[IMPORTANT: The user has invoked the "paper-recommender" skill, indicating they want you to follow its instructions. The full skill content is loaded below.]
---
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"
version: 2.2.0
author: Hermes
tags: [PubMed, 论文推荐, Claude评估, 文献解读, 科研]
---
# 📚 每日论文推荐工作流 (Paper Recommender)
## 职责
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。
## 用户研究方向
1. 帕金森病(PD) / GZR18 / α-synuclein
2. 神经炎症 / 小胶质细胞 / 星形胶质细胞
3. 细胞死亡方式 (Mitoxyperiosis / 铁死亡 / 焦亡 / 泛素化降解)
4. 外泌体 / 细胞外囊泡 / 神经退行性疾病
5. 脑缺血 / 脑卒中 / 神经保护
6. 生信分析 / 单细胞测序 / 多组学
## 定时推送安排
| 时间 | 主题 | 关键词 |
|:----:|------|--------|
| 08:00 | PD/帕金森病 | Parkinson's disease, α-synuclein, MPTP, dopamine neuron |
| 11:00 | 神经炎症/胶质细胞 | neuroinflammation, microglia, astrocyte, NLRP3 |
| 13:00 | 细胞死亡/信号通路 | cell death, mitoxyperiosis, ferroptosis, ubiquitination |
| 15:00 | 外泌体/细胞通讯 | exosome, extracellular vesicle, neural, brain |
| 17:00 | 脑缺血/神经保护 | cerebral ischemia, stroke, neuroprotection, MCAO |
| 19:00 | 生信/前沿技术 | single-cell, multi-omics, bioinformatics, spatial transcriptomics |
## ⚠️ 已知工具陷阱
### 文件系统隔离（重要！）
`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。
- ❌ 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
- ✅ 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）
- ✅ 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
### 大文件HTML生成
当HTML嵌入base64图片时（5张Nature原图 ≈ 4MB），`write_file`会因大小限制失败。
- ❌ 不要直接用write_file写4MB+的HTML
- ✅ 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
### Claude CLI 长提示词超时陷阱
claude -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。
- ❌ 一次性传入4篇论文的完整摘要+评估指令 → 超时
- ✅ 策略：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
### Cell Press PII清理模式（重要！）
PubMed 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：
- ❌ `tr -d '()'` → 只去除括号，留下连字符 → CDN返回404
- ✅ `tr -d '()-'` → 同时去除括号和连字符 → CDN返回200
- 详见 `references/figure-download-patterns.md` 中的修正实例
### Windows Python路径陷阱
在 Windows git-bash 中，Python 脚本不识别 MSYS 路径格式（`/c/Users/...`）：
- ❌ `open("/c/Users/forgase/fig1_b64.txt")` → FileNotFoundError
- ✅ `open("C:/Users/forgase/fig1_b64.txt")` — 正斜杠在 Windows Python 中可识别
- 同理，`python3` 命令在 Windows 上可能被应用执行别名拦截 → 始终使用 `python`
## 执行流程（完整版）
### Step 1: PubMed检索 — 两阶段策略
**方式：Python urllib**（推荐，避免curl的SSL/编码问题）
```python
import urllib.request, urllib.parse, json
params = {
'db': 'pubmed', 'term': query,
'mindate': '<3个月前>', 'maxdate': '<今天>',
'datetype': 'pdat', 'retmax': 15, 'retmode': 'json'
}
url = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?' + urllib.parse.urlencode(params)
```
**阶段A — 主题搜索**：用关键词搜该方向近期论文
**阶段B — 高IF期刊过滤**：用主题词 + `("Nature"[Journal] OR "Cell"[Journal] OR ...)` 格式搜
⚠️ 关键陷阱：
- `sort=date` 被PubMed忽略（返回warning），不要用
- 期刊名必须用 `"全称"[Journal]` 格式，裸词会被翻译为MeSH词条
- 复杂查询在curl中容易URL编码失败，优先用Python
### Step 2: 获取论文详情并初筛
```python
# 获取元数据
url = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&id=<PMIDs>&retmode=json'
# 获取摘要
url = 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=<PMIDs>&retmode=xml'
```
**初筛硬性门槛**（必须同时满足）：
1. IF > 10 或领域顶刊
2. 2026年3月后发表
3. 与用户研究方向直接相关
4. 原创研究（pubtype不含Review）
5. 非 News & Views / Letter / 编辑评论
### Step 3: Claude Code深度评估（Hermes + Claude 双重评判）
将经过初筛的候选论文交给 Claude Code 严格评估：
```
claude -p "严格评估以下论文，从5个维度各评1-10分..."
```
**5维度评分**：
1. **逻辑完整性** (1-10)：完整正反验证（gain+loss of function）、KO/KI模型
2. **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）
3. **创新性** (1-10)：新概念/新机制/新方法，首次报道
4. **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**
5. **临床转化潜力** (1-10)：体内验证或治疗意义
### Step 4: 唯一推荐（核心规则）
- Claude评分 < 30分（平均<6分）或任何单维度 < 5分 → **不推荐**，跳过
- 多个候选都达标 → **只选最优的1篇**，不要让用户选
- Hermes再次确认质量 + 相关性 + 可借鉴性 → 只有双方都确认才通过
- **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**
### Step 5: 下载PDF + 提取Figure图片
**PDF下载**：
- Nature: `https://www.nature.com/articles/{article_id}.pdf`
- Cell Press/Elsevier: PDF有ScienceDirect防护，通常无法通过curl下载
- 所有期刊的Figure图片可通过CDN下载（详见`references/figure-download-patterns.md`）
- 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
**Figure提取（Nature系列通用模式 — 已验证 Nature & Nat Neurosci）**：
```bash
# 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）
curl -s -L -H "User-Agent: Mozilla/5.0" "https://www.nature.com/articles/{article_id}" \
| grep -oP 'https://media\.springernature\.com/[^"'"'"'<>]+s415\d\d[^"'"'"'<>]*\.(?:png|jpg|webp)' \
| sort -u
# 2. 下载每个figure为base64（用于HTML嵌入）
# 先用grep确定实际的journal_id/year/article_num，然后：
FIG_URL="https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F{s415XX-...}/MediaObjects/{journal_id}_{year}_{article_num}_Fig{N}_HTML.png"
curl -s "$FIG_URL" -H "User-Agent: Mozilla/5.0" | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt
```
**分辨率选择**：
- `/full/` — 最高分辨率（推荐用于Fig1）
- `/lw1200/` — 宽1200px（其余Figures用此即可）
- `/m685/` — 宽685px（小尺寸）
**已验证的图片URL模式**：
| 期刊 | article_id 示例 | journal_id | URL模式 |
|------|----------------|------------|---------|
| Nature | s41586-026-10597-2 | 41586 | `41586_{year}_{article_num}_Fig{N}_HTML.png` |
| Nat Neurosci | s41593-026-02317-w | 41593 | `41593_{year}_{article_num}_Fig{N}_HTML.png` |
- 参考 `references/figure-download-patterns.md` 获取各期刊的详细URL模式
### Step 6: 制作公众号风格HTML深度解读 — Python Builder模式
HTML文件要求：
1. 所有图片用JS变量(base64)嵌入，不使用file://协议
2. 仿公众号排版（简洁卡片风格）
3. 每条结果配"复现建议"（🔬 复现建议：...）
4. 包含论文原图 + 逐图解读 + 文章小结
5. 保存到桌面，文件命名规范：`{主题关键词}_文献解读.html`
**实现方法**（大文件HTML必须用此方式）：
由于HTML含5张base64图片（~4MB），不能直接用`write_file`写入。
```python
# 1. 先读取base64数据（terminal工具写入的文件）
# ⚠️ 重要：Windows Python不识别 MSYS 路径 /c/Users/，必须用 C:/Users/ 格式
fig_b64 = {}
for i in range(1, 7):
with open(f"C:/Users/<user>/fig{i}_b64.txt", "r") as f:
fig_b64[f"fig{i}"] = f.read().strip()
# 2. 构建HTML字符串（用f-string嵌入base64）
html = f'''...<img src="data:image/png;base64,{fig_b64['fig1']}">...'''
# 3. 写入文件（使用正斜杠路径，Windows Python可识别）
with open("C:/Users/<user>/Desktop/外泌体_文献解读.html", "w", encoding="utf-8") as f:
f.write(html)
```
**流程总结**（6步）：
1. terminal中`curl | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt` 下载所有图片（保存到用户目录，/tmp/在沙箱中不可用）
2. 用`write_file`将HTML builder脚本写入磁盘（不含base64数据，仅模板）
3. terminal中执行该Python脚本（读取base64文件 + 构建完整HTML + 写入桌面）
4. 验证HTML和PDF文件存在：`ls -la /c/Users/<user>/Desktop/`
**HTML模板风格指南**：
- 头部：渐变深蓝背景 + 白色文字 + 标签徽章
- 评分卡片：flex网格布局，5维度评分条
- 图文解读：Fig依次排列，每个配canvas+caption+复现建议
- 文章小结：渐变紫色卡片
- 参考 `references/html-template-structure.md` 获取模板框架
### Step 7: 微信推送（⚠️ 关键：必须附上HTML文件）
**格式要求**（最终消息末尾必须加上 `MEDIA:路径` 发送HTML文件）：
```
🔥 {时间} {主题} 论文推荐
🏆 标题...
📅 日期 | 📰 期刊
⭐ Claude评分：X/50
💡 推荐理由：...
MEDIA:C:\Users\forgase\Desktop\{文件名}.html
```
**如果当天没有好论文**：
```
📭 {时间} {主题}
今天这个方向没有找到特别适合你的论文，下次继续关注。
```
**⚠️ 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。
## 核心原则
- **只推1篇** —— 不要让用户从多个候选中选择
- **宁缺毋滥** —— 没有好论文就不推，不强塞
- **Hermes + Claude 双重把关** —— 都确认完美适合才推
- **不推荐综述**（除非极高价值）
- **不推荐与用户研究方向无关的论文**（即使评分高）
- **推送语言用中文**，但保留英文标题和期刊名
- **⚠️ 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
## 参考文件
- `references/pubmed-API-patterns.md` — PubMed E-utilities API详细笔记
- `references/figure-download-patterns.md` — Nature/Cell/Elsevier等期刊的图片URL提取模式
The user has provided the following instruction alongside the skill invocation: [IMPORTANT: You are running as a scheduled cron job. DELIVERY: Your final response will be automatically delivered to the user — do NOT use send_message or try to deliver the output yourself. Just produce your report/output as your final response and the system handles the rest. SILENT: If there is genuinely nothing new to report, respond with exactly "[SILENT]" (nothing else) to suppress delivery. Never combine [SILENT] with content — either report your findings normally, or say [SILENT] and nothing more.]
你是Hermes，用户的科研助手。加载 paper-recommender skill。
今日任务：搜索**细胞死亡机制/信号通路**相关高质量论文（mitoxyperiosis/ferroptosis/pyroptosis/ubiquitination），经过Hermes+Claude双重评判后，**只推最优的1篇**，做成HTML深度解读并**必须通过MEDIA:路径附在消息末尾一起发送**。
主题关键词：cell death, mitoxyperiosis, ferroptosis, pyroptosis, ubiquitination, necroptosis
日期范围：最近3个月内发表
期刊要求：IF > 10 或领域顶刊
遵循 paper-recommender skill 的完整6步流程（PubMed检索→获取详情→Claude评估→唯一选定→下载PDF+提取原图→Python builder生成HTML）。
**⚠️ 关键：最终微信消息末尾必须加上一行 `MEDIA:C:\Users\forgase\Desktop\{文件名}.html`，这样HTML文件才会作为附件发送给用户。**
论文推荐-13-细胞死亡 · Jun 12 13:12
2026-06-12 13:00 · 61 条 · deepseek-v4-flash
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"success": true, "name": "paper-recommender", "file": "references/figure-download-patterns.md", "content": "# 学术期刊Figure下载模式速查\n\n## Nature 系列\n**已验证模式（2026年6月）**\n\n### URL结构\n```\n文章页: https://www.nature.com/articles/{article_id}\nFigure URL: https://media.springernature.com/{size}/springer-static/image/\n art%3A10.1038%2F{article_id}/MediaObjects/\n {journal_id}_{year}_{article_num}_Fig{N}_HTML.png\n```\n\n### 关键参数\n- `{article_id}`: DOI中`/`后面的部分，如 `s41586-026-10597-2` 或 `s41593-026-02317-w`\n- `{journal_id}`: 期刊对应数字ID，如 Nature=41586, Nat Neurosci=41593\n- `{year}`: 4位年份\n- `{article_num}`: 文章编号（DOI中期刊ID后的数字部分，去连字符）\n- `{N}`: Figure编号（1-7）\n\n### 实例1 (Nature — 已验证 2026-06)\n```\narticle_id = s41586-026-10597-2\njournal_id = 41586\nyear = 2026\narticle_num = 10597\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41586-026-10597-2/MediaObjects/41586_2026_10597_Fig1_HTML.png\n\nFig2 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41586-026-10597-2/MediaObjects/41586_2026_10597_Fig2_HTML.png\n```\n\n### 实例2 (Nature Neuroscience — 已验证 2026-06)\n```\narticle_id = s41593-026-02317-w\njournal_id = 41593\nyear = 2026\narticle_num = 2317\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41593-026-02317-w/MediaObjects/41593_2026_2317_Fig1_HTML.png\n\nFig4 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41593-026-02317-w/MediaObjects/41593_2026_2317_Fig4_HTML.png\n```\n\n### 实例3 (Nature Medicine — 已验证 2026-06-11)\n```\narticle_id = s41591-026-04393-8\njournal_id = 41591\nyear = 2026\narticle_num = 4393\n\nFig1 全尺寸:\nhttps://media.springernature.com/full/springer-static/image/art%3A10.1038%2Fs41591-026-04393-8/MediaObjects/41591_2026_4393_Fig1_HTML.png\n\nFig2-Fig5 中等尺寸:\nhttps://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41591-026-04393-8/MediaObjects/41591_2026_4393_Fig2_HTML.png\n...\nhttps://media.springernature.com/lw1200/...41591_2026_4393_Fig5_HTML.png\n\narticle_num提取: DOI \"s41591-026-04393-8\" → 取s41591后的两段 \"026\"+\"04393\" → 截取最终段的数字部分去前导零 → 4393\n```\n\n### 快速提取命令（curl + grep）\n```bash\n# 1. 从HTML提取所有Figure URL（通用模式，匹配所有s415XX系列期刊）\ncurl -s -L -H \"User-Agent: Mozilla/5.0\" \\\n \"https://www.nature.com/articles/{article_id}\" \\\n | grep -oP 'https://media\\.springernature\\.com/[^\"'\"'\"'<>]+s415\\d\\d[^\"'\"'\"'<>]*\\.(?:png|jpg|webp)' \\\n | sort -u\n\n# 2. 下载某张Figure为base64（用于HTML嵌入）\nFIG_URL=\"https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F{article_id}/MediaObjects/{journal_id}_{year}_{article_num}_Fig{N}_HTML.png\"\ncurl -s \"$FIG_URL\" -H \"User-Agent: Mozilla/5.0\" | base64 -w 0 > /c/Users/<user>/fig{N}_b64.txt\n```\n\n### 分辨率控制\n| 前缀 | 尺寸 | 说明 |\n|------|------|------|\n| `/full/` | 全尺寸 | 最高分辨率，推荐用于Fig1 |\n| `/lw1200/` | 宽1200px | 中等尺寸，适用于其余Figures |\n| `/m685/` | 宽685px | 小尺寸 |\n| `/w215h120/` | 215x120px | 缩略图 |\n\n### 已测试的期刊ID\n| 期刊 | ID | DOI前缀 | 验证状态 |\n|------|----|---------|---------|\n| Nature | 41586 | s41586 | ✅ 2026-06 |\n| **Nature Medicine** | **41591** | **s41591** | **✅ 2026-06** |\n| **Nature Neuroscience** | **41593** | **s41593** | **✅ 2026-06** |\n| Nature Communications | 41467 | s41467 | 🟢 已验证 |\n| Cell Death & Differentiation | 41418 | s41418 | 🟢 已验证 |\n| Scientific Reports | 41598 | s41598 | 🟢 已验证 |\n| Cell Discovery | 41420 | s41420 | 🟢 已验证 |\n\n## Cell Press / Elsevier 系列（Cell Metabolism, Cell, Neuron, Cell Reports 等）\n**已验证模式（2026年6月）**\n\n### 关键发现：主页面有Cloudflare防护，但CDN图片可直接访问\nCell Press 主页面（www.cell.com）使用 Cloudflare 防护，curl/browser 直接访问被拦截。\n但图片通过 `ars.els-cdn.com` CDN 分发，**可以直接通过 curl 下载**。\n\n### URL结构（已成功用于 Cell Metabolism）\n```\nFigure N (大尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-gr{N}_lrg.jpg\n\nFigure N (小尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-gr{N}.jpg\n\nGraphical Abstract (大尺寸):\nhttps://ars.els-cdn.com/content/image/1-s2.0-{PII}-fx1_lrg.jpg\n```\n\n### 关键参数\n- `{PII}`: 文章的PII（Publisher Item Identifier），可从PubMed esummary结果中获取（idtype='pii'），或从DOI对应的ScienceDirect URL中提取\n- `{N}`: Figure编号（1-7），Cell Press系列使用 `gr1, gr2, ..., gr7` 格式（非 `Fig1`）\n- `fx1`: Graphical Abstract的固定标识\n\n### 实例（Neuron — 已验证 2026-06-12）\n```bash\nPMID: 42127911\nDOI: 10.1016/j.neuron.2026.04.033\nPII: S0896-6273(26)00328-4 # 含有括号和连字符，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"}
tool · 2026-06-12 13:12
{"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"}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Search URL: https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=%28%28ferroptosis%5BTitle%2FAbstract%5D+OR+pyroptosis%5BTitle%2FAbstract%5D+...\r\n\r\nTotal results: 0\r\nPMIDs: \r\n", "tool_calls_made": 0, "duration_seconds": 0.61}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Query 1: Count=0, PMIDs: \r\n\r\nQuery 2: Count=0, PMIDs: \r\n\r\nQuery 3: Count=0, PMIDs: \r\n\r\nQuery 4: Count=0, PMIDs: \r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.81}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Query 'ferroptosis[Title/Abstract] AND 2026[dp]...': Count=0, PMIDs: \r\n\r\nQuery 'ferroptosis[Title/Abstract]...': Count=0, PMIDs: \r\n\r\nQuery 'Nature[Journal] AND 2026[dp]...': Count=0, PMIDs: \r\n\r\n", "tool_calls_made": 0, "duration_seconds": 4.62}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Full URL: https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=ferroptosis%5BTitle%2FAbstract%5D&retmax=5&retmode=json\r\nResponse: {\"header\":{\"type\":\"esearch\",\"version\":\"0.3\"},\"esearchresult\":{\"count\":\"27980\",\"retmax\":\"5\",\"retstart\":\"0\",\"idlist\":[\"42276463\",\"42276441\",\"42276388\",\"42276195\",\"42275906\"],\"translationset\":[],\"querytranslation\":\"\\\"ferroptosis\\\"[Title/Abstract]\"}}\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 0.61}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "{'mindate': '2026/03/12', 'maxdate': '2026/06/12', 'datetype': 'pdat'}: Count=0, PMIDs=[]\r\n\r\n{'mindate': '2026-03-12', 'maxdate': '2026-06-12', 'datetype': 'pdat'}: Count=0, PMIDs=[]\r\n\r\n{'mindate': '2026/03/01', 'maxdate': '2026/06/12', 'datetype': 'pdat'}: Count=0, PMIDs=[]\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.42}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Count=0, PMIDs=[]\r\n\r\nCount=0, PMIDs=[]\r\n\r\nCount=0, PMIDs=[]\r\n\r\n", "tool_calls_made": 0, "duration_seconds": 1.81}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Recent ferroptosis PMIDs: []\r\n", "tool_calls_made": 0, "duration_seconds": 1.02}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "Full response: {\r\n \"header\": {\r\n \"type\": \"esearch\",\r\n \"version\": \"0.3\"\r\n },\r\n \"esearchresult\": {\r\n \"count\": \"27980\",\r\n \"retmax\": \"10\",\r\n \"retstart\": \"0\",\r\n \"idlist\": [\r\n \"42276463\",\r\n \"42276441\",\r\n \"42276388\",\r\n \"42276195\",\r\n \"42275906\",\r\n \"42275866\",\r\n \"42275647\",\r\n \"42\r\n", "tool_calls_made": 0, "duration_seconds": 0.61}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "2026年06月12日 13:07:34\n---\nPython 3.11.15", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"status": "success", "output": "IDs: []\r\n", "tool_calls_made": 0, "duration_seconds": 1.22}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Python was not found; run without arguments to install from the Microsoft Store, or disable this shortcut from Settings > Apps > Advanced app settings > App execution aliases.", "exit_code": 49, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Traceback (most recent call last):\r\n File \"<string>\", line 14, in <module>\r\nKeyError: 'IdList'", "exit_code": 1, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Full result: {\r\n \"header\": {\r\n \"type\": \"esearch\",\r\n \"version\": \"0.3\"\r\n },\r\n \"esearchresult\": {\r\n \"count\": \"27980\",\r\n \"retmax\": \"5\",\r\n \"retstart\": \"0\",\r\n \"idlist\": [\r\n \"42276463\",\r\n \"42276441\",\r\n \"42276388\",\r\n \"42276195\",\r\n \"42275906\"\r\n ],\r\n \"translationset\": [],\r\n \"querytranslation\": \"\\\"ferroptosis\\\"[Title/Abstract]\"\r\n }\r\n}", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Count: 160\r\nIDs: ['42270976', '42270660', '42265110', '42259813', '42251040', '42236947', '42236908', '42230599', '42225830', '42215722', '42209505', '42203761', '42191968', '42191733', '42185629', '42185286', '42174135', '42174134', '42173913', '42173883']", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "PMID:42270976\r\n Nat Cell Biol [2026 Jun 10]\r\n DOI:10.1038/s41556-026-01974-0\r\n Type:Journal Article\r\n Mitochondria-ER contacts function as an iron supply hub.\r\n\r\nPMID:42270660\r\n Nat Commun [2026 Jun 10]\r\n DOI:10.1038/s41467-026-74117-6\r\n Type:Journal Article\r\n A mitochondria-driven quality control mechanism for peroxisomal membrane proteins.\r\n\r\nPMID:42265110\r\n Nat Commun [2026 Jun 9]\r\n DOI:10.1038/s41467-026-74080-2\r\n Type:Journal Article\r\n CLPX acquires an iron-sulfur cluster to sustain mitochondrial proteostasis in cancer cells.\r\n\r\nPMID:42259813\r\n Nat Commun [2026 Jun 8]\r\n DOI:10.1038/s41467-026-74032-w\r\n Type:Journal Article\r\n Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.\r\n\r\nPMID:42251040\r\n Nat Commun [2026 Jun 6]\r\n DOI:10.1038/s41467-026-74021-z\r\n Type:Journal Article\r\n Ameliorating calcium homeostasis improves longevity and healthspan in progeroid and naturally aged mice.\r\n\r\nPMID:42236947\r\n Nature [2026 Jun 3]\r\n DOI:10.1038/s41586-026-10597-2\r\n Type:Journal Article\r\n Spermine is an endogenous iron chelator that inhibits ferroptosis.\r\n\r\nPMID:42236908\r\n Cell Death Differ [2026 Jun 3]\r\n DOI:10.1038/s41418-026-01775-w\r\n Type:Journal Article\r\n Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.\r\n\r\nPMID:42230599\r\n Nat Commun [2026 Jun 2]\r\n DOI:10.1038/s41467-026-73710-z\r\n Type:Journal Article\r\n A Rras2-BMPR2 feedback loop sustains osteogenesis and represents a therapeutic target for osteoporosis.\r\n\r\nPMID:42225830\r\n Nat Cell Biol [2026 Jun 1]\r\n DOI:10.1038/s41556-026-01972-2\r\n Type:Journal Article, Review\r\n Emerging roles of ferroptosis in modulating the immune landscape of glial tumours.\r\n\r\nPMID:42215722\r\n Cell Death Differ [2026 May 29]\r\n DOI:10.1038/s41418-026-01773-y\r\n Type:Journal Article\r\n Akt-mediated RALY phosphorylation functions as a molecular switch governing c-Myc stability.\r\n\r\nPMID:42209505\r\n Nat Commun [2026 May 28]\r\n DOI:10.1038/s41467-026-73702-z\r\n Type:Journal Article\r\n Metabolic characterization of the tumor microenvironment orchestrates therapeutic strategies and clinical outcomes in pancreatic c\r\n\r\nPMID:42203761\r\n Nat Commun [2026 May 27]\r\n DOI:10.1038/s41467-026-73498-y\r\n Type:Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't\r\n Cuproptosis inducers mediate cold lethality via SLCR-46.1 in C. elegans.\r\n\r\nPMID:42191968\r\n Cell Death Differ [2026 May 26]\r\n DOI:10.1038/s41418-026-01766-x\r\n Type:Journal Article\r\n Fatty acid channelling into triglycerides and oxylipins drives ferroptosis resistance during oncogenic BRAF-induced senescence.\r\n\r\nPMID:42191733\r\n Nat Commun [2026 May 26]\r\n DOI:10.1038/s41467-026-73538-7\r\n Type:Journal Article\r\n Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate im\r\n\r\nPMID:42185629\r\n Cell Death Differ [2026 May 25]\r\n DOI:10.1038/s41418-026-01767-w\r\n Type:Journal Article\r\n GSDME acts as an epigenetic modifier to promote melanoma development via centriole biogenesis regulator PLK4.\r\n\r\nPMID:42185286\r\n Nat Commun [2026 May 25]\r\n DOI:10.1038/s41467-026-73682-0\r\n Type:Journal Article\r\n An HDAC4-specific PROTAC degrader achieves radiation sensitization by enhancing ferroptosis in lung cancer.\r\n\r\nPMID:42174135\r\n Nat Cell Biol [2026 May 22]\r\n DOI:10.1038/s41556-026-01950-8\r\n Type:Journal Article\r\n Stress granules shape ferroptosis in cancer.\r\n\r\nPMID:42174134\r\n Nat Cell Biol [2026 May 22]\r\n DOI:10.1038/s41556-026-01953-5\r\n Type:Journal Article\r\n Stress granules restrain ferroptosis by sequestering ferritin.\r\n\r\nPMID:42173913\r\n Nat Commun [2026 May 22]\r\n DOI:10.1038/s41467-026-73379-4\r\n Type:Journal Article\r\n Iron overload in the tumor microenvironment induces CD8(+) T cell ferroptosis and dysfunction.\r\n\r\nPMID:42173883\r\n Nat Commun [2026 May 22]\r\n DOI:10.1038/s41467-026-73350-3\r\n Type:Journal Article\r\n TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "=== PMID: 42236947 | ? ===\r\nDOI: 10.1038/s41586-026-10597-2\r\nTitle: Spermine is an endogenous iron chelator that inhibits ferroptosis.\r\nAbstract: Ferroptosis is an iron-dependent form of cell death driven by lipid peroxidation1. Here we identify spermine-a polyamine derived from spermidine2-as an endogenous iron chelator that directly suppresses ferroptosis. Integrating metabolomics, stable isotope tracing and biophysical studies of the interaction between spermine and Fe2+ ions, we demonstr...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42270976 | ? ===\r\nDOI: 10.1038/s41556-026-01974-0\r\nTitle: Mitochondria-ER contacts function as an iron supply hub.\r\nAbstract: Mitochondrial iron dynamics are essential for cellular respiration and metabolic homeostasis, yet the molecular mechanisms governing iron supply to mitochondria remain poorly understood. Here we identify a pathway in which haem serves as an iron source for mitochondria, maintaining mitochondrial iron homeostasis and mitochondrial supercomplex integ...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42259813 | ? ===\r\nDOI: 10.1038/s41467-026-74032-w\r\nTitle: Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.\r\nAbstract: Mycobacterium tuberculosis (M.tb) actively reprograms host lipid metabolism during infection; however, the underlying mechanism remains poorly understood. How M.tb manipulates macrophage lipid metabolism to induce lipid peroxidation and ferroptosis for bacterial persistence remains a fundamental question. Here, using single-cell RNA sequencing and ...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42174135 | ? ===\r\nDOI: 10.1038/s41556-026-01950-8\r\nTitle: Stress granules shape ferroptosis in cancer.\r\nAbstract: ...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42174134 | ? ===\r\nDOI: 10.1038/s41556-026-01953-5\r\nTitle: Stress granules restrain ferroptosis by sequestering ferritin.\r\nAbstract: Glioblastoma stem cells (GSCs) are refractory to first-line treatment in the clinic, which includes irradiation (IR) and temozolomide (TMZ). Here we find that disrupting stress granules (SGs) sensitizes GSCs to IR/TMZ through ferroptosis. The profiling of SG proteins reveals the recruitment of iron-related proteins including ferritin. Mechanistical...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42185286 | ? ===\r\nDOI: 10.1038/s41467-026-73682-0\r\nTitle: An HDAC4-specific PROTAC degrader achieves radiation sensitization by enhancing ferroptosis in lung cancer.\r\nAbstract: Post-translational modifications (PTMs) play a critical role in cancer radioresistance, yet how they regulate ferroptosis to influence radiotherapy response remains poorly understood. Here, we show that HDAC4 promotes radiation resistance in lung cancer by inhibiting ferroptosis. Through a CRISPR screen in patient-derived organoids, we identify HDA...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42203761 | ? ===\r\nDOI: 10.1038/s41467-026-73498-y\r\nTitle: Cuproptosis inducers mediate cold lethality via SLCR-46.1 in C. elegans.\r\nAbstract: Cuproptosis denotes cell death triggered by copper accumulation. However, its role in natural environmental responses remains unclear. Here, we demonstrate that cuproptosis contributes to cold-induced lethality in C. elegans. A mutant for the lysosomal copper transporter gene slcr-46.1 exhibited defective cold tolerance due to copper accumulation i...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article', 'Research Support, N.I.H., Extramural', \"Research Support, Non-U.S. Gov't\"]\r\n\r\n=== PMID: 42173883 | ? ===\r\nDOI: 10.1038/s41467-026-73350-3\r\nTitle: TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.\r\nAbstract: Inflammasomes are cytosolic multiprotein complexes facilitating the maturation and release of the inflammatory cytokines interleukin (IL)-1β and IL-18 and pyroptosis. ASC (apoptosis-associated-speck-like protein containing a CARD) is the central inflammasome adaptor. ASC polymerization is crucial for inflammasome assembly, and ASC particle re...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42185629 | ? ===\r\nDOI: 10.1038/s41418-026-01767-w\r\nTitle: GSDME acts as an epigenetic modifier to promote melanoma development via centriole biogenesis regulator PLK4.\r\nAbstract: Gasdermins have been traditionally recognized for their canonical pore-forming activity in pyroptosis and generally considered as a tumor suppressor due to their low endogenous expression in various types of cancers. However, the pyroptosis-independent role of gasdermins in cellular biological processes remains poorly understood, sparking debates o...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42191968 | ? ===\r\nDOI: 10.1038/s41418-026-01766-x\r\nTitle: Fatty acid channelling into triglycerides and oxylipins drives ferroptosis resistance during oncogenic BRAF-induced senescence.\r\nAbstract: Oncogene-induced senescence (OIS), a cellular programme initiated by activation of oncogenic signalling, provides a barrier to transformation and is accompanied by major reprogramming of cellular metabolism. We show here that induction of OIS by BRAFV600E expression in human diploid fibroblasts led to global changes in the cellular lipidome, charac...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42270660 | ? ===\r\nDOI: 10.1038/s41467-026-74117-6\r\nTitle: A mitochondria-driven quality control mechanism for peroxisomal membrane proteins.\r\nAbstract: Peroxisomes are essential organelles involved in lipid and reactive oxygen species metabolism, and their function requires proper targeting of peroxisomal membrane proteins (PMPs). When peroxisome biogenesis fails, as occurs in peroxisome biogenesis disorders, PMP levels decrease markedly, yet the underlying mechanisms remain unclear. Here, using q...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42265110 | ? ===\r\nDOI: 10.1038/s41467-026-74080-2\r\nTitle: CLPX acquires an iron-sulfur cluster to sustain mitochondrial proteostasis in cancer cells.\r\nAbstract: Mitochondrial proteostasis-maintaining mechanisms are crucial for protecting cells from the toxicity of misfolded protein accumulation. Although excessive stress is known to inactivate these mechanisms and thereby induce mitophagy in cancer cells, the detailed molecular mechanisms coordinating these mitochondrial quality control processes remain un...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42236908 | ? ===\r\nDOI: 10.1038/s41418-026-01775-w\r\nTitle: Cell death-induced release of the pro-aging protein acyl CoA binding protein (ACBP) into the circulation.\r\nAbstract: Acyl-CoA-binding protein (ACBP, encoded by diazepam binding inhibitor, DBI) is an abundant intracellular regulator of lipid metabolism that also circulates systemically, yet the mechanisms governing its release and its relationship to organ injury remain unresolved. Herein, we combine human multi-omics, mechanistic mouse models and controlled cell ...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42191733 | ? ===\r\nDOI: 10.1038/s41467-026-73538-7\r\nTitle: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.\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 immun...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\n\r\n=== PMID: 42173913 | ? ===\r\nDOI: 10.1038/s41467-026-73379-4\r\nTitle: Iron overload in the tumor microenvironment induces CD8+ T cell ferroptosis and dysfunction.\r\nAbstract: While iron homeostasis in cancer cells is well-established, its role in mediating crosstalk between tumors and CD8+ T cells within the tumor microenvironment (TME) remains largely elusive. In this study, we compare iron levels across primary tissues populated by CD8+ T cells. Contrary to the systemic iron deficiency commonly found in cancer patient...\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "PMID: 42236947\r\nDOI: 10.1038/s41586-026-10597-2\r\nTitle: Spermine is an endogenous iron chelator that inhibits ferroptosis.\r\nAbstract: Ferroptosis is an iron-dependent form of cell death driven by lipid peroxidation1. Here we identify spermine-a polyamine derived from spermidine2-as an endogenous iron chelator that directly suppresses ferroptosis. Integrating metabolomics, stable isotope tracing and biophysical studies of the interaction between spermine and Fe2+ ions, we demonstrate that aldehyde dehydrogenase 18 family member A1 (ALDH18A1) promotes an alternative glutamine-dependent pathway for de novo spermine synthesis. This process limits iron availability and lipid peroxidation in hepatocellular carcinoma. Genetic or pharmacological inhibition of ALDH18A1-through knockout, short hairpin RNA delivered using adeno-associated virus (AAV), or the small molecule inhibitor YG1702-triggers ferroptosis and impairs both\r\n---END---\r\n\r\nPMID: 42174134\r\nDOI: 10.1038/s41556-026-01953-5\r\nTitle: Stress granules restrain ferroptosis by sequestering ferritin.\r\nAbstract: Glioblastoma stem cells (GSCs) are refractory to first-line treatment in the clinic, which includes irradiation (IR) and temozolomide (TMZ). Here we find that disrupting stress granules (SGs) sensitizes GSCs to IR/TMZ through ferroptosis. The profiling of SG proteins reveals the recruitment of iron-related proteins including ferritin. Mechanistically, G3BP1, an SG core protein, directly interacts with ferritin light chain in an IR/TMZ-induced G3BP1 methionine-333 oxidation-dependent manner. This interaction facilitates recruiting and sequestering ferritin into SGs, thereby restricting ferroptosis by limiting Fe2+ content in the labile iron pool and preventing ferritinophagy. Disrupting G3BP1 and ferritin light chain binding using a screened small molecule, ciwujianoside C3, mitigates the r\r\n---END---\r\n\r\nPMID: 42185286\r\nDOI: 10.1038/s41467-026-73682-0\r\nTitle: An HDAC4-specific PROTAC degrader achieves radiation sensitization by enhancing ferroptosis in lung cancer.\r\nAbstract: Post-translational modifications (PTMs) play a critical role in cancer radioresistance, yet how they regulate ferroptosis to influence radiotherapy response remains poorly understood. Here, we show that HDAC4 promotes radiation resistance in lung cancer by inhibiting ferroptosis. Through a CRISPR screen in patient-derived organoids, we identify HDAC4 as a key mediator. Mechanistically, HDAC4 acts as an E3 SUMO ligase that SUMOylates MBD1, preventing its ubiquitination and degradation. Stabilized MBD1 represses TP53 and CYP1A1 transcription, thereby suppressing lipid reactive oxygen species formation and ferroptosis. To target HDAC4, we develop a proteolysis-targeting chimera (PROTAC), TP1, based on tasquinimod, which binds and degrades HDAC4 specifically, as confirmed by surface plasmon re\r\n---END---\r\n\r\nPMID: 42173883\r\nDOI: 10.1038/s41467-026-73350-3\r\nTitle: TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.\r\nAbstract: Inflammasomes are cytosolic multiprotein complexes facilitating the maturation and release of the inflammatory cytokines interleukin (IL)-1β and IL-18 and pyroptosis. ASC (apoptosis-associated-speck-like protein containing a CARD) is the central inflammasome adaptor. ASC polymerization is crucial for inflammasome assembly, and ASC particle release propagates inflammasome responses to bystander cells. However, control of inflammasome and ASC particle assembly to limit chronic inflammation and the emergence of autoinflammatory diseases is still incompletely understood. Here, we show that the E3 ubiquitin ligase TRIM (tripartite-motif-containing protein) 21, a common autoantigen in autoimmune diseases, is involved in inflammasome assembly. Specifically, TRIM21 binds to and ubiquitinates ASC t\r\n---END---\r\n\r\nPMID: 42191733\r\nDOI: 10.1038/s41467-026-73538-7\r\nTitle: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.\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 t\r\n---END---\r\n\r\nPMID: 42270976\r\nDOI: 10.1038/s41556-026-01974-0\r\nTitle: Mitochondria-ER contacts function as an iron supply hub.\r\nAbstract: Mitochondrial iron dynamics are essential for cellular respiration and metabolic homeostasis, yet the molecular mechanisms governing iron supply to mitochondria remain poorly understood. Here we identify a pathway in which haem serves as an iron source for mitochondria, maintaining mitochondrial iron homeostasis and mitochondrial supercomplex integrity, regulated at mitochondria-endoplasmic reticulum contact sites (MERCs). We demonstrate that haem oxygenase 2 (HMOX2), an ER-resident enzyme, is also localized to MERCs and facilitates the supply of haem-derived iron to mitochondria. This process is orchestrated by the mitochondrial ubiquitin ligase MITOL (also known as MARCH5/MARCHF5), which ubiquitinates HMOX2 at K68 with K63-linked polyubiquitin chains, enhancing its haem-degrading activit\r\n---END---\r\n\r\nPMID: 42259813\r\nDOI: 10.1038/s41467-026-74032-w\r\nTitle: Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.\r\nAbstract: Mycobacterium tuberculosis (M.tb) actively reprograms host lipid metabolism during infection; however, the underlying mechanism remains poorly understood. How M.tb manipulates macrophage lipid metabolism to induce lipid peroxidation and ferroptosis for bacterial persistence remains a fundamental question. Here, using single-cell RNA sequencing and proteomics, we show that M.tb infection substantially upregulates peroxisome proliferator-activated receptor gamma (PPARγ) in macrophages. Mechanistically, M.tb isocitrate dehydrogenase (IDH) interacts with PPARγ and impairs its proteasomal degradation. Elevated PPARγ suppresses glutathione peroxidase 4 (Gpx4) expression by recruiting the NCOR/SMRT corepressor complex to the Gpx4 promoter, resulting in increased lipid peroxidation and ferroptosis\r\n---END---\r\n\r\nPMID: 42173913\r\nDOI: 10.1038/s41467-026-73379-4\r\nTitle: Iron overload in the tumor microenvironment induces CD8+ T cell ferroptosis and dysfunction.\r\nAbstract: While iron homeostasis in cancer cells is well-established, its role in mediating crosstalk between tumors and CD8+ T cells within the tumor microenvironment (TME) remains largely elusive. In this study, we compare iron levels across primary tissues populated by CD8+ T cells. Contrary to the systemic iron deficiency commonly found in cancer patients, the TME exhibits marked iron enrichment compared to lymphatic fluid and peripheral blood, a phenomenon primarily attributed to tumor necrosis. However, this iron-overloaded TME is detrimental to CD8+ T cells, triggering their ferroptosis and dysfunction. Mechanistically, tumoral T cell receptor (TCR) hyperactivation and tumor-derived hepcidin cooperatively downregulate the iron exporter SLC40A1 in CD8+ T cells, leading to intracellular iron ac\r\n---END---", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "/c/Users/forgase/AppData/Local/hermes/node/claude", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "# 5篇细胞死亡机制论文严格评估\n\n---\n\n## 📊 评分矩阵\n\n| 维度 | 论文1 (Nature) | 论文2 (Nat Cell Biol) | 论文3 (Nat Commun) | 论文4 (Nat Commun) | 论文5 (Nat Commun) |\n|------|:---:|:---:|:---:|:---:|:---:|\n| **1. 逻辑完整性** | 8 | 7 | 8 | **9** | 8 |\n| **2. 方法学水平** | 8 | 8 | **9** | **9** | 7 |\n| **3. 创新性** | **9** | 8 | 8 | 7 | 7 |\n| **4. 可借鉴性** | 8 | 6 | 7 | **10** | 8 |\n| **5. 临床转化潜力** | 7 | 6 | 7 | **8** | 7 |\n| **总分** | **40** | **35** | **39** | **43** | **37** |\n\n---\n\n## 🔬 逐篇详细评析\n\n### 论文1 — 精胺/铁死亡 (Nature, 40/50)\n\n| 维度 | 得分 | 评语 |\n|------|:---:|------|\n| 逻辑完整性 | 8 | ALDH18A1 GOF/LOF → 多胺合成 → 铁螯合，因果链清晰；AAV/shRNA + YG1702双向验证。缺：神经退行性病变体内KO模型。 |\n| 方法学水平 | 8 | 代谢组学鉴定内源螯合剂、铁螯合定量、AAV递送。Nature级别，但未见结构生物学（如精胺-Fe²⁺共晶结构）。 |\n| 创新性 | **9** | ⭐ **首次发现**精胺为内源性铁螯合剂，连接多胺代谢↔铁死亡全新通路，YG1702为新化学探针。概念原创性极高。 |\n| 可借鉴性 | 8 | 多胺（精胺/亚精胺）在脑内高度富集；铁稳态异常是PD核心特征；AAV策略可直接迁移至神经科学。 |\n| 临床转化 | 7 | 精胺已是膳食补充剂，但系统性铁螯合副作用大；YG1702处于极早期。 |\n\n### 论文2 — 应激颗粒/铁蛋白 (Nat Cell Biol, 35/50)\n\n| 维度 | 得分 | 评语 |\n|------|:---:|------|\n| 逻辑完整性 | 7 | G3BP1-FTL结合→限制铁死亡的逻辑成立，ciwujianoside C3为工具分子。缺：G3BP1铁蛋白结合域特异性突变体、体内遗传学验证不足。 |\n| 方法学水平 | 8 | 应激颗粒生物学+蛋白互作筛选+天然产物探针，方法扎实。 |\n| 创新性 | 8 | 应激颗粒↔铁死亡是全新连接；铁蛋白在应激颗粒中被\"扣押\"的概念新颖。 |\n| 可借鉴性 | 6 | 胶质瘤干细胞为模型，应激颗粒虽与ALS/FTD相关，但铁蛋白扣押机制在神经元中可能不保守；ciwujianoside C3的CNS穿透性未知。 |\n| 临床转化 | 6 | 肿瘤导向；天然产物PK/PD未明；靶向应激颗粒的选择性存疑。 |\n\n### 论文3 — HDAC4-PROTAC/铁死亡 (Nat Commun, 39/50)\n\n| 维度 | 得分 | 评语 |\n|------|:---:|------|\n| 逻辑完整性 | 8 | CRISPR筛选→HDAC4→SUMO化MBD1→TP53/CYP1A1，PROTAC TP1降解验证，因果链完整。 |\n| 方法学水平 | **9** | CRISPR全基因组筛选+PROTAC开发（前沿化学生物学）+SUMO化生化+放射生物学，方法多样性突出。 |\n| 创新性 | 8 | 首个HDAC4特异性PROTAC；HDAC4-MBD1-TP53-CYP1A1新轴线；PROTAC诱导铁死亡策略新颖。但HDAC4在肿瘤中已有较多研究。 |\n| 可借鉴性 | 7 | PROTAC技术高度可迁移（神经退行性E3连接酶靶向）；HDAC4参与神经元存活/突触可塑性。但CYP1A1与神经退行关联弱，放射增敏场景难以迁移。 |\n| 临床转化 | 7 | PROTAC已是临床模态（ARV-471等），但TP1为研究工具；放疗增敏限定肿瘤场景。 |\n\n### 论文4 — EPG5/线粒体自噬/神经退行 (Nat Commun, 43/50) 🥇\n\n| 维度 | 得分 | 评语 |\n|------|:---:|------|\n| 逻辑完整性 | **9** | 人类遗传学（EPG5致病变异）→ iPSC皮层神经元→线粒体自噬缺陷→线粒体功能障碍→Ca²⁺过载→cGAS-STING先天免疫激活，**基因到表型完整链路**，多层级验证。 |\n| 方法学水平 | **9** | iPSC定向分化为皮层神经元（金标准）、线粒体自噬流定量、Ca²⁺成像、先天免疫通路报告系统、人类遗传学，**疾病模型+机制研究双前沿**。 |\n| 创新性 | 7 | EPG5-线粒体自噬关联在Vici综合征中已有报道；新在：Ca²⁺过载→先天免疫激活的**下游机制**。概念原创性中等，但机制整合度好。 |\n| 可借鉴性 | **10** | 🔥 **直接命中**：iPSC-神经元平台可**无缝迁移**至PD模型（PINK1/Parkin线粒体自噬通路）；线粒体自噬-神经炎症轴是PD核心；Ca²⁺稳态失调在PD中关键；cGAS-STING在神经退行中新兴热点。实验框架**整包可移植**。 |\n| 临床转化 | 8 | Vici综合征虽罕见，但机制照亮PD/AD共同通路；cGAS-STING通路已有抑制剂在研；线粒体自噬增强策略开发中；iPSC平台支持药物筛选。 |\n\n### 论文5 — TRIM21/炎症小体/焦亡 (Nat Commun, 37/50)\n\n| 维度 | 得分 | 评语 |\n|------|:---:|------|\n| 逻辑完整性 | 8 | TRIM21（E3泛素连接酶）→泛素化ASC→促进炎症小体组装→焦亡。Gain/loss of function验证完善。 |\n| 方法学水平 | 7 | 泛素化生化+ASC斑点成像+自身炎症模型。领域内标准方法，无突出技术亮点。 |\n| 创新性 | 7 | TRIM21已知功能为抗体依赖性胞内中和（Fc受体+E3连接酶双功能）；新发现其参与炎症小体——拓展了TRIM21生物学。但ASC泛素化已有多个E3连接酶报道，增量创新。 |\n| 可借鉴性 | 8 | NLRP3/ASC/焦亡是神经炎症核心通路；TRIM21在脑中表达；ASC斑点传播与神经退行性病变扩散有平行性。但模型为自身炎症而非神经退行模型。 |\n| 临床转化 | 7 | 自身炎症疾病有明确适应证；但E3连接酶靶向挑战大；NLRP3抑制剂已有临床竞争者。 |\n\n---\n\n## 🏆 最终推荐\n\n> ## **论文4** — EPG5 pathogenic variants drive neurodegeneration through mitochondrial dysfunction and innate immune activation (Nat Commun, 43/50)\n\n### 一句话推荐理由：\n\n**该论文是5篇中唯一直接在神经退行性疾病模型（iPSC-皮层神经元）中构建了从基因→线粒体自噬缺陷→Ca²⁺过载→先天免疫激活的完整因果链，其实验框架可无缝迁移至帕金森病（PINK1/Parkin通路）的线粒体自噬-神经炎症轴研究，且iPSC平台+多层级方法学组合对神经科学实验室具有最高的可复制性和借鉴价值。**\n\n---", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "=== Step 1: Extract figure URLs from article HTML ===\n\n=== Step 2: Download PDF ===\nHTTP 200, Size: 254841 bytes\n-rw-r--r-- 1 forgase 197121 254841 6月 12 13:10 /c/Users/forgase/Desktop/EPG5_ND_ncomms.pdf", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "https://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs12276-026-01644-z/MediaObjects/12276_2026_1644_Fig1_HTML.png\nhttps://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs42003-023-05238-7/MediaObjects/42003_2023_5238_Fig1_HTML.png\nhttps://media.springernature.com/w215h120/springer-static/image/art%3A10.1038%2Fs44324-025-00049-2/MediaObjects/44324_2025_49_Fig1_HTML.png\nhttps://verify.nature.com/verify/nature.png\nhttps://www.springernature.com/app-sn/public/images/logo-springernature.png", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Fig1: HTTP 200\n Saved fig1_b64.txt (1849116 bytes)\nFig2: HTTP 200\n Saved fig2_b64.txt (1144568 bytes)\nFig3: HTTP 200\n Saved fig3_b64.txt (2235896 bytes)\nFig4: HTTP 200\n Saved fig4_b64.txt (1203428 bytes)\nFig5: HTTP 200\n Saved fig5_b64.txt (961444 bytes)\nFig6: HTTP 200\n Saved fig6_b64.txt (2042704 bytes)\nFig7: HTTP 200\n Saved fig7_b64.txt (1897264 bytes)\nFig1 full: HTTP 200", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "TITLE: Pathogenic variants in the autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation.\r\n\r\nJOURNAL: ?\r\nPUBDATE: 2026-May-26\r\nAUTHORS: Kritarth Singh, Hormos Salimi Dafsari, Olivia Gillham, Haoyu Chi, Ivet Mandzhukova, Ioanna Kourouzidou, Preethi Sheshadri, Chih-Yao Chung et al.\r\nKEYWORDS: \r\n\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.", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "Journal: Nature communications\r\nISO: Nat Commun\r\nEID: 10.1038/s41467-026-73538-7\r\nDOI: 10.1038/s41467-026-73538-7", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"bytes_written": 15576, "dirs_created": true, "lint": {"status": "ok", "output": ""}, "resolved_path": "C:\\Users\\forgase\\build_epg5_html.py", "files_modified": ["C:\\Users\\forgase\\build_epg5_html.py"]}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "fig1: 1354 KB loaded\r\n fig2: 838 KB loaded\r\n fig3: 1638 KB loaded\r\n fig4: 881 KB loaded\r\n fig5: 704 KB loaded\r\n fig6: 1496 KB loaded\r\n fig7: 1390 KB loaded\r\nLoaded 7/7 figures\r\n\r\n✅ HTML saved to: C:/Users/forgase/Desktop/线粒体自噬_EPG5_文献解读.html\r\n Size: 10.8 MB\r\nDone!", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "-rw-r--r-- 1 forgase 197121 11349071 6月 12 13:12 /c/Users/forgase/Desktop/线粒体自噬_EPG5_文献解读.html\n-rw-r--r-- 1 forgase 197121 254841 6月 12 13:10 /c/Users/forgase/Desktop/EPG5_ND_ncomms.pdf", "exit_code": 0, "error": null}
assistant · 2026-06-12 13:12
tool · 2026-06-12 13:12
{"output": "", "exit_code": 0, "error": null}