默 → 小胶质细胞功能丧失），但ZFP384在损伤后期如何被\"开启\"的上游机制未交代；\"细胞命运分析\"到ZFP384发现的过渡逻辑略显跳跃。 |\n| 方法学水平 | **9/10** | 细胞命运追踪 + 转录调控 + 染色质构象 + ASO干预，多层次验证体系符合Nature水准。ASO靶向策略有良好的特异性控制。 |\n| 创新性 | **8/10** | 核心洞见——修复性小胶质细胞并非\"消失\"而是\"功能沉默\"——具有概念新颖性；ZFP384-YY1轴作为该过程的分子开关是原创发现。但ASO作为干预手段本身并非创新。 |\n| 可借鉴性 | **9/10** | 命运分析→机制解析→干预验证的三段式实验设计范式值得借鉴；特别是证明了\"维持已有修复功能\"比\"重新激活修复程序\"更具可行性的思路，对神经科学实验设计有启示意义。 |\n| 临床转化潜力 | **8/10** | ASO药物已有成熟临床路径（如nusinersen）；但脑内小胶质细胞的ASO递送效率和脱靶效应仍是转化瓶颈；仅在小鼠中验证、治疗时间窗未明确。 |\n| **总分** | **42/50** | |\n\n### 核心优势\n\n- **概念突破**：颠覆了领域内\"修复窗口期后微胶质细胞退出\"的传统认知，提出\"细胞存在但功能沉默\"的新范式，为慢性期干预提供了理论依据\n- **靶点清晰**：ZFP384作为单一转录调控节点，可撬动广泛的修复基因网络，靶点成药潜力明确\n- **实验逻辑完整**：从现象发现（命运分析）→ 机制阐明（ZFP384/YY1/染色质）→ 干预验证（ASO），逻辑递进严密\n\n### 潜在缺憾\n\n- 仅在小鼠模型中验证，缺乏大动物或人源化数据\n- ZFP384的上游调控信号（是什么导致其在慢性期被诱导？）未阐明，机制链最上游缺失\n- 功能恢复评估的行为学指标细节未在摘要中呈现，无法判断其临床相关性\n- 小胶质细胞\"修复功能\"的具体分子效应器（分泌哪些因子？影响哪些细胞类型？）描述不足\n\n### 推荐意见\n\n**推荐优先级: #2**\n\n值得推荐。该研究为脑卒中慢性期的神经修复提供了新的治疗窗口和分子靶点。对脑缺血/神经保护方向的研究者而言，其\"维持内源性修复\"的思路比传统的\"外源性补充\"更值得关注。但其转化距离相对较远（仅小鼠数据），且摘要未充分展示神经保护（相对于修复）的直接证据。\n\n---\n\n## 📄 候选论文 2: Cell Metabolism — Astrocytic collagen drives neuronal death in stroke\n\n### 评分表格\n\n| 维度 | 得分 | 理由 |\n|------|------|------|\n| 逻辑完整性 | **9/10** | 机制级联极其完整：H₂O₂ → miR-29↓ + FUT8↑（双重调控）→ COL1核心岩藻糖化 → 整合素信号 → 神经元死亡 → 胶质屏障 → 神经功能缺损。每个节点均有干预验证（COL1沉默、FUT8沉默、KDS12025），形成闭环。 |\n| 方法学水平 | **10/10** | 三种干预策略（遗传学×2 + 药理学×1）在**两个物种**（小鼠+NHP）中验证；氧化还原-糖基化偶联的生化机制分析精细。NHP卒中模型中的药效验证是转化研究中的金标准级别证据。 |\n| 创新性 | **9/10** | \"氧化应激→星形胶质细胞胶原合成→胶质屏障→神经元死亡\"是一条全新的病理通路；氧化还原-糖基化偶联（redox-glycosylation coupling）作为翻译后调控的整合机制是原创概念；KDS12025（过氧化物酶增强剂）提供了新的药理学策略。 |\n| 可借鉴性 | **10/10** | 多模态验证策略（遗传+药理，啮齿类+灵长类）是转化神经科学研究的标杆；\"从代谢紊乱中发现病理性结构屏障\"的思路具有跨疾病借鉴意义。 |\n| 临床转化潜力 | **9/10** | NHP验证极大增强了转化信心；KDS12025作为小分子药物具有良好成药性；星形胶质细胞特异性靶向降低了系统性副作用风险。唯一不足：摘要未提及治疗时间窗和NHP行为学恢复的详细程度。 |\n| **总分** | **47/50** | |\n\n### 核心优势\n\n- **转化证据等级最高**：小鼠+NHP双物种验证 + 遗传学/药理学双路径干预，是本次评审三篇中最接近临床转化的研究\n- **机制深度与广度兼备**：从miRNA转录后调控到糖基化翻译后修饰，双重调控层面的整合分析达到了很高的生化深度；而COL1→整合素→神经元死亡的细胞间信号传导又拓展了机制的细胞广度\n- **病理性结构屏障概念**：星形胶质细胞来源的COL1形成\"胶质屏障\"直接驱动神经元死亡，这个概念既有生物学新颖性，又为药物干预提供了明确的病理靶标\n- **KDS12025的药理学策略**：以增强内源性过氧化物酶来降低H₂O₂负担，相比于直接抗氧化，是一种更持续和生理性的干预方式\n\n### 潜在缺憾\n\n- (摘要中)代谢角度（Cell Metabolism的定位）与神经病理机制的衔接可更紧密——COL1合成对星形胶质细胞整体代谢网络的影响未被描述\n- 胶质屏障的物理/功能特性（是否真的是扩散屏障？还是信号屏障？）需要更多结构证据\n- 光化学血栓模型中H₂O₂的时间动态是否与人类卒中匹配值得讨论\n- KDS12025的特异性和脱靶效应在大动物中的评估信息不足\n\n### 推荐意见\n\n**推荐优先级: #1 ⭐（最佳推荐）**\n\n**强烈推荐。** 该研究在脑缺血/神经保护领域几乎无短板：完整的机制链、多物种验证、遗传学和药理学双重干预、明确的临床转化路径。对于脑缺血研究者而言，其从\"氧化应激代谢紊乱→细胞外基质病理性重塑→神经元死亡\"的研究框架具有高度的可借鉴性和扩展性。NHP验证使KDS12025成为极具潜力的临床候选分子。\n\n---\n\n## 📄 候选论文 3: Neuron — SARM1 executes neuronal parthanatos\n\n### 评分表格\n\n| 维度 | 得分 | 理由 |\n|------|------|------|\n| 逻辑完整性 | **9/10** | PARP1超活化 → NAD⁺耗竭 → NMN/NAD⁺比值↑ → SARM1变构激活 → 线粒体去极化 → AIF核转位 → parthanatos，逻辑链条明确。在多种遗传学和药理学模型中均验证了SARM1的必要性。 |\n| 方法学水平 | **8/10** | 多种DNA损伤剂 + 多种疾病模型（MPTP/PD、兴奋性毒性、ALS），模型广度好。但主要依赖遗传学功能缺失策略；缺乏药理学干预验证（SARM1抑制剂）；AIF核转位等经典指标虽可靠但传统。 |\n| 创新性 | **9/10** | 将SARM1（经典轴突变性执行者）与parthanatos（经典DNA损伤-细胞死亡通路）连接，完成了PARP1→SARM1→AIF这一死亡信号轴的\"缺失环节\"填补，具有重要的概念整合价值。 |\n| 可借鉴性 | **8/10** | 跨疾病模型的验证策略值得借鉴；parthanatos的判定标准（线粒体去极化+AIF核转位+细胞死亡）可作为其他研究者的参考框架。但实验设计整体偏传统（主要在遗传学层面操作）。 |\n| 临床转化潜力 | **7/10** | SARM1已有活跃的药物发现项目（轴突变性领域），靶点成药性良好。但SARM1作为核心死亡执行者，抑制可能带来安全性风险（如肿瘤监测、感染防御）。摘要中未展示任何治疗性干预的验证。对于卒中特异性场景的验证缺失。 |\n| **总分** | **41/50** | |\n\n### 核心优势\n\n- **概念整合力强**：将两个之前相对独立的领域（SARM1/轴突变性与PARP1/parthanatos）进行了机制性桥接，填补了parthanatos通路中\"PARP1下游、AIF上游\"的关键执行者空白\n- **疾病模型覆盖面广**：从DNA损伤到PD（MPTP）、兴奋性毒性（NMDA/红藻氨酸）到ALS相关毒性，展示了SARM1-parthanatos轴的广泛病理相关性\n- **机制层次清晰**：从生化激活（NMN/NAD⁺比值）到细胞器事件（线粒体去极化）到核事件（AIF转位）到终点（细胞死亡），层次分明\n- **学术影响力高**：发表于Neuron，对于基础神经生物学研究者而言具有较高的引用价值和讨论热度\n\n### 潜在缺憾\n\n- **脑缺血/卒中场景的缺失**：尽管兴奋性毒性在卒中亚急性期重要，但摘要未直接验证SARM1在体内卒中模型中的作用，对于脑缺血方向的研究者而言缺乏直接证据\n- **缺乏治疗性验证**：所有实验均为功能缺失（loss-of-function）验证SARM1必要性，但未测试SARM1抑制剂在疾病模型中的疗效或治疗时间窗\n- **SARM1激活的上游特异性**：NMN/NAD⁺比值变化可能由多种代谢紊乱触发，parthanatos场景下的特异性有待进一步讨论\n- **体内数据描述不足**：摘要强调机制，体内模型的行为学/病理学终点数据薄弱\n\n### 推荐意见\n\n**推荐优先级: #3**\n\n可推荐，但优先级低于前两篇。该研究对于理解神经元死亡的基础机制具有重要学术价值，SARM1作为parthanatos执行者的发现是领域内的重要进展。然而，对于**脑缺血/神经保护方向**的研究者而言，该论文缺乏直接的卒中模型验证和治疗性干预策略，其转化距离较远。更适合基础神经生物学或神经退行性疾病方向的读者。\n\n---\n\n## 📊 综合对比与推荐排序\n\n| 排名 | 论文 | 总分 | 核心标签 |\n|------|------|------|----------|\n| **#1 ⭐** | 论文2: Cell Metabolism | **47/50** | 机制最完整、转化证据最强、NHP验证 |\n| **#2** | 论文1: Nature | **42/50** | 概念新颖、修复窗口再定义、ASO策略 |\n| **#3** | 论文3: Neuron | **41/50** | 基础机制重要、但缺乏卒中直接验证 |\n\n### 推荐逻辑\n\n**对于脑缺血/神经保护方向的研究者，推荐优先级为 2 > 1 > 3**，理由如下：\n\n1. **论文2（Cell Metabolism）位列第一**，因为它是三篇中唯一在非人灵长类卒中模型中验证了药效的研究，同时具备完整机制链、多干预策略和明确的小分子药物候选（KDS12025）——这意味着从实验台到病床的每一步都有了关键证据支撑。\n\n2. 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{"status": "success", "output": "标题: Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic stroke.\r\n来源: Cell Metab\r\n属性: ['Has Abstract']\r\n ID: pubmed = 42049021\r\n ID: doi = 10.1016/j.cmet.2026.04.001\r\n ID: pii = S1550-4131(26)00139-7\r\n", "tool_calls_made": 0, "duration_seconds": 2.02}

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{"status": "success", "output": "=== 论文元数据 ===\r\n标题: Oxidative stress-induced astrocytic collagen biosynthesis drives glial barrier formation and neuronal death in ischemic stroke.\r\n作者: Jae-Hun Lee; In-Young Hwang; Hyun Jun Jang; Hyeon-Gu Yeo; Jiwoon Lim; Jinyoung Won; Benedict Reve Delmo; Myungju Kim 等\r\n期刊: Cell metabolism (Cell Metab)\r\n日期: 2026 Apr 27\r\nDOI: 10.1016/j.cmet.2026.04.001\r\n关键词: extracellular matrix, fucosylation, glial barrier, hydrogen peroxide, ischemic stroke, neuronal death, oxidative stress, photothrombosis, reactive astrocyte, type I collagen\r\n\r\n机构样本: ['Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea.', 'Futuristic Animal Resource & Research Center, KRIBB, Cheongju 28116, Republic of Korea; KRIBB School, Korea University of Science and Technology (UST), Daejeon 34113, Republic of Korea.', 'Department of Biomedical Engineering, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.']\r\n\r\n摘要HTML(前500): Astrocytes regulate brain metabolism and homeostasis, but how oxidative stress reshapes astrocytic metabolism to drive neuronal damage remains unclear. Here, we demonstrate that oxidative stress turns on astrocytic type I collagen (COL1) production via a redox-glycosylation coupling mechanism. Hydrogen peroxide (H2O2) suppresses miR-29 and enhances fucosyltransferase 8 (FUT8)-mediated core fucosylation, integrating post-transcriptional and glycosylation-dependent regulation of COL1. Astrocyte-de\r\n", "tool_calls_made": 0, "duration_seconds": 1.22}

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