论文推荐-08-PD · Jun 13 08:12

{"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: 2.4.0\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## ⚡ 用户核心课题（跨所有方向的超优先主题）\n**博一课题**：Warburg乳酸 → PCAF介导RhoA K118/K162乳酸化 → RhoA持续激活 → 线粒体远离质膜 → 拮抗mitoxyperiosis\n\n所有方向的论文推荐，只要与以下关键词相关的论文**自动获得更高优先级**，应优先于同评分不相关的论文推送：\n- Mitoxyperiosis / 线粒体-质膜接触 / 新型细胞死亡\n- 乳酸化修饰(Kla) / PCAF / p300 / 组蛋白乳酸化\n- RhoA信号 / 细胞骨架重排 / 小G蛋白修饰\n- Warburg效应 / 肿瘤代谢 / LDHA抑制\n- 糖酵解 / 乳酸代谢 / 肿瘤免疫代谢\n- 禁食疗法 / 卡路里限制 / 联合免疫治疗\n- 代谢组学 / 能量代谢 / 肿瘤微环境\n\n评估论文时，额外增加一个维度：**\"课题借鉴价值\"** — 这篇论文中有什么技术、概念、实验设计可以直接复用到用户的mitoxyperiosis-乳酸化课题？\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### Claude CLI 长提示词超时陷阱\nclaude -p 传入大段文本时容易超时（exit code 124，返回空），特别是在Windows git-bash环境。\n- ❌ 一次性传入4篇论文的完整摘要+评估指令 → 超时\n- ✅ 策略1：将评估指令简化，每篇论文控制到1-3句关键信息；或拆分为多次调用分别评估单篇\n- ✅ 策略2：用 `head -N` 或 `tail -N` 截断输出（如 `claude -p \"评估...\" 2>&1 | head -60`），防止Claude生成过长内容导致超时。即使Claude内部未完成，前60行通常已包含评分结果\n\n### Cell Press PII清理模式（重要！）\nPubMed esummary返回的PII含括号和连字符（如 `S0896-6273(26)00386-7`），CDN URL需要去掉这些字符：\n- ❌ `tr -d '()'` → 只去除括号，留下连字符 → CDN返回404\n- ✅ `tr -d '()-'` → 同时去除括号和连字符 → CDN返回200\n- 详见 `references/figure-download-patterns.md` 中的修正实例\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**执行位置：terminal 而非 execute_code**\nPubMed API调用应在 `terminal` 中通过 `python -c \"...\"` 或写脚本后执行。`terminal` 中的 Python 连接更稳定，且结果可被后续terminal命令使用（写入文件、管道传递）。避免在 `execute_code` 中做PubMed检索——沙箱环境的网络连接可能不稳定，且JSON结果无法跨沙箱传递给terminal。\n\n**日期范围两种方式（方式B更可靠）**：\n```python\n# 方式A: mindate/maxdate 参数（有时返回0结果，不可靠）\nparams = {\n 'db': 'pubmed', 'term': query,\n 'mindate': '<3个月前>', 'maxdate': '<今天>',\n 'datetype': 'pdat', 'retmax': 15, 'retmode': 'json'\n}\n\n# 方式B: [dp] 查询语法（推荐，已验证可靠）\nquery = '(ferroptosis[Title/Abstract] OR ...) AND (\"2026/03/01\"[dp] : \"2026/06/12\"[dp])'\nparams = {\n 'db': 'pubmed', 'term': query,\n 'retmax': 15, 'retmode': 'json'\n}\n```\n`dp` (Date - Publication) 语法格式：`\"YYYY/MM/DD\"[dp] : \"YYYY/MM/DD\"[dp]`。日期之间需要空格+冒号+空格。此方式不受 `mindate/maxdate` 参数兼容性问题影响。\n详见 `references/pubmed-API-patterns.md` 第4节。\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- PubMed JSON返回的ID列表键名为小写 `idlist`，不是 `IdList`（驼峰）\n\n### Step 2: 获取论文详情并初筛\n\n```python\nimport urllib.request, json, time\n\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\n6. **有作者（`hascreator == 'Y'`）** — `esummary`返回的`hascreator`字段为`'N'`时表示\"No authors listed\"，通常是社论/News & Views，pubtype字段无法区分此类内容。检查方式：`r.get('hascreator', 'N') == 'Y'`\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系列: `https://www.nature.com/articles/{article_id}.pdf`（已验证：Nature, Nat Neurosci, Nat Med, Nat Commun均可下载）\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, Nat Med, Nat Commun）**：\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. 暴力枚举法（推荐，因为url模式固定—不依赖HTML解析）\nfor fig in 1 2 3 4 5 6 7; do\n url=\"https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F${ARTICLE_ID}/MediaObjects/${JOURNAL_ID}_${YEAR}_${ARTICLE_NUM}_Fig${fig}_HTML.png\"\n code=$(curl -s -o /dev/null -w \"%{http_code}\" -L \"$url\" -H \"User-Agent: Mozilla/5.0\")\n if [ \"$code\" != \"404\" ]; then\n curl -s -L \"$url\" -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > \"/c/Users/forgase/fig${fig}_b64.txt\"\n fi\ndone\n```\n\n**Figure Caption提取（Nature系列 — 紧跟图片下载之后执行）**：\n提取的caption将用于Step 6 HTML的逐图解读部分。\n```bash\ncurl -s -L -H \"User-Agent: Mozilla/5.0\" \"https://www.nature.com/articles/${ARTICLE_ID}\" \\\n | python -c \"\nimport sys, re\nhtml = sys.stdin.read()\nfigs = re.findall(r'<fig[^>]*>.*?<figcaption[^>]*>(.*?)</figcaption>', html, re.DOTALL)\nfor i, fig in enumerate(figs):\n clean = re.sub(r'<[^>]+>', '', fig).strip()\n print(f'{i+1}|{clean}')\n\"\n```\n然后将captions嵌入Python builder脚本中的字典变量。\n详见 `references/figure-download-patterns.md` 中的\"Figure Caption Extraction\"节。\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| Nat Med | s41591-026-04393-8 | 41591 | `41591_{year}_{article_num}_Fig{N}_HTML.png` |\n| Nat Commun | s41467-026-73538-7 | 41467 | `41467_{year}_{article_num}_Fig{N}_HTML.png` |\n\n- article_num 提取规则：从DOI中提取期刊ID后的倒数第二段（年份后的数字段），去前导零。如 `s41591-026-04393-8` → 编号段为 `04393` → 去前导零 → `4393`；`s41586-026-10480-0` → `10480`(无前导零即可直接使用) → `10480`；`s41593-026-02317-w` → `02317` → `2317`\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base64 data URI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含多张base64图片（5-7张原图≈10MB），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, 8):\n path = f\"C:/Users/forgase/fig{i}_b64.txt\"\n if os.path.exists(path):\n with open(path, \"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/forgase/Desktop/主题_文献解读.html\", \"w\", encoding=\"utf-8\") as f:\n f.write(html)\n```\n\n**流程总结**（4步）：\n1. terminal中`curl | base64 -w 0 > /c/Users/forgase/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Python builder脚本写入磁盘（不含base64数据，仅模板）\n3. terminal中执行该Python脚本（`python C:/Users/forgase/build_html.py` — 读取base64文件 + 构建完整HTML + 写入桌面）\n4. 验证文件存在：`ls -la /c/Users/forgase/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（⚠️ 关键：必须附上HTML文件）\n\n**格式要求**（最终消息末尾必须加上 `MEDIA:路径` 发送HTML文件）：\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\nMEDIA:C:\\Users\\forgase\\Desktop\\{文件名}.html\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**⚠️ 不做这个动作等于白做**：最终推送消息的末尾必须包含 `MEDIA:C:\\Users\\forgase\\Desktop\\{文件名}.html` 这一行，这样微信才会把HTML文件当作附件发送给用户。只发文字说\"已生成\"用户收不到文件。\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- **⚠️ 必须将HTML文件附在消息中一起发送** — 在最终消息末尾加上 `MEDIA:/path/to/file`，确保用户直接收到文件，不是只发文字\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- `references/github-access-patterns.md` — 国内网络环境下载GitHub资源的优先级策略\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\\github-access-patterns.md", "references\\html-template-structure.md", "references\\pubmed-API-patterns.md", "references\\user-project-context.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"}

{"todos": [{"id": "step1", "content": "PubMed检索PD方向论文 (最近3个月)", "status": "in_progress"}, {"id": "step2", "content": "获取论文详情并初筛", "status": "pending"}, {"id": "step3", "content": "Claude Code深度评估候选论文", "status": "pending"}, {"id": "step4", "content": "确定唯一推荐论文", "status": "pending"}, {"id": "step5", "content": "下载PDF + 提取Figure图片 + Captions", "status": "pending"}, {"id": "step6", "content": "制作公众号风格HTML深度解读", "status": "pending"}, {"id": "step7", "content": "推送消息（含MEDIA附件路径）", "status": "pending"}], "summary": {"total": 7, "pending": 6, "in_progress": 1, "completed": 0, "cancelled": 0}}

{"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| Nature Cell Biology | `\"Nat Cell Biol\"[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⚠️ JSON的id列表键名是小写 `idlist`（如 `data['esearchresult']['idlist']`），不是驼峰的 `IdList`。\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（需要去除XML标签+解码HTML实体）\n- `<AbstractText>` → 摘要段落（可以有多段，Label属性区分BACKGROUND/METHODS/RESULTS/CONCLUSIONS）\n- `<ELocationID EIdType=\"doi\">` → DOI\n- `<Journal><Title>` → 期刊全名\n- `<PubDate><Year>` + `<Month>` → 发表日期\n\nXML转义字符需要手动替换：`&#x3b1;`=α, `&#x3b2;`=β, `&#x3b3;`=γ, `&#xa0;`=空格, `&#x2060;`='', `&amp;`=&, `&lt;`=<, `&gt;`=>\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>`（含多个Label段落）\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. `mindate`/`maxdate` + `datetype` 日期过滤可能返回0结果（2026-06发现）\n使用 `mindate` + `maxdate` + `datetype=pdat/ppub/edat` 参数组合对常见查询（如 `ferroptosis[Title/Abstract]`）返回 Count=0，不返回任何PMID。PubMed API的日期参数在此环境下不可靠。\n- **修复**：改用 `dp` (Date - Publication) 范围语法直接在查询串中限定日期：\n ```python\n query = 'ferroptosis[Title/Abstract] AND (\"2026/03/01\"[dp] : \"2026/06/12\"[dp])'\n params = {'db': 'pubmed', 'term': query, 'retmax': 20, 'retmode': 'json'}\n ```\n `dp` 语法格式：`\"YYYY/MM/DD\"[dp] : \"YYYY/MM/DD\"[dp]`（日期之间需加空格、冒号、空格）。此方式已验证可靠（2026-06-12），可与其他搜索条件自由组合（如 AND 期刊过滤）。\n\n### 5. execute_code 中 PubMed API 不稳定\n在 `execute_code` 沙箱中连续调用 PubMed API 时，部分请求返回空结果（即使同一查询在前一个调用中返回了完整的 count 和 idlist）。推测与沙箱环境的连接复用或速率限制有关。\n- 修复：将 PubMed API 调用移至 `terminal(\"python -c \\\"...\\\"\")` 中执行。terminal 中的 Python 连接更稳定，返回结果一致。\n- 如果结果仍然为空，在两次 API 调用之间添加 `time.sleep(0.5)` 避免速率限制。\n\n### 6. 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- 但 Cell Press 的 Figure 图片通过 `ars.els-cdn.com` CDN 分发，可直接通过 curl 下载（详见 figure-download-patterns.md）。\n- PII 中的括号和连字符需要清理：`tr -d '()-'`\n\n## 搜索策略（两阶段工作流）\n\n### 阶段A：主题搜索\n```python\n# 方式A: mindate/maxdate（可能不可靠）\nparams = {\n 'db': 'pubmed', 'term': query,\n 'mindate': '<3月前>', 'maxdate': '<今天>',\n 'datetype': 'pdat', 'retmax': 10, 'retmode': 'json'\n}\n# 方式B: [dp] 语法（推荐，已验证可靠）\nquery = 'Parkinson disease AND (\"2026/03/01\"[dp] : \"2026/06/12\"[dp])'\nparams = {\n 'db': 'pubmed', 'term': query,\n '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}) AND (\"<3月前>\"[dp] : \"<今天>\"[dp])'\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\n5. 从XML提取时注意HTML实体和Unicode转义符的处理\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。", "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4 (Nature Neuroscience — 新验证 2026-06-12, PMID: 42151483)\n```\narticle_id = s41593-026-02267-3\njournal_id = 41593\nyear = 2026\narticle_num = 2267 # 从DOI \"02267\" 去前导零 → 2267\n\nFig1-Fig7 (lw1200): 全部 HTTP 200 ✅\nFig1-Fig3 (full): 全部 HTTP 200 ✅\nPDF: https://www.nature.com/articles/s41593-026-02267-3.pdf → HTTP 200, 26.7MB ✅\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。**注意：Nature系列通常在`/full/`下所有Figure都可用，非仅Fig1**（已验证：Nature s41586-026-10480-0, Fig1-Fig6全部200） |\n| `/lw1200/` | 宽1200px | 中等尺寸，适用于其余Figures。备选方案——若`/full/`偶有404，降级到此 |\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 (Fig1-Fig6 all HTTP 200 full/) |\n| **Nature Medicine** | **41591** | **s41591** | **✅ 2026-06** |\n| **Nature Neuroscience** | **41593** | **s41593** | **✅ 2026-06 (两篇独立验证)** |\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## Figure Caption Extraction (Nature系列 — HTML解析)\n\n### 为什么需要提取caption\nStep 6的HTML深度解读需要为每张Figure配caption文字。直接从Nature文章页HTML中提取比手动编写更准确、更快速。\n\n### 方法：Python regex解析 `<figcaption>`\n\nNature系列文章将figure caption放在 `<figcaption>` 标签内，可通过Python regex可靠提取：\n\n```bash\ncurl -s -L -H \"User-Agent: Mozilla/5.0\" \"https://www.nature.com/articles/{article_id}\" \\\n | python -c \"\nimport sys, re\nhtml = sys.stdin.read()\nfigs = re.findall(r'<fig[^>]*>.*?<figcaption[^>]*>(.*?)</figcaption>', html, re.DOTALL)\nfor i, fig in enumerate(figs):\n clean = re.sub(r'<[^>]+>', '', fig).strip()\n print(f'Figure {i+1}: {clean}')\n print()\n\"\n```\n\n### 已验证（2026-06-12，Nat Neurosci s41593-026-02267-3）\n所有7张Figure的caption均正确提取，如：\n```\nFigure 1: Fig. 1: CODEX workflow for neuroscience applications.\nFigure 2: Fig. 2: Multicellular characterization of the Aβ plaque microenvironment at the proteomic level.\nFigure 3: Fig. 3: CODEX-CNS reveals specific cellular interactions in human AD brain.\n...\n```\n\n### 在Builder脚本中使用captions\n将提取到的captions以Python变量形式嵌入builder脚本：\n```python\ncaptions = {\n 1: \"CODEX workflow for neuroscience applications.\",\n 2: \"Multicellular characterization of the Aβ plaque microenvironment at the proteomic level.\",\n # ...\n}\n```\n\n### 已知注意事项\n- Nature系列的 `<figcaption>` 目前为纯文本加少量 `<sup>` 标签，清理 `<sup>` 后即可得到干净文本\n- Cell Press系列因Cloudflare防护，页面HTML不可直接解析→caption需从PDF或手动输入\n- 部分文章可能有Extended Data Figures（Fig S1, S2等），主文章通常只含Fig1-Fig7\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 # 含有括号和连字符，需全部去除\nURL-PII: S0896627326003284 # 去除括号和连字符后的实际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# ⚠️ 必须同时去除括号和连字符：tr -d '()-'\n# \"S0896-6273(26)00328-4\" → tr -d '()-' → \"S0896627326003284\"\nPII_URL=$(echo \"$PII\" | tr -d '()-')\necho \"$PII_URL\" # → S0896627326003284\n\n```\n\n### 实例2（Neuron — 新验证 2026-06-12）\n```bash\nPMID: 42263678\nDOI: 10.1016/j.neuron.2026.05.015\nPII: S0896-6273(26)00386-7\nURL-PII: S0896627326003867 # 经 tr -d '()-' 处理\n\n# gr1-gr7 全部 HTTP 200 ✅ (含 _lrg 和无 _lrg 两种尺寸均可用)\ncurl -s \"https://ars.els-cdn.com/content/image/1-s2.0-S0896627326003867-gr1_lrg.jpg\" | base64 -w 0 > fig1_b64.txt\n# fx1: HTTP 404（非所有Cell Press文章都有Graphical Abstract）\n```\n\n### 实例（Cell Metabolism — 已验证 2026-06-11，需 tr -d '()-'）\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# ⚠️ 同样需要 tr -d '()-' 去除括号和连字符\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（修复版）\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. ⚠️ 关键：清理PII中的括号和连字符，否则CDN URL会404\nPII_CLEAN=$(echo \"$PII\" | tr -d '()-')\n\n# 3. 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-${PII_CLEAN}-gr${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# 4. 下载Graphical Abstract (可能不存在→404，正常)\ncurl -s \"https://ars.els-cdn.com/content/image/1-s2.0-${PII_CLEAN}-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全部通过，HTTP 200；PMID 42127911 + PMID 42263678** |\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"}

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{"output": "=== Phase A: Broad PD Search ===\r\nTotal count: 3304\r\nPMIDs (20): 42284533, 42283407, 42283246, 42283143, 42283118, 42282950, 42282907, 42282839, 42282830, 42282733, 42282709, 42282604, 42282569, 42282567, 42282274, 42282215, 42282212, 42282179, 42281553, 42281443\r\n\r\n=== Phase B: High-IF Journal Filtered ===\r\nTotal count: 85\r\nPMIDs (20): 42275211, 42271071, 42259820, 42234754, 42217054, 42213789, 42209780, 42204590, 42192124, 42191733, 42190663, 42186854, 42174197, 42166327, 42161331, 42161327, 42160433, 42157002, 42153334, 42140967", "exit_code": 0, "error": null}

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{"output": "PMID | Title | Journal | PubType | HasAbstract | HasCreator | DOI | PubDate\r\n------------------------------------------------------------------------------------------------------------------------\r\n42275211 | STING dampens the unfolded protein response to enable the presentation of self-a... | Cell Rep | Journal Article | Abs:Y | Cre:N | DOI:10.1016/j.celrep.2026.117497 | 2026 Jun 11\r\n42271071 | Dual-target gene therapy in Parkinson's disease: a multicenter phase 1 trial. | Nat Med | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41591-026-04436-0 | 2026 Jun 10\r\n42259820 | Ultrastructural diversity and subcellular organization of nigral Lewy pathology ... | Nat Commun | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41467-026-74083-z | 2026 Jun 8\r\n42234754 | Charting the human-specific properties of gene expression networks in the infant... | Sci Adv | Comparative Study, Journal Article | Abs:Y | Cre:N | DOI:10.1126/sciadv.aea3316 | 2026 Jun 5\r\n42217054 | GRP78 associates with alpha-synuclein in vulnerable neurons of the Parkinson's d... | Acta Neuropathol | Letter | Abs:N | Cre:N | DOI:10.1007/s00401-026-03034-1 | 2026 May 30\r\n42213789 | Action and rest tremor map to distinct networks within the primary motor cortex. | Cell Rep | Journal Article | Abs:Y | Cre:N | DOI:10.1016/j.celrep.2026.117404 | 2026 May 28\r\n42209780 | Gut microbiome screens could identify risk of Parkinson's disease years before s... | Nat Med | Journal Article | Abs:N | Cre:N | DOI:10.1038/s41591-026-04458-8 | 2026 May 28\r\n42204590 | Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic... | Mol Neurodegener | Journal Article, Review | Abs:Y | Cre:N | DOI:10.1186/s13024-026-00951-3 | 2026 May 28\r\n42192124 | Transmembrane domain switching controls PINK1 import and fate in mitochondria. | EMBO J | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s44318-026-00789-x | 2026 May 26\r\n42191733 | Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegenerati... | Nat Commun | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41467-026-73538-7 | 2026 May 26\r\n42190663 | TPPP/p25 amyloid seeding activity as a specific biomarker for multiple system at... | Cell | Journal Article | Abs:Y | Cre:N | DOI:10.1016/j.cell.2026.04.050 | 2026 May 26\r\n42186854 | Is SORL1 a common genetic target across neurodegenerative diseases? A multi-ance... | Brain | Journal Article | Abs:Y | Cre:N | DOI:10.1093/brain/awag187 | 2026 May 26\r\n42174197 | Neuroprotective effect of astrocytic dopamine Drd2 receptor on mitochondrial com... | Cell Death Differ | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41418-026-01756-z | 2026 May 22\r\n42166327 | Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autoph... | Cell Rep | Journal Article | Abs:Y | Cre:N | DOI:10.1016/j.celrep.2026.117364 | 2026 May 21\r\n42161331 | Large-scale antagonistic cerebral networks drive amplitude variability in Parkin... | Brain | Journal Article | Abs:Y | Cre:N | DOI:10.1093/brain/awag182 | 2026 May 20\r\n42161327 | CYP2D6 variants in amyotrophic lateral sclerosis: an association study of risk a... | Brain | Journal Article | Abs:Y | Cre:N | DOI:10.1093/brain/awag178 | 2026 May 20\r\n42160433 | The immunoproteome and multimorbidity: A Mendelian randomization study. | Sci Adv | Journal Article | Abs:Y | Cre:N | DOI:10.1126/sciadv.adz7117 | 2026 May 22\r\n42157002 | A multimodal biomarker strategy to enhance diagnostic precision in neurodegenera... | Nat Med | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41591-026-04398-3 | 2026 May 19\r\n42153334 | Parkinson's disease beyond the brain: erythrocyte α-synuclein transfer across th... | Brain | Journal Article | Abs:Y | Cre:N | DOI:10.1093/brain/awag179 | 2026 May 19\r\n42140967 | α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity t... | Nat Commun | Journal Article | Abs:Y | Cre:N | DOI:10.1038/s41467-026-73136-7 | 2026 May 15", "exit_code": 0, "error": null}

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{"output": "================================================================================\r\nPMID: 42271071\r\nTitle: Dual-target gene therapy in Parkinson's disease: a multicenter phase 1 trial.\r\nSource: Nat Med\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 Jun 10\r\ndoi: 10.1038/s41591-026-04436-0\r\npii: 10.1038/s41591-026-04436-0\r\n\r\n================================================================================\r\nPMID: 42259820\r\nTitle: Ultrastructural diversity and subcellular organization of nigral Lewy pathology in Parkinson's disease.\r\nSource: Nat Commun\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 Jun 8\r\ndoi: 10.1038/s41467-026-74083-z\r\npii: 10.1038/s41467-026-74083-z\r\n\r\n================================================================================\r\nPMID: 42190663\r\nTitle: TPPP/p25 amyloid seeding activity as a specific biomarker for multiple system atrophy.\r\nSource: Cell\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 26\r\ndoi: 10.1016/j.cell.2026.04.050\r\npii: S0092-8674(26)00517-9\r\n\r\n================================================================================\r\nPMID: 42174197\r\nTitle: Neuroprotective effect of astrocytic dopamine Drd2 receptor on mitochondrial complex I in a mouse model of Parkinson's disease through β-arrestin2-NDUFA10 regulation.\r\nSource: Cell Death Differ\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 22\r\ndoi: 10.1038/s41418-026-01756-z\r\npii: 10.1038/s41418-026-01756-z\r\n\r\n================================================================================\r\nPMID: 42140967\r\nTitle: α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.\r\nSource: Nat Commun\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 15\r\ndoi: 10.1038/s41467-026-73136-7\r\npii: 10.1038/s41467-026-73136-7\r\n\r\n================================================================================\r\nPMID: 42153334\r\nTitle: Parkinson's disease beyond the brain: erythrocyte α-synuclein transfer across the blood-brain barrier.\r\nSource: Brain\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 19\r\ndoi: 10.1093/brain/awag179\r\npii: 8687270\r\n\r\n================================================================================\r\nPMID: 42192124\r\nTitle: Transmembrane domain switching controls PINK1 import and fate in mitochondria.\r\nSource: EMBO J\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 26\r\ndoi: 10.1038/s44318-026-00789-x\r\npii: 10.1038/s44318-026-00789-x\r\n\r\n================================================================================\r\nPMID: 42166327\r\nTitle: Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autophagy and exacerbates alpha-synuclein aggregation.\r\nSource: Cell Rep\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 21\r\ndoi: 10.1016/j.celrep.2026.117364\r\npii: S2211-1247(26)00442-0\r\n\r\n================================================================================\r\nPMID: 42157002\r\nTitle: A multimodal biomarker strategy to enhance diagnostic precision in neurodegenerative parkinsonism.\r\nSource: Nat Med\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 19\r\ndoi: 10.1038/s41591-026-04398-3\r\npii: 10.1038/s41591-026-04398-3\r\n\r\n================================================================================\r\nPMID: 42191733\r\nTitle: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.\r\nSource: Nat Commun\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 26\r\ndoi: 10.1038/s41467-026-73538-7\r\npii: 10.1038/s41467-026-73538-7\r\n\r\n================================================================================\r\nPMID: 42127911\r\nTitle: Secreted GPNMB enhances uptake of fibrillar alpha-synuclein in a non-cell-autonomous process that can be blocked by anti-GPNMB antibodies.\r\nSource: Neuron\r\nPubTypes: ['Journal Article']\r\nHasCreator: N\r\nAttributes: ['Has Abstract']\r\nPubDate: 2026 May 12\r\ndoi: 10.1016/j.neuron.2026.04.033\r\npii: S0896-6273(26)00328-4", "exit_code": 0, "error": null}

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{"output": "================================================================================\r\nPMID: 42271071\r\nTitle: Dual-target gene therapy in Parkinson's disease: a multicenter phase 1 trial.\r\nJournal: Nature medicine\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Restoring striatal dopamine synthesis is a promising gene therapy strategy for Parkinson's disease. Previous adeno-associated virus-mediated aromatic L-amino acid decarboxylase (AADC) monotherapies remain dependent on exogenous levodopa, whereas multigene delivery is constrained by strict adeno-asso...\r\n\r\n================================================================================\r\nPMID: 42259820\r\nTitle: Ultrastructural diversity and subcellular organization of nigral Lewy pathology in Parkinson's disease.\r\nJournal: Nature communications\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Lewy bodies, the defining pathological feature of Parkinson's disease, are intraneuronal inclusions enriched in aggregated alpha-synuclein (αSyn). We used correlative light and electron microscopy to selectively investigate phosphorylated αSyn (αSynpS129)-positive inclusions in the substantia nigra ...\r\n\r\n================================================================================\r\nPMID: 42140967\r\nTitle: α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.\r\nJournal: Nature communications\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Tunneling nanotubes (TNTs) enable direct intercellular transfer of macromolecules, organelles, and pathogenic protein aggregates. While α-synuclein (α-Syn) aggregates are known to promote TNT formation, the underlying mechanisms remain poorly defined. Here, using human neuronal and microglial cell l...\r\n\r\n================================================================================\r\nPMID: 42174197\r\nTitle: Neuroprotective effect of astrocytic dopamine Drd2 receptor on mitochondrial complex I in a mouse model of Parkinson's d\r\nJournal: Cell death and differentiation\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Parkinson's disease (PD) is a progressive neurodegenerative disease. Current treatment strategies for PD mainly focus on dopamine replacement and regulation of dopaminergic signaling. Here, we reveal the unique role of the astrocytic dopamine D2 (Drd2) receptor in regulating mitochondrial function, ...\r\n\r\n================================================================================\r\nPMID: 42166327\r\nTitle: Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autophagy and exacerbates alpha-synuclein aggr\r\nJournal: Cell reports\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Parkinson disease (PD)-associated mutations in the LRRK2 gene hyperactivate LRRK2 kinase activity, leading to increased phosphorylation of a subset of RAB GTPases, which are master regulators of intracellular trafficking. In neurons, processive retrograde transport of autophagosomes is essential for...\r\n\r\n================================================================================\r\nPMID: 42191733\r\nTitle: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and\r\nJournal: Nature communications\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: The autophagy-tethering factor ectopic P-granule 5 autophagy protein (EPG5) plays a key role in autophagosome-lysosome fusion. Impaired autophagy associated with pathogenic variants in EPG5 causes a rare devastating multisystem disorder known as Vici syndrome, which features neurodevelopmental defec...\r\n\r\n================================================================================\r\nPMID: 42127911\r\nTitle: Secreted GPNMB enhances uptake of fibrillar alpha-synuclein in a non-cell-autonomous process that can be blocked by anti\r\nJournal: Neuron\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Glycoprotein nonmetastatic melanoma B (GPNMB) is critical to cellular uptake of pathological forms of alpha-synuclein (aSyn), the hallmark disease protein in Parkinson's disease (PD). Here, we demonstrate that the non-membrane-anchored, extracellular domain of GPNMB can function in a non-cell-autono...\r\n\r\n================================================================================\r\nPMID: 42153334\r\nTitle: Parkinson's disease beyond the brain: erythrocyte α-synuclein transfer across the blood-brain barrier.\r\nJournal: Brain : a journal of neurology\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Parkinson's disease is characterized by the accumulation and propagation of α-synuclein pathology in the central nervous system, yet the contribution of peripheral α-synuclein sources remains unclear. Here, we identify erythrocytes as an important reservoir of α-synuclein and demonstrate that bone m...\r\n\r\n================================================================================\r\nPMID: 42192124\r\nTitle: Transmembrane domain switching controls PINK1 import and fate in mitochondria.\r\nJournal: The EMBO journal\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Mitochondrial targeting of the PINK1 kinase results, under normal conditions, in membrane-potential-driven inner membrane penetration and cleavage by the resident protease PARL before retro-translocation and proteasomal degradation. In compromised mitochondria, with reduced membrane potential, inner...\r\n\r\n================================================================================\r\nPMID: 42190663\r\nTitle: TPPP/p25 amyloid seeding activity as a specific biomarker for multiple system atrophy.\r\nJournal: Cell\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Detection of α-synuclein (α-syn) amyloid seeds in human biofluids has attracted great interest for clinical diagnosis of synucleinopathies. However, as a common biomarker, α-syn lacks specificity in reliably differentiating distinct disorders. Here, we report tubulin polymerization promoting protein...\r\n\r\n================================================================================\r\nPMID: 42157002\r\nTitle: A multimodal biomarker strategy to enhance diagnostic precision in neurodegenerative parkinsonism.\r\nJournal: Nature medicine\r\nAuthors: 0\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Differential diagnosis of neurodegenerative parkinsonian syndromes is complicated by overlapping clinical features and frequent co-pathology that challenges the interpretation of single-protein biomarkers. We evaluated a multimodal, minimally invasive biomarker strategy integrating dermal α-synuclei...", "exit_code": 0, "error": null}

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{"output": "PD+Lactate: Count=0, IDs=\r\nPD+RhoA_GTPase: Count=0, IDs=\r\nPD+Mitochondria: Count=13, IDs=42275211, 42204590, 42192124, 42174197, 42140184, 42066086, 42062290, 42052893, 41997149, 41992946\r\nPD+Fasting: Count=5, IDs=42204590, 42161327, 42052893, 42015416, 41997149", "exit_code": 0, "error": null}

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{"output": "PMID: 42140184\r\nTitle: Transplantation of encapsulated mitochondria alleviates dysfunction in mitochondrial and Parkinson's disease models.\r\nJournal: Cell\r\nDOI: 10.1016/j.cell.2026.05.004\r\nPubTypes: <PublicationType UI=\"D016425\">Published Erratum\r\nAbstract: \r\n\r\nPMID: 42066086\r\nTitle: Piezoelectric neuromodulation of the subthalamic nucleus ameliorates motor and nonmotor symptoms of Parkinson's disease.\r\nJournal: Science advances\r\nDOI: 10.1126/sciadv.aec6955\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Traditional deep-brain stimulation via implanted electrodes can effectively treat neurological disorders, but surgical injury limits its clinical application. Here, we developed ultrasound-responsive piezoelectric nanoparticles for minimal-invasive a...\r\n\r\nPMID: 42062290\r\nTitle: Nuclear genetic modulation of tissue-specific mitochondrial RNA processing contributes to common disease risk.\r\nJournal: Nature communications\r\nDOI: 10.1038/s41467-026-72649-5\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Mitochondrial dysfunction is widely implicated in human disease, yet whether it plays a causal role and why effects are tissue-specific remain unclear. Here, we analyse over 15,000 RNA-sequencing datasets from 49 tissue types integrated with germline...\r\n\r\nPMID: 42052893\r\nTitle: Comparative transcriptomics reveal molecular convergence and divergence in parkinsonian disorders.\r\nJournal: Brain : a journal of neurology\r\nDOI: 10.1093/brain/awag153\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Neurodegenerative parkinsonisms are phenotypically diverse disorders including Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration. These currently incurable diseases ...\r\n\r\nPMID: 41997149\r\nTitle: SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\nJournal: Neuron\r\nDOI: 10.1016/j.neuron.2026.03.027\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: 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 ...\r\n\r\nPMID: 41992946\r\nTitle: Blood mtDNA markers of mitochondrial subtype and early-onset Parkinson's disease biology.\r\nJournal: Brain : a journal of neurology\r\nDOI: 10.1093/brain/awag135\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Mitochondrial dysfunction is central to the pathogenesis of Parkinson's disease (PD), integrating both genetic and environmental factors. Therefore, reliable blood-based biomarkers reflecting mitochondrial alterations are needed. Emerging evidence su...\r\n\r\nPMID: 42015416\r\nTitle: Machine learning model based on plasma proteomics for the identification of Parkinson's disease.\r\nJournal: Brain : a journal of neurology\r\nDOI: 10.1093/brain/awag140\r\nPubTypes: <PublicationType UI=\"D016428\">Journal Article\r\nAbstract: Developing reliable biomarkers capable of differentiating Parkinson's disease from other neurological conditions is crucial for both patient care and research. In this study, we leveraged recent advances in high-throughput proteomic technology and ma...", "exit_code": 0, "error": null}

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{"output": "=== PAPER ===\r\nPMID: 42140967\r\nTITLE: α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication.\r\nJOURNAL: Nature communications (2026)\r\nDOI: 10.1038/s41467-026-73136-7\r\nABSTRACT: Tunneling nanotubes (TNTs) enable direct intercellular transfer of macromolecules, organelles, and pathogenic protein aggregates. While α-synuclein (α-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 α-Syn aggregates induce severe mitochondrial damage, leading to cytosolic release of mitochondrial DNA (mtDNA) and activation of the cGAS-STING-NF-κB-IRF3 pathway. This innate immune response drives actin cytoskeleton remodeling and the formation of TNT-like structures, promoting intercellular transfer of α-Syn from neurons to microglia. Additionally, neuronal cells transfer damaged mitochondria to microglia, where they undergo lysosome-mediated degradation. Neuron-to-microglia communication under α-Syn-induced stress also triggers a bystander inflammatory response in microglia, suggesting a neuroimmune activation. Our findings identify mitochondrial damage and STING-mediated inflammation as key drivers of TNT formation and α-Syn propagation, highlighting potential targets to modulate disease progression in Synucleinopathies. \r\n\r\n=== PAPER ===\r\nPMID: 42259820\r\nTITLE: Ultrastructural diversity and subcellular organization of nigral Lewy pathology in Parkinson's disease.\r\nJOURNAL: Nature communications (2026)\r\nDOI: 10.1038/s41467-026-74083-z\r\nABSTRACT: Lewy bodies, the defining pathological feature of Parkinson's disease, are intraneuronal inclusions enriched in aggregated alpha-synuclein (αSyn). We used correlative light and electron microscopy to selectively investigate phosphorylated αSyn (αSynpS129)-positive inclusions in the substantia nigra of end-stage postmortem Parkinson's disease brain. Here we show that somatic αSynpS129 inclusions in nigral dopaminergic neurons are consistently fibrillar, whereas the membranous-type inclusions are restricted to neuritic processes. These neuritic inclusions displayed marked ultrastructural heterogeneity, ranging from predominantly membranous to mixed membranous-fibrillar forms. The selective targeting of defined inclusions enabled detailed structural characterization of Lewy pathology, rather than quantitative or disease-stage comparisons. Our findings highlight clear ultrastructural differences between somatic and neuritic αSynpS129 pathology and demonstrate the structural complexity and heterogeneity of Lewy pathology in human Parkinson's disease brain. \r\n\r\n=== PAPER ===\r\nPMID: 42174197\r\nTITLE: Neuroprotective effect of astrocytic dopamine Drd2 receptor on mitochondrial complex I in a mouse model of Parkinson's disease through β-arrestin2-NDUFA10 regulation.\r\nJOURNAL: Cell death and differentiation (2026)\r\nDOI: 10.1038/s41418-026-01756-z\r\nABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disease. Current treatment strategies for PD mainly focus on dopamine replacement and regulation of dopaminergic signaling. Here, we reveal the unique role of the astrocytic dopamine D2 (Drd2) receptor in regulating mitochondrial function, thereby improving Parkinson's disease-like symptoms in a mouse model. Transcriptome sequencing and metabolomics suggest that deletion of astrocytic Drd2 receptor significantly aggravates mitochondrial dysfunction. Mechanistically, we demonstrate that the Drd2 receptor regulates mitochondrial complex I activity by recruiting the scaffold protein β-arrestin2, which facilitates its interaction with NDUFA4 and NDUFA10, two subunits of mitochondrial complex I. Notably, the neuroprotective effect of Drd2 activation in vivo was completely abolished upon selective knockdown of NDUFA10 in mouse astrocytes. The identification of this novel mechanistic axis not only elucidates how astrocytes maintain neuronal mitochondrial homeostasis via dopaminergic signaling but also establishes a transformative framework for the development of targeted combination therapies that concurrently address mitochondrial dysfunction and dopamine receptor dysregulation as a promising avenue for advancing PD treatment strategies. \r\n\r\n=== PAPER ===\r\nPMID: 42127911\r\nTITLE: Secreted GPNMB enhances uptake of fibrillar alpha-synuclein in a non-cell-autonomous process that can be blocked by anti-GPNMB antibodies.\r\nJOURNAL: Neuron (2026)\r\nDOI: 10.1016/j.neuron.2026.04.033\r\nABSTRACT: Glycoprotein nonmetastatic melanoma B (GPNMB) is critical to cellular uptake of pathological forms of alpha-synuclein (aSyn), the hallmark disease protein in Parkinson's disease (PD). Here, we demonstrate that the non-membrane-anchored, extracellular domain of GPNMB can function in a non-cell-autonomous manner. In the human brain, GPNMB is widely expressed in neurons and microglia. In induced pluripotent stem cell-derived microglia (iMicroglia), GPNMB expression and secretion increase with exposure to apoptotic neurons. In the aSyn fibril-seeded model of PD, iMicroglia-derived GPNMB enhances neuronal aSyn uptake and development of aSyn pathology, including in GPNMB knockout neurons. Conversely, anti-GPNMB antibodies rescue neurons from developing aSyn pathology. Finally, in 1,675 human postmortem cases, GPNMB genotypes conferring higher GPNMB expression are associated with more widespread aSyn pathology. Our data suggest a positive feedback loop, where neurodegeneration triggers increased microglial GPNMB secretion, leading to increased neuronal aSyn pathology and neurodegeneration. Importantly, this cycle can be therapeutically interrupted by anti-GPNMB antibodies. \r\n\r\n=== PAPER ===\r\nPMID: 42191733\r\nTITLE: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.\r\nJOURNAL: Nature communications (2026)\r\nDOI: 10.1038/s41467-026-73538-7\r\nABSTRACT: The autophagy-tethering factor ectopic P-granule 5 autophagy protein (EPG5) plays a key role in autophagosome-lysosome fusion. Impaired autophagy associated with pathogenic variants in EPG5 causes a rare devastating multisystem disorder known as Vici syndrome, which features neurodevelopmental defects, severe progressive neurodegeneration and immunodeficiency. The pathophysiological mechanisms driving disease presentation and progression are only partially understood. In patient-derived fibroblasts and iPS cells differentiated to cortical neurons, we find that impaired mitophagy leads to mitochondrial bioenergetic dysfunction. Physiological cytosolic Ca2+ transients result in unexpected mitochondrial Ca2+ overload despite a decrease in mitochondrial membrane potential. This is attributed to downregulation of MICU1. Ca2+ signals cause mitochondrial depolarisation, mtDNA release and activation of the cGAS-STING pathway, reversed by pharmacological inhibition of the mitochondrial permeability transition pore (mPTP) or of the STING pathway. Thus, we identify a pathophysiological cascade driving disease progression associated with EPG5 deficiency, including impaired mitochondrial bioenergetics, mitochondrial Ca2+ overload, vulnerability to mPTP opening and activation of innate immune signalling, signposting multiple potential therapeutic targets. \r\n\r\n=== PAPER ===\r\nPMID: 41997149\r\nTITLE: SARM1 executes neuronal parthanatos and promotes excitotoxic cell death.\r\nJOURNAL: Neuron (2026)\r\nDOI: 10.1016/j.neuron.2026.03.027\r\nABSTRACT: 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 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-pyridinium (MPP+) dopaminergic neuron toxicity and N-methyl-D-aspartate (NMDA) excitotoxicity, are potently protected by SARM1 inhibition. These findings place SARM1 at the nexus of multiple mechanisms driving neuronal cell death, thereby greatly expanding the potential clinical utility of SARM1 inhibitors beyond diseases of axon loss. \r\n\r\n=== PAPER ===\r\nPMID: 42271071\r\nTITLE: Dual-target gene therapy in Parkinson's disease: a multicenter phase 1 trial.\r\nJOURNAL: Nature medicine (2026)\r\nDOI: 10.1038/s41591-026-04436-0\r\nABSTRACT: Restoring striatal dopamine synthesis is a promising gene therapy strategy for Parkinson's disease. Previous adeno-associated virus-mediated aromatic L-amino acid decarboxylase (AADC) monotherapies remain dependent on exogenous levodopa, whereas multigene delivery is constrained by strict adeno-associated virus packaging limits. A 'dual approach' targeting the two rate-limiting enzymes, tyrosine hydroxylase (TH) and AADC, offers the potential for autonomous dopamine synthesis. We report the 12-month primary safety and tolerability outcomes of a multicenter, open-label, dose-escalation, phase 1 trial evaluating BBM-P002, a new adeno-associated virus vector-AAVT42-codelivering constitutively active TH and AADC. Ten participants with moderate-to-advanced Parkinson's disease were enrolled and received bilateral intraputaminal infusions across doses of 4.0 × 1011 vg (Cohort 1; n = 1), 6.0 × 1011 vg (Cohort 2; n = 2), 1.0 × 1012 vg (Cohort 3; n = 2) and 1.2 × 1012 vg (Cohort 4; n = 5). The trial achieved its primary outcome, as BBM-P002 demonstrated a favorable safety and tolerability profile within 12 months post-treatment. No dose-limiting toxicities or drug-related serious adverse events occurred. A total of 23 adverse events were reported, all judged unrelated to BBM-P002 and primarily mild and transient. Systemic toxicity and clinically meaningful immunogenicity were absent. In conclusion, intraputaminal delivery of BBM-P002 was safe and well tolerated in this phase 1 trial, supporting continued clinical development. ClinicalTrials.gov registration: NCT05822739 . \r\n\r\n=== PAPER ===\r\nPMID: 42166327\r\nTITLE: Knockout of the LRRK2-counteracting RAB phosphatase PPM1H disrupts axonal autophagy and exacerbates alpha-synuclein aggregation.\r\nJOURNAL: Cell reports (2026)\r\nDOI: 10.1016/j.celrep.2026.117364\r\nABSTRACT: Parkinson disease (PD)-associated mutations in the LRRK2 gene hyperactivate LRRK2 kinase activity, leading to increased phosphorylation of a subset of RAB GTPases, which are master regulators of intracellular trafficking. In neurons, processive retrograde transport of autophagosomes is essential for autophagosome maturation and effective degradation of autophagosomal cargo in the axon. Here, we show that knockout of the LRRK2-counteracting RAB phosphatase PPM1H causes a gene-dose-dependent disruption of the axonal transport of autophagosomes, leading to impaired degradation of axonal alpha-synuclein (aSyn), a key protein in PD pathophysiology. Defective autophagosome transport and impaired aSyn degradation correlate with increased aSyn aggregation in primary PPM1H knockout neurons exposed to preformed fibrils of aSyn, an effect that is dependent on LRRK2 kinase activity. These findings mechanistically link LRRK2-mediated RAB hyperphosphorylation to defective autophagosomal degradation and enhanced aggregation of aSyn, positioning the LRRK2-RAB axis as a key driver of PD pathophysiology. \r\n\r\n=== PAPER ===\r\nPMID: 42192124\r\nTITLE: Transmembrane domain switching controls PINK1 import and fate in mitochondria.\r\nJOURNAL: The EMBO journal (2026)\r\nDOI: 10.1038/s44318-026-00789-x\r\nABSTRACT: Mitochondrial targeting of the PINK1 kinase results, under normal conditions, in membrane-potential-driven inner membrane penetration and cleavage by the resident protease PARL before retro-translocation and proteasomal degradation. In compromised mitochondria, with reduced membrane potential, inner membrane incorporation is not achieved, which leads to surface activation of the full-length protein, Parkin recruitment and mitophagy. Here, we identify a third pathway in which PINK1 is imported into the mitochondrial matrix. Structural modelling predicts that PINK1's transmembrane domain (TMD) is conformationally plastic, forming either an α-helix or α/β-hybrid at the interface between Tim17 of the TIM23-complex for engagement of either ROMO1 or PARL. These mutually exclusive assemblies define distinct protein-import channels with differing biological roles. PINK1's α-helical TMD adopts a pose suggestive of translocation through the ROMO1/Tim17-channel, while the α/β-hybrid engages PARL and is cleaved. We propose that TMD structural plasticity determines whether PINK1 is imported into the matrix or cleaved and retro-translocated. The results expand the role of PINK1 beyond that of a damage sensor and imply a role in healthy mitochondrial function with potential relevance to Parkinson's disease.", "exit_code": 0, "error": null}

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{"todos": [{"id": "step1", "content": "PubMed检索PD方向论文 (最近3个月)", "status": "completed"}, {"id": "step2", "content": "获取论文详情并初筛", "status": "completed"}, {"id": "step3", "content": "Claude Code深度评估候选论文", "status": "in_progress"}, {"id": "step4", "content": "确定唯一推荐论文", "status": "pending"}, {"id": "step5", "content": "下载PDF + 提取Figure图片 + Captions", "status": "pending"}, {"id": "step6", "content": "制作公众号风格HTML深度解读", "status": "pending"}, {"id": "step7", "content": "推送消息（含MEDIA附件路径）", "status": "pending"}], "summary": {"total": 7, "pending": 4, "in_progress": 1, "completed": 2, "cancelled": 0}}

{"output": "{\"total\": 38, \"dimensions\": {\"logic\": 8, \"methods\": 8, \"innovation\": 7, \"relevance\": 8, \"translation\": 7}, \"recommend\": true, \"reason\": \"线粒体损伤→肌动蛋白重塑→细胞间通讯的逻辑链与RhoA乳酰化驱动线粒体位移拮抗mitoxyperiosis高度平行，cGAS-STING通路及TNT成像策略可直接借鉴。\"}", "exit_code": 0, "error": null}

{"output": "{\"total\": 39, \"dimensions\": {\"logic\": 9, \"methods\": 8, \"innovation\": 7, \"relevance\": 6, \"translation\": 9}, \"recommend\": true, \"reason\": \"SARM1-NAD+-mitochondrial depolarization axis parallels the user's mitochondrial displacement mechanism in neuronal death, offering transferable methodology for mitochondrial phenotyping in cell death studies despite distinct upstream pathways.\"}", "exit_code": 0, "error": null}

{"output": "{\"total\": 36, \"dimensions\": {\"logic\": 8, \"methods\": 8, \"innovation\": 8, \"relevance\": 5, \"translation\": 7}, \"recommend\": false, \"reason\": \"Novel Drd2-beta-arrestin2-NDUFA10 axis in astrocytic mitochondria but limited mechanistic overlap with Warburg-lactate-PCAF-RhoA lactylation-mitoxyperiosis project\"}", "exit_code": 0, "error": null}

{"output": "{\"total\": 41, \"dimensions\": {\"logic\": 9, \"methods\": 9, \"innovation\": 9, \"relevance\": 5, \"translation\": 9}, \"recommend\": true, \"reason\": \"Top-tier aSyn propagation mechanism with antibody therapy; limited mechanistic overlap with lactylation/mitoxyperiosis but methodological paradigms (iPSC, human genetics, non-cell-autonomous logic) transferable.\"}", "exit_code": 0, "error": null}

{"output": "```json\n{\n \"逻辑完整性\": 8,\n \"方法学水平\": 7,\n \"创新性\": 8,\n \"可借鉴性\": 6,\n \"临床转化潜力\": 7\n}\n```", "exit_code": 0, "error": null}

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