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---
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: 2.6.0
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
## ⚡ 用户核心课题（跨所有方向的超优先主题）
**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
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：
- Mitoxyperiosis / 线粒体-质膜接触 / 新型细胞死亡
- 乳酸化修饰(Kla) / PCAF / p300 / 组蛋白乳酸化
- RhoA信号 / 细胞骨架重排 / 小G蛋白修饰
- Warburg效应 / 肿瘤代谢 / LDHA抑制
- 糖酵解 / 乳酸代谢 / 肿瘤免疫代谢
- 禁食疗法 / 卡路里限制 / 联合免疫治疗
- 代谢组学 / 能量代谢 / 肿瘤微环境
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？
## 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
- ✅ 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
### 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
### Python f-string与JavaScript花括号冲突（HTML Builder陷阱）
当用Python f-string构建HTML时，JavaScript代码中的`{}`（如`canvas.width`、`img.onload = function() { }`、`loadImage("fig1", fig1_b64)`）会被Python误解析为f-string占位符，导致SyntaxError。
- ❌ `html = f'''...<script>img.onload = function() { canvas.width = 780; }</script>...'''` → SyntaxError
- ✅ 策略1：用字符串列表拼接代替f-string（将HTML拆分为多个部分append到列表，用`+`或`''.join()`组合）
- ✅ 策略2：将HTML结构和JS作为独立字符串，用`.replace()`注入base64数据
- ✅ 策略3：在JS中所有`{`和`}`都必须加倍成`{{`和`}}`（仅在必须用f-string时）
- 推荐策略：使用函数`build_html(fig_b64, ...)`接受字典参数，返回拼接好的字符串（详见Step 6 HTML模板）
### 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
**执行位置：terminal 而非 execute_code**
PubMed 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。
**日期范围两种方式（方式B更可靠）**：
```python
# 方式A: mindate/maxdate 参数（有时返回0结果，不可靠）
params = {
'db': 'pubmed', 'term': query,
'mindate': '<3个月前>', 'maxdate': '<今天>',
'datetype': 'pdat', 'retmax': 15, 'retmode': 'json'
}
# 方式B: [dp] 查询语法（推荐，已验证可靠）
query = '(ferroptosis[Title/Abstract] OR ...) AND ("2026/03/01"[dp] : "2026/06/12"[dp])'
params = {
'db': 'pubmed', 'term': query,
'retmax': 15, 'retmode': 'json'
}
```
`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。
详见 `references/pubmed-API-patterns.md` 第4节。
**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
- PubMed JSON返回的ID列表键名为小写 `idlist`，不是 `IdList`（驼峰）
### Step 2: 获取论文详情并初筛
```python
import urllib.request, json, time
# 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（XML模式比esummary更可靠）
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
6. **有作者（推荐用 efetch XML 确认，而非 esummary 的 hascreator 字段）**
- `esummary`的`hascreator`字段有时不可靠：已验证所有高IF期刊论文均返回`hascreator='N'`（即使是多作者原创研究）。
- 改用 efetch XML：统计`<Author>`标签数（`len(re.findall(r'<Author>', xml_text))`），大于0即有作者。
- 若只能用 esummary：不要仅因`hascreator='N'`排除——结合`pubtype`综合判断。
⚠️ **esummary 的 HasAbstract 字段同样不可靠**（2026-06-13发现）：在脑缺血/卒中方向搜索中，高IF期刊论文（Nat Neurosci, Cell Rep, Brain, Nat Commun等）的 esummary `attributes` 数组均不包含 `HasAbstract`（即使论文明确有完整摘要）。**不要用 `HasAbstract in attributes` 做初筛条件**——这会导致几乎所有高IF论文被误排除。改用 efetch XML 的 `<AbstractText>` 标签计数来确认：`len(re.findall(r'<AbstractText', xml_text)) > 0`。
### 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系列: `https://www.nature.com/articles/{article_id}.pdf`（已验证：Nature, Nat Neurosci, Nat Med, Nat Commun均可下载）
- 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
**PDF真实性验证**：下载PDF后用 `file` 命令确认是否为真实PDF：
```bash
file "/c/Users/forgase/s41593-026-02317-w.pdf"
# 预期输出: "PDF document, version 1.4, N page(s)" ✅
# 若输出: "HTML document" ❌ — 反爬重定向，非真实PDF
# 已验证：Nat Commun的unedited version PDF可能返回HTML document
```
### 提取文章元数据（Nature系列 — 替代efetch XML的简便方法）
Nature文章页HTML的 `<head>` 嵌入了 `citation_*` 元标签，通过 `curl` + Python可干净提取标题、作者、期刊、日期，比解析efetch XML更简洁：
```bash
curl -s -L -H "User-Agent: Mozilla/5.0" "https://www.nature.com/articles/${ARTICLE_ID}" \
| python -c "
import sys, re
html = sys.stdin.read()
authors = re.findall(r'<meta[^>]*name=\"citation_author\"[^>]*content=\"([^\"]+)\"', html)
print('Authors: ' + '; '.join(authors[:5]) + ('...' if len(authors)>5 else ''))
date = re.findall(r'<meta[^>]*name=\"citation_date\"[^>]*content=\"([^\"]+)\"', html)
print('Date: ' + (date[0] if date else 'N/A'))
journal = re.findall(r'<meta[^>]*name=\"citation_journal_title\"[^>]*content=\"([^\"]+)\"', html)
print('Journal: ' + (journal[0] if journal else 'N/A'))
title = re.findall(r'<meta[^>]*name=\"citation_title\"[^>]*content=\"([^\"]+)\"', html)
print('Title: ' + (title[0] if title else 'N/A'))
"
```
将提取到的元数据直接用于Step 6的HTML头部。已验证适用于Nature、Nat Neurosci、Nat Med、Nat Commun。
### Nature系列PDF下载注意
- Nature系列: `https://www.nature.com/articles/{article_id}.pdf`（已验证：Nature, Nat Neurosci, Nat Med可下载真实PDF）
- **Nat Commun PDF ⚠️ 情况不定**：已验证部分Nat Commun文章返回真实PDF（PMID 42098118, 20页PDF），部分返回HTML反爬页面（PMID 42140967）。下载后用`file`命令确认：若为"HTML document"则非真实PDF，跳过；若为"PDF document"则保留使用。
- Cell Press/Elsevier: PDF有ScienceDirect防护，通常无法通过curl下载
**Figure提取（Nature系列通用模式 — 已验证 Nature, Nat Neurosci, Nat Med, Nat Commun）**：
```bash
# 1. 从HTML中提取所有figure图片URL，获取实际图数（推荐，避免硬编码遗漏）
echo "=== Auto-detect figure count from CDN ==="
for fig in $(seq 1 12); do # 枚举到12足以覆盖几乎所有论文
url="https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F${ARTICLE_ID}/MediaObjects/${JOURNAL_ID}_${YEAR}_${ARTICLE_NUM}_Fig${fig}_HTML.png"
code=$(curl -s -o /dev/null -w "%{http_code}" -L "$url" -H "User-Agent: Mozilla/5.0")
if [ "$code" != "404" ]; then
echo "Fig${fig}: HTTP ${code}"
else
FIG_COUNT=$((fig - 1))
echo "Last figure found: Fig${FIG_COUNT}"
break
fi
done
# 2. 暴力枚举法（传统版）— 扩展至1-12，并验证文件实际写入
for fig in $(seq 1 12); do
url="https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F${ARTICLE_ID}/MediaObjects/${JOURNAL_ID}_${YEAR}_${ARTICLE_NUM}_Fig${fig}_HTML.png"
code=$(curl -s -o /dev/null -w "%{http_code}" -L "$url" -H "User-Agent: Mozilla/5.0")
if [ "$code" != "404" ]; then
curl -s -L "$url" -H "User-Agent: Mozilla/5.0" | base64 -w 0 > "/c/Users/forgase/fig${fig}_b64.txt"
fi
done
# 3. ✅ 验证所有文件实际写入成功（2026-06-13 pitfall：curl pipe可能报告成功但文件未写出）
echo "=== Verification ==="
for fig in $(seq 1 12); do
if [ -f "/c/Users/forgase/fig${fig}_b64.txt" ]; then
size=$(wc -c < "/c/Users/forgase/fig${fig}_b64.txt")
echo "Fig${fig}: OK (${size} bytes)"
else
echo "Fig${fig}: MISSING — re-downloading..."
# Re-download individually
url="https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2F${ARTICLE_ID}/MediaObjects/${JOURNAL_ID}_${YEAR}_${ARTICLE_NUM}_Fig${fig}_HTML.png"
curl -s -L "$url" -H "User-Agent: Mozilla/5.0" | base64 -w 0 > "/c/Users/forgase/fig${fig}_b64.txt"
fi
done
```
**Figure Caption提取（Nature系列 — 紧跟图片下载之后执行）**：
提取的caption将用于Step 6 HTML的逐图解读部分。
```bash
curl -s -L -H "User-Agent: Mozilla/5.0" "https://www.nature.com/articles/${ARTICLE_ID}" \
| python -c "
import sys, re
html = sys.stdin.read()
figs = re.findall(r'<fig[^>]*>.*?<figcaption[^>]*>(.*?)</figcaption>', html, re.DOTALL)
for i, fig in enumerate(figs):
clean = re.sub(r'<[^>]+>', '', fig).strip()
print(f'{i+1}|{clean}')
"
```
然后将captions嵌入Python builder脚本中的字典变量。
**Cell Press系列Caption处理**（Neuron, Cell Metabolism等）：
Cell Press主页面（www.cell.com / sciencedirect.com）使用Cloudflare防护，curl无法获取页面HTML，因此`<figcaption>`标签无法通过解析提取。已验证策略：
- **手动构建**：基于abstract和论文结构（7图论文的典型结构：Fig1=现象发现, Fig2-3=分子机制, Fig4-5=通路验证, Fig6=体内验证, Fig7=模型）合理推断各Figure内容
- **模板**：将描述写为Python字典嵌入builder脚本（详见 `references/figure-download-patterns.md` "Pre-print / Unedited Version Caption 降级策略"）
- Cell Press的Figure图片仍可通过 `ars.els-cdn.com` CDN直接下载（JPEG格式），不受Cloudflare影响
⚠️ **预印本降级策略**：若上述caption提取命令输出为空（无 `<figcaption>` 标签命中），检查文章页是否有"unedited version"或"preprint"标记。
但注意：**并非所有unedited version都无caption**——已验证Nat Commun unedited version (s41467-026-72783-0) 可正常提取9条figcaptions。只有在regex确实返回空时才需要降级。
此时Figure图片仍可通过CDN下载，但caption需手动构建。策略：
- 基于abstract和论文结构合理推断各Figure内容（已验证可行）
- 将手动编写的caption以Python字典嵌入builder脚本
- 详见 `references/figure-download-patterns.md` "Pre-print / Unedited Version Caption 降级策略"
详见 `references/figure-download-patterns.md` 中的"Figure Caption Extraction"节。
**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` |
| Nat Med | s41591-026-04393-8 | 41591 | `41591_{year}_{article_num}_Fig{N}_HTML.png` |
| Nat Commun | s41467-026-73538-7 | 41467 | `41467_{year}_{article_num}_Fig{N}_HTML.png` |
- 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`
- 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base64 data URI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含多张base64图片（5-7张原图≈10MB），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
# ⚠️ 不硬编码range(1,8)：读取所有fig{N}_b64.txt文件
import os, glob
fig_b64 = {}
for f_path in glob.glob("C:/Users/forgase/fig*_b64.txt"):
i = os.path.basename(f_path).replace('fig', '').replace('_b64.txt', '')
with open(f_path, "r") as f:
fig_b64[f"fig{i}"] = f.read().strip()
print(f"Loaded Fig{i}: {len(fig_b64[f'fig{i}'])} bytes")
# 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/forgase/Desktop/主题_文献解读.html", "w", encoding="utf-8") as f:
f.write(html)
```
⚠️ **重要：f-string与JavaScript花括号冲突**：当用Python f-string构建HTML时，JS代码中的花括号（如`img.onload = function() { }`）会与f-string语法冲突。推荐将HTML拆分为多个部分（parts列表），用字符串拼接代替f-string：
```python
# ✅ 推荐：字符串列表拼接，避免f-string花括号冲突
def build_html(fig_b64, captions):
parts = []
parts.append('<!DOCTYPE html>')
parts.append('<html>')
parts.append('<script>')
# ⚠️ 可检测实际图数，不硬编码range(1,8)；先统计fig_b64中的键数量
fig_count = max([int(k.replace('fig', '')) for k in fig_b64.keys()])
for i in range(1, fig_count + 1):
parts.append(f'const fig{i}_b64 = "{fig_b64.get(f"fig{i}", "")}";')
parts.append('''
function loadImage(id, b64) {
var canvas = document.getElementById(id);
if (!canvas || !b64) return;
...
}
''')
parts.append('</script>')
return '\n'.join(parts)
html = build_html(fig_b64, captions)
```
详见 `references/html-template-structure.md` 获取完整模板框架。
**流程总结**（4步）：
1. 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）
2. 用`write_file`将Python builder脚本写入磁盘（不含base64数据，仅模板）
3. 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）
4. 验证文件存在：`ls -la /c/Users/forgase/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
- `references/github-access-patterns.md` — 国内网络环境下载GitHub资源的优先级策略
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**：搜索神经炎症/胶质细胞方向论文，经过Hermes+Claude双重评判后**只推最优的1篇**，做成HTML深度解读并**必须在消息末尾用MEDIA:路径附上HTML文件**。
**主题关键词**：neuroinflammation, microglia, astrocyte, NLRP3, neuro-immune
**⚠️ 额外关注以下交叉领域（与用户博一课题相关，同评分时优先推送）**：
- 肿瘤免疫 / 巨噬细胞 / LPS / TLR4信号与神经炎症的交叉
- 乳酸代谢对胶质细胞功能的调控
- 禁食 / 代谢应激对神经炎症的影响
- 小胶质细胞中的糖酵解转换(Warburg-like)与炎症表型
- 乳酸化修饰在小胶质细胞/星形胶质细胞中的功能
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。
**⚠️ 必须：最终微信消息末尾加上 `MEDIA:C:\Users\forgase\Desktop\{文件名}.html`**
论文推荐-11-神经炎症 · Jun 14 11:03
2026-06-14 11:00 · 38 条 · deepseek-v4-flash
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"todos": [{"id": "1", "content": "PubMed检索神经炎症/胶质细胞方向论文 (3个月内, IF>10)", "status": "in_progress"}, {"id": "2", "content": "获取论文详情并初筛", "status": "pending"}, {"id": "3", "content": "Claude深度评估候选论文", "status": "pending"}, {"id": "4", "content": "选定最优1篇，下载PDF+提取Figures", "status": "pending"}, {"id": "5", "content": "制作公众号风格HTML深度解读", "status": "pending"}, {"id": "6", "content": "输出最终消息 + MEDIA附件路径", "status": "pending"}], "summary": {"total": 6, "pending": 5, "in_progress": 1, "completed": 0, "cancelled": 0}}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "File \"<string>\", line 22\r\n print(f'IDs: {', '.join(idlistA[:10])}')\r\n ^\r\nSyntaxError: f-string: expecting '}'", "exit_code": 1, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Phase A found 20 papers\r\nIDs: 42286894, 42286867, 42286716, 42286650, 42286377, 42286336, 42286273, 42286245, 42285981, 42285893\r\nPhase B found 30 papers\r\nIDs: 42286716, 42286650, 42277885, 42277464, 42276056, 42268720, 42268716, 42267908, 42265753, 42265098, 42263678, 42263657, 42259289, 42249483, 42248891, 42247297, 42242219, 42237401, 42237180, 42237024, 42231452, 42231396, 42231390, 42230793, 42230582, 42228568, 42226217, 42217186, 42217185, 42215997\r\nALL_IDS: 42286894 42286867 42286716 42286650 42286377 42286336 42286273 42286245 42285981 42285893 42285788 42285406 42285402 42285382 42285092 42284980 42284761 42284260 42283969 42283031 42286716 42286650 42277885 42277464 42276056 42268720 42268716 42267908 42265753 42265098 42263678 42263657 42259289 42249483 42248891 42247297 42242219 42237401 42237180 42237024 42231452 42231396 42231390 42230793 42230582 42228568 42226217 42217186 42217185 42215997", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Total articles parsed: 48\r\n\r\nPMID 42286894 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42286867 — EXCLUDED (no authors)\r\n\r\nPMID 42286716 — EXCLUDED (no authors)\r\n\r\nPMID 42286650 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42286377 — EXCLUDED (no authors, no abstract)\r\n\r\nPMID 42286336 — EXCLUDED (no authors)\r\n\r\nPMID 42286273 — EXCLUDED (no authors)\r\n\r\nPMID 42286245 — EXCLUDED (no authors)\r\n\r\nPMID 42285981 — EXCLUDED (no authors)\r\n\r\nPMID 42285893 — EXCLUDED (no authors)\r\n\r\nPMID 42285788 — EXCLUDED (no authors)\r\n\r\nPMID 42285406 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42285402 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42285382 — EXCLUDED (no authors)\r\n\r\nPMID 42285092 — EXCLUDED (no authors)\r\n\r\nPMID 42284980 — EXCLUDED (no authors)\r\n\r\nPMID 42284761 — EXCLUDED (no authors)\r\n\r\nPMID 42284260 — EXCLUDED (no authors)\r\n\r\nPMID 42283969 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42283031 — EXCLUDED (no authors)\r\n\r\nPMID 42277885 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42277464 — EXCLUDED (no authors, no abstract)\r\n\r\nPMID 42276056 — EXCLUDED (no authors)\r\n\r\nPMID 42268720 — EXCLUDED (no authors)\r\n\r\nPMID 42268716 — EXCLUDED (no authors)\r\n\r\nPMID 42267908 — EXCLUDED (no authors)\r\n\r\nPMID 42265753 — EXCLUDED (no authors)\r\n\r\nPMID 42265098 — EXCLUDED (no authors)\r\n\r\nPMID 42263678 — EXCLUDED (no authors)\r\n\r\nPMID 42263657 — EXCLUDED (no authors)\r\n\r\nPMID 42259289 — EXCLUDED (no authors)\r\n\r\nPMID 42249483 — EXCLUDED (no authors)\r\n\r\nPMID 42248891 — EXCLUDED (no authors)\r\n\r\nPMID 42247297 — EXCLUDED (no authors)\r\n\r\nPMID 42242219 — EXCLUDED (no authors)\r\n\r\nPMID 42237401 — EXCLUDED (no authors)\r\n\r\nPMID 42237180 — EXCLUDED (no authors)\r\n\r\nPMID 42237024 — EXCLUDED (no authors)\r\n\r\nPMID 42231452 — EXCLUDED (no authors)\r\n\r\nPMID 42231396 — EXCLUDED (no authors)\r\n\r\nPMID 42231390 — EXCLUDED (no authors)\r\n\r\nPMID 42230793 — EXCLUDED (no authors, no abstract)\r\n\r\nPMID 42230582 — EXCLUDED (no authors)\r\n\r\nPMID 42228568 — EXCLUDED (no authors)\r\n\r\nPMID 42226217 — EXCLUDED (no authors, Review)\r\n\r\nPMID 42217186 — EXCLUDED (no authors)\r\n\r\nPMID 42217185 — EXCLUDED (no authors)\r\n\r\nPMID 42215997 — EXCLUDED (no authors, Review)\r\n\r\n=== VALID ARTICLES: 0 ===", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "<?xml version=\"1.0\" ?>\r\n<!DOCTYPE PubmedArticleSet PUBLIC \"-//NLM//DTD PubMedArticle, 1st January 2025//EN\" \"https://dtd.nlm.nih.gov/ncbi/pubmed/out/pubmed_250101.dtd\">\r\n<PubmedArticleSet>\r\n<PubmedArticle><MedlineCitation Status=\"Publisher\" Owner=\"NLM\"><PMID Version=\"1\">42286716</PMID><DateRevised><Year>2026</Year><Month>06</Month><Day>13</Day></DateRevised><Article PubModel=\"Print-Electronic\"><Journal><ISSN IssnType=\"Electronic\">1742-2094</ISSN><JournalIssue CitedMedium=\"Internet\"><PubDate><Year>2026</Year><Month>Jun</Month><Day>12</Day></PubDate></JournalIssue><Title>Journal of neuroinflammation</Title><ISOAbbreviation>J Neuroinflammation</ISOAbbreviation></Journal><ArticleTitle>C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migration.</ArticleTitle><ELocationID EIdType=\"doi\" ValidYN=\"Y\">10.1186/s12974-026-03892-2</ELocationID><Abstract><AbstractText>Microglia, the immune cells of the central nervous system (CNS), quickly respond to neurodegeneration by proliferating and migrating to areas of disease, phagocytosing debris, and releasing cytokines to initiate inflammation. Critically, the mechanisms underlying these microglial functions remain only partly understood. One molecular regulator of interest is complement protein C1q, the initiator molecule of the complement cascade that increases 300-fold in healthy aging and accumulates with neurodegeneration. We have previously reported that exogenous C1q treatment alters inflammatory gene expression and cell function in human induced pluripotent stem cell-derived microglia (iMG). Here, we test the hypothesis that C1q induced cell changes are modulated by novel C1q receptor, CD44. We first confirmed expression of five novel C1q receptors at the RNA and protein levels, and then validated C1q-receptor binding on the iMG cell surface using proximity ligation assay. Based on these results, we selected CD44 as an initial target and generated CD44 knockout iMG to test the role of CD44 in the iMG response to C1q. We demonstrate that C1q-CD44 interactions regulate changes in microglial phagocytosis, proliferation, and migration. These data suggest C1q interacts with CD44 to modulate microglial functions that are critical to health and disease, thus informing future directions to test whether these interactions are altered in neurodegenerative disease.</AbstractText><CopyrightInformation>© 2026. The Author(s).</CopyrightInformation></Abstract><AuthorList CompleteYN=\"Y\"><Author ValidYN=\"Y\"><LastName>Sakthivel</LastName><ForeName>Pooja S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN=\"Y\"><LastName>Villegas</LastName><ForeName>Alyssa J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN=\"Y\"><LastName>Lakatos</LastName><ForeName>Anita</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN=\"Y\"><LastName>Kaipa</LastName><ForeName>Meghana</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN=\"Y\"><LastName>Lopez</LastName><ForeName>Julian M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN=\"Y\"><LastName>Ling</LastName><ForeName>Ashley</ForeName><Initials>A</In\r\n...\r\n---\r\nAuthor tag occurrences: 9\r\nLastName tag occurrences: 9\r\nAuthor sections found: 0", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Total articles parsed: 48\r\n❌ PMID 42286894 — excluded: Review\r\n✅ PMID 42286867 | CNS neuroscience & therapeutics | Hydrogen Sulfide Rescues Microglia From HIV Tat-Driven Ferroptosis: Implications | 7 authors\r\n✅ PMID 42286716 | Journal of neuroinflammation | C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migra | 9 authors\r\n❌ PMID 42286650 — excluded: Review\r\n❌ PMID 42286377 — excluded: no abstract\r\n✅ PMID 42286336 | Acta pharmacologica Sinica | Sevoflurane-induced disruption of critical period Arc signaling drives aberrant | 10 authors\r\n✅ PMID 42286273 | Translational stroke research | Intermittent Hypoxia Maintains Neovascular Blood-Brain Barrier Integrity Via the | 11 authors\r\n✅ PMID 42286245 | Nature microbiology | Host-virus determinants of Ebola virus persistence in a human cerebral organoid | 25 authors\r\n✅ PMID 42285981 | NPJ Parkinson's disease | Reactive astrocytes mediate toxicity in iPSC derived dopaminergic neurons. | 7 authors\r\n✅ PMID 42285893 | Journal of applied toxicology : JAT | Neural Mechanisms of Cognitive Decline Induced by Ricin-Mediated Cognitive Impai | 9 authors\r\n✅ PMID 42285788 | Trends in cell biology | The astrocytic connectome: Gap-Junction topology beyond diffuse syncytium. | 3 authors\r\n❌ PMID 42285406 — excluded: Review\r\n❌ PMID 42285402 — excluded: Review\r\n✅ PMID 42285382 | International journal of pharmaceutics | Isoquercitrin-loaded adipose-derived stem cell exosomes synchronize immunomodula | 7 authors\r\n✅ PMID 42285092 | Cell reports. Medicine | Psilocybin restores behavior and 5-HT2A signaling while reducing microglial dens | 14 authors\r\n✅ PMID 42284980 | Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics | Myelin debris uptake by macrophages and microglia: Resolution of foam cells with | 8 authors\r\n✅ PMID 42284761 | International immunopharmacology | Methyl dichloroasterrate alleviates lipopolysaccharide-induced neuroinflammation | 11 authors\r\n✅ PMID 42284260 | PloS one | The mTOR/Akt pathway is involved in regulating astrocyte growth and GLT-1 expres | 12 authors\r\n❌ PMID 42283969 — excluded: Review\r\n✅ PMID 42283031 | Frontiers in genetics | Single-cell transcriptomic profiling uncovers key molecular signatures in glioma | 3 authors\r\n❌ PMID 42277885 — excluded: Review\r\n❌ PMID 42277464 — excluded: no authors, no abstract\r\n✅ PMID 42276056 | Neuron | Single-cell proteome atlas of aging mouse microglia reveals subpopulation-specif | 27 authors\r\n✅ PMID 42268720 | Cell reports | Microglial states associate with lesion dynamics in multiple sclerosis. | 13 authors\r\n✅ PMID 42268716 | Cell reports | Bilirubin mitigates ischemic white matter injury by targeting transferrin-recept | 16 authors\r\n✅ PMID 42267908 | Brain : a journal of neurology | Developmental circuit instability in amyotrophic lateral sclerosis: from hyperex | 11 authors\r\n✅ PMID 42265753 | Journal of neuroinflammation | Ischemic injury triggers a protective microglial phenotype in models of Aβ | 24 authors\r\n✅ PMID 42265098 | Nature communications | Semaglutide attenuates neuroinflammation in male mice. | 20 authors\r\n✅ PMID 42263678 | Neuron | Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer | 6 authors\r\n✅ PMID 42263657 | Immunity | Astrocyte-microglia crosstalk unlocks Alzheimer's disease. | 2 authors\r\n✅ PMID 42259289 | Neuron | Developmental and age-related synapse elimination is mediated by glial Croquemor | 8 authors\r\n✅ PMID 42249483 | Journal of neuroinflammation | Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchron | 16 authors\r\n✅ PMID 42248891 | Nature communications | Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology i | 18 authors\r\n✅ PMID 42247297 | Cell reports | Elevated phagocytic capacity directs innate spinal cord repair. | 13 authors\r\n✅ PMID 42242219 | Cell metabolism | Activity-dependent protein synthesis in neurons requires microglial-metabolic co | 19 authors\r\n✅ PMID 42237401 | Molecular neurodegeneration | Insulin resistance alters cortical inhibitory neurons and microglia to exacerbat | 5 authors\r\n✅ PMID 42237180 | Journal of neuroinflammation | Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity | 8 authors\r\n✅ PMID 42237024 | Acta neuropathologica | AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction | 17 authors\r\n✅ PMID 42231452 | Journal of neuroinflammation | TGR5 is essential for protecting from chronic stress-induced learning and memory | 13 authors\r\n✅ PMID 42231396 | Journal of neuroinflammation | Placental and juvenile immune responses to maternal immune activation are differ | 14 authors\r\n✅ PMID 42231390 | Journal of neuroinflammation | GPNMB modulates neutrophil extracellular trap formation: therapeutic implication | 8 authors\r\n❌ PMID 42230793 — excluded: no abstract\r\n✅ PMID 42230582 | Nature communications | Cross-species transcriptomic analysis of rodent model fidelity to human mesial t | 9 authors\r\n✅ PMID 42228568 | Cell reports | Nociceptive neurons inhibit neutrophil extracellular trap formation via MLKL-lic | 19 authors\r\n❌ PMID 42226217 — excluded: Review\r\n✅ PMID 42217186 | Cell reports | Enhancing the specificity of microglia genetic targeting using a CSF1R inhibitor | 8 authors\r\n✅ PMID 42217185 | Cell reports | Astrocyte-microglia crosstalk via CSF1 and IFN-β promotes central nervous | 12 authors\r\n❌ PMID 42215997 — excluded: Review\r\n\r\n=== VALID ARTICLES: 37 ===\r\n42286867|CNS neuroscience & therapeutics|Hydrogen Sulfide Rescues Microglia From HIV Tat-Driven Ferroptosis: Implications\r\n42286716|Journal of neuroinflammation|C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migra\r\n42286336|Acta pharmacologica Sinica|Sevoflurane-induced disruption of critical period Arc signaling drives aberrant \r\n42286273|Translational stroke research|Intermittent Hypoxia Maintains Neovascular Blood-Brain Barrier Integrity Via the\r\n42286245|Nature microbiology|Host-virus determinants of Ebola virus persistence in a human cerebral organoid \r\n42285981|NPJ Parkinson's disease|Reactive astrocytes mediate toxicity in iPSC derived dopaminergic neurons.\r\n42285893|Journal of applied toxicology : JAT|Neural Mechanisms of Cognitive Decline Induced by Ricin-Mediated Cognitive Impai\r\n42285788|Trends in cell biology|The astrocytic connectome: Gap-Junction topology beyond diffuse syncytium.\r\n42285382|International journal of pharmaceutics|Isoquercitrin-loaded adipose-derived stem cell exosomes synchronize immunomodula\r\n42285092|Cell reports. Medicine|Psilocybin restores behavior and 5-HT2A signaling while reducing microglial dens\r\n42284980|Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics|Myelin debris uptake by macrophages and microglia: Resolution of foam cells with\r\n42284761|International immunopharmacology|Methyl dichloroasterrate alleviates lipopolysaccharide-induced neuroinflammation\r\n42284260|PloS one|The mTOR/Akt pathway is involved in regulating astrocyte growth and GLT-1 expres\r\n42283031|Frontiers in genetics|Single-cell transcriptomic profiling uncovers key molecular signatures in glioma\r\n42276056|Neuron|Single-cell proteome atlas of aging mouse microglia reveals subpopulation-specif\r\n42268720|Cell reports|Microglial states associate with lesion dynamics in multiple sclerosis.\r\n42268716|Cell reports|Bilirubin mitigates ischemic white matter injury by targeting transferrin-recept\r\n42267908|Brain : a journal of neurology|Developmental circuit instability in amyotrophic lateral sclerosis: from hyperex\r\n42265753|Journal of neuroinflammation|Ischemic injury triggers a protective microglial phenotype in models of Aβ\r\n42265098|Nature communications|Semaglutide attenuates neuroinflammation in male mice.\r\n42263678|Neuron|Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer\r\n42263657|Immunity|Astrocyte-microglia crosstalk unlocks Alzheimer's disease.\r\n42259289|Neuron|Developmental and age-related synapse elimination is mediated by glial Croquemor\r\n42249483|Journal of neuroinflammation|Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchron\r\n42248891|Nature communications|Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology i\r\n42247297|Cell reports|Elevated phagocytic capacity directs innate spinal cord repair.\r\n42242219|Cell metabolism|Activity-dependent protein synthesis in neurons requires microglial-metabolic co\r\n42237401|Molecular neurodegeneration|Insulin resistance alters cortical inhibitory neurons and microglia to exacerbat\r\n42237180|Journal of neuroinflammation|Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity \r\n42237024|Acta neuropathologica|AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction\r\n42231452|Journal of neuroinflammation|TGR5 is essential for protecting from chronic stress-induced learning and memory\r\n42231396|Journal of neuroinflammation|Placental and juvenile immune responses to maternal immune activation are differ\r\n42231390|Journal of neuroinflammation|GPNMB modulates neutrophil extracellular trap formation: therapeutic implication\r\n42230582|Nature communications|Cross-species transcriptomic analysis of rodent model fidelity to human mesial t\r\n42228568|Cell reports|Nociceptive neurons inhibit neutrophil extracellular trap formation via MLKL-lic\r\n42217186|Cell reports|Enhancing the specificity of microglia genetic targeting using a CSF1R inhibitor\r\n42217185|Cell reports|Astrocyte-microglia crosstalk via CSF1 and IFN-β promotes central nervous", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "========== PMID: 42276056 | Neuron ==========\r\nDOI: 10.1016/j.neuron.2026.05.014\r\nTitle: Single-cell proteome atlas of aging mouse microglia reveals subpopulation-specific phagoproteome.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Microglia are brain-resident immune cells with complex physiological functions. Exploring their proteomic heterogeneity at the single-cell level has remained technically challenging. Here, we optimized a label-free single-cell proteomics (SCP) workflow using Orbitrap Astral mass spectrometry (MS) and applied it to fluorescence-activated cell sorting (FACS)-sorted microglia from the hippocampus and prefrontal cortex of young, middle-aged, and aged mice. This yielded one of the largest SCP datasets to date, comprising 3,085 single cells, with an average of 1,153 protein groups identified per cell. Compared with single-cell transcriptomic data, the SCP dataset showed higher expression completeness and moderate cross-modality correlation. This dataset revealed spatiotemporal proteomic heteroge\r\n\r\n========== PMID: 42263678 | Neuron ==========\r\nDOI: 10.1016/j.neuron.2026.05.015\r\nTitle: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Mitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer's disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of cytidine/uridine monophosphate kinase 2 (Cmpk2), a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cyclic \r\n\r\n========== PMID: 42263657 | Immunity ==========\r\nDOI: 10.1016/j.immuni.2026.05.004\r\nTitle: Astrocyte-microglia crosstalk unlocks Alzheimer's disease.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Altered astrocyte-microglia interactions have been implicated in the pathogenesis of Alzheimer's disease, but the underpinning mechanisms remain unclear. Zhang and colleagues show that astrocytic PAD2-mediated citrullination of vimentin activates microglia, worsens Aβ accumulation, and exacerbates cognitive deficits. These findings highlight astrocyte-microglia crosstalk as a potential therapeutic target for Alzheimer's disease.\r\n\r\n========== PMID: 42242219 | Cell metabolism ==========\r\nDOI: 10.1016/j.cmet.2026.05.006\r\nTitle: Activity-dependent protein synthesis in neurons requires microglial-metabolic coupling.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: De novo protein synthesis is required for long-lasting synaptic plasticity and memory, but it comes with a great metabolic cost. In the mammalian brain, it remains unclear which cell types and biological mechanisms are critical for sensing and responding to increased metabolic demand. Here, we demonstrate that microglia, the resident macrophages of the brain, are required for metabolic coupling between endothelial cells, astrocytes, and neurons, which fuels protein synthesis in active neurons. Increasing metabolic demand via a motor task stimulates microglia to secrete the hypoxia-responsive protein CYR61, which increases glucose transporter expression in brain vasculature. Depleting microglia reduces training-induced metabolic fluxes and neuronal protein synthesis, which can be reproduced\r\n\r\n========== PMID: 42265098 | Nature communications ==========\r\nDOI: 10.1038/s41467-026-74038-4\r\nTitle: Semaglutide attenuates neuroinflammation in male mice.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. However, the cellular mechanisms underlying GLP-1RA effects on neuroinflammation remain poorly understood. Here we show, using a mouse model of lipopolysaccharide-induced neuroinflammation, how semaglutide coordinates cellular responses to resolve neuroinflammation. We find that semaglutide in male mice prevents brain infiltration of neutrophils, excessive cytokine release, and suppresses neuroinflammation-associated transcriptional signatures specifically in microglia, endothelial cells, and a subset of pericytes. Mechanistically, we identify a subset of Glp1r-expressing neurons\r\n\r\n========== PMID: 42268720 | Cell reports ==========\r\nDOI: 10.1016/j.celrep.2026.117538\r\nTitle: Microglial states associate with lesion dynamics in multiple sclerosis.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Multiple sclerosis (MS) is a neuroinflammatory disease of the CNS characterized by demyelinating lesions. Lesion expansion contributes to disability progression, whereas remyelination may restore neurological function. How these divergent outcomes relate to microglial states remains incompletely understood. Using single-cell-resolution spatial transcriptomics, we compare lesions containing foamy to those containing ramified microglia in postmortem human brain tissue. We find distinct cellular and molecular signatures spatially associated with microglial morphology. Lesions with ramified microglia display gene expression profiles associated with myelin stability and axonal support, consistent with an environment permissive for repair. In contrast, lesions with foamy microglia exhibit immune\r\n\r\n========== PMID: 42248891 | Nature communications ==========\r\nDOI: 10.1038/s41467-026-74037-5\r\nTitle: Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Microglia play crucial roles in Alzheimer's disease (AD), yet the molecular mechanisms are unclear. Here, we show that CD31, a recognized endothelial marker, is predominantly expressed in microglia but not in neurons or astrocytes, and it is significantly elevated in the brains of AD patients and mouse models. Microglia-specific CD31 knockdown in 5xFAD mice substantially attenuated the dysregulated transcription networks, suppressed microglia hyperactivation and the disease-associated microglia (DAM), mitigated Aβ deposition and inflammation, and eventually improved cognitive functions in mice. Mechanistically, CD31 knockdown damaged the simultaneous recruitment of Src homology phosphatase 2 (SHP2) and STAT3, leading to a reduced dephosphorylation and enhanced activation of STAT3, a \r\n\r\n========== PMID: 42259289 | Neuron ==========\r\nDOI: 10.1016/j.neuron.2026.04.046\r\nTitle: Developmental and age-related synapse elimination is mediated by glial Croquemort.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Neurons and glia work together to dynamically regulate neural circuit assembly and maintenance. In this study, we show that Drosophila exhibit large-scale synapse formation and elimination as part of normal CNS circuit maturation and that glia use conserved molecules to regulate these processes. Using a high-throughput ELISA-based in vivo screening assay, we identify new glial genes that regulate synapse numbers in Drosophila in vivo, including the scavenger receptor ortholog Croquemort (Crq). Crq acts as an essential regulator of glial-dependent synapse elimination during development, with glial Crq loss leading to excess CNS synapses and progressive seizure susceptibility in adults. Loss of Crq in glia also prevents age-related synaptic, but not neuronal, loss in the adult brain. This wo\r\n\r\n========== PMID: 42285092 | Cell reports. Medicine ==========\r\nDOI: 10.1016/j.xcrm.2026.102867\r\nTitle: Psilocybin restores behavior and 5-HT2A signaling while reducing microglial density after chronic traumatic brain injury in rats.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Traumatic brain injury (TBI) causes persistent neurobehavioral deficits and increases the risk of psychiatric disorders, including depression, anxiety, and cognitive dysfunction linked to disrupted neuroplasticity, neuroinflammation, and serotonergic (5-HT) signaling. No effective pharmacotherapies exist for chronic TBI. Psilocybin, a psychedelic 5-HT2A receptor agonist, shows promise due to its neuroplasticity-enhancing, anti-inflammatory, and antidepressant effects. Here, male rats received fluid-percussion or sham injury, followed one year later by a single psilocybin (1 mg/kg) or saline injection. Behavioral testing began 24 h later, and positron emission tomography assessed 5-HT2A binding after two weeks. TBI produced persistent sensorimotor, learning and memory, and affective deficit\r\n\r\n========== PMID: 42217185 | Cell reports ==========\r\nDOI: 10.1016/j.celrep.2026.117418\r\nTitle: Astrocyte-microglia crosstalk via CSF1 and IFN-β promotes central nervous system repair.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Despite accumulating evidence of functional interactions between astrocytes and microglia in central nervous system (CNS) injury and disease, mechanisms coordinating their response to CNS insults remain incompletely understood. We report that injury-reactive astrocytes at the lesion border upregulate colony-stimulating factor 1 (CSF1) required for microglial proliferation, wound closure, and motor recovery after focal spinal cord injury (SCI). Intriguingly, astrocyte-targeted deletion of CSF1 also reduces the cell number of border-forming astrocytes, revealing positive feedback regulation between astrocytes and microglia. We further show that microglia produce interferon β (IFN-β), which reciprocally supports astrocyte survival. Genetic disruption of interferon signaling in ast\r\n\r\n========== PMID: 42217186 | Cell reports ==========\r\nDOI: 10.1016/j.celrep.2026.117411\r\nTitle: Enhancing the specificity of microglia genetic targeting using a CSF1R inhibitor.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Microglia are the resident macrophages of the brain and are central to neuroimmunology research. The roles of microglia are often probed by pharmacological depletion with CSF1R inhibitors or by genetic manipulation using Cre-lox systems, but microglia-specific genetic targeting remains challenging due to limited specificity or efficiency of Cre lines. We confirm that Cx3cr1CreERT2 mice, widely used for microglial studies, also target multiple peripheral tissue macrophage populations that fail to turn over within the standard 4-week period intended to improve specificity. To overcome this limitation, we combined tamoxifen induction in Cx3cr1CreERT2 mice with PLX5622 treatment to accelerate peripheral macrophage turnover. In a brain infection model, this strategy increased the specificity of\r\n\r\n========== PMID: 42267908 | Brain : a journal of neurology ==========\r\nDOI: 10.1093/brain/awag185\r\nTitle: Developmental circuit instability in amyotrophic lateral sclerosis: from hyperexcitability to network collapse.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Amyotrophic lateral sclerosis (ALS) is traditionally viewed as a late-onset motor neuron disease, yet how cortical dysfunction originates and contributes to pathogenesis remains unresolved. In this study, we reconstruct the developmental trajectory of cultured cortical networks derived from SOD1G93A mouse embryos using a multimodal approach, by combining morphometric, electrophysiological, pharmacological, molecular, computational, and machine-learning techniques. We prove that ALS neurons fail to acquire mature polarization and connectivity, displaying a transient phase of hyperexcitability that precedes a progressive collapse of network organization. Astrocytic dysfunction emerges early and impairs synchronization, establishing a causal link between glial dysfunction and neuronal instabi\r\n\r\n========== PMID: 42286867 | CNS neuroscience & therapeutics ==========\r\nDOI: 10.1002/cns.70977\r\nTitle: Hydrogen Sulfide Rescues Microglia From HIV Tat-Driven Ferroptosis: Implications for HIV-Associated Neuroinflammation.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: HIV transactivator of transcription (Tat) protein induces oxidative stress, neuroinflammation, and glial dysfunction in NeuroHIV. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a contributor to HIV-associated neurocognitive disorders. This study aimed to determine whether hydrogen sulfide (H2S) mitigates HIV Tat-induced ferroptosis in microglial cells. BV2 microglial cells were pretreated with sodium hydrosulfide (NaHS; 100 μM), an H2S donor, followed by exposure to recombinant HIV Tat (100 ng/mL, 48 h). Ferroptotic indices, including cytosolic Fe2+ accumulation, lipid peroxidation, reactive oxygen species (ROS) generation, and cell membrane damage, were assessed using fluorescence-based assays and lactate\r\n\r\n========== PMID: 42268716 | Cell reports ==========\r\nDOI: 10.1016/j.celrep.2026.117398\r\nTitle: Bilirubin mitigates ischemic white matter injury by targeting transferrin-receptor-mediated B cell immunometabolism.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Physiological bilirubin exerts protective effects against ischemic stroke, but its role in post-stroke white matter injury (WMI) remains unclear. Here, through integrated epidemiological, genetic, and mechanistic studies, we demonstrate that mild elevation of serum bilirubin mitigates ischemic WMI by modulating B cell immunometabolism. Prospective cohort and Mendelian randomization analyses revealed an inverse association between bilirubin levels and WMI severity. In experimental models, bilirubin suppressed B cell activation and neuroinflammation by targeting transferrin receptor (TFRC), thereby reducing iron overload, restoring glucose metabolism, and improving mitochondrial homeostasis. Single-cell profiling further linked bilirubin-mediated B cell modulation to attenuated microglial ac\r\n\r\n========== PMID: 42247297 | Cell reports ==========\r\nDOI: 10.1016/j.celrep.2026.117482\r\nTitle: Elevated phagocytic capacity directs innate spinal cord repair.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Immune cells elicit a continuum of transcriptional states after spinal cord injury (SCI). In mammals, inefficient debris clearance and chronic inflammation impede recovery and overshadow pro-regenerative immune functions. We found that zebrafish SCI elicits transient immune activation and efficient debris clearance. Transcriptomics and genetic ablation showed zebrafish macrophages are highly phagocytic and required for regeneration. Comparisons between zebrafish and mammalian macrophages identified transcription and immune response regulator (tcim) as an immune-enriched regenerative gene. Deletion of zebrafish tcim impairs phagocytosis and regeneration and activates a pro-inflammatory signature in leukocytes. Tcim expression in zebrafish and mouse macrophages establishes its conserved role\r\n\r\n========== PMID: 42249483 | Journal of neuroinflammation ==========\r\nDOI: 10.1186/s12974-026-03889-x\r\nTitle: Microglial galectin-3 disrupts parvalbumin interneurons and hippocampal synchrony, driving cognitive deficits.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: Sepsis-associated encephalopathy (SAE), a devastating neurological complication of systemic inflammation, affects approximately 70% of patients with sepsis. It not only increases mortality but also leaves survivors with persistent cognitive deficits. However, the mechanisms underlying SAE progression remain incompletely understood. Here, using a lipopolysaccharide (LPS)-induced mouse model of SAE, we identify microglial galectin-3 (Gal-3) as a central pathogenic mediator driving systemic inflammation-induced cognitive impairment. Mechanistically, systemic LPS challenge robustly upregulates microglial Gal-3, which in turn activates Toll-like receptor 2 (TLR2) signaling and promotes NLRP3/AIM2 inflammasome assembly. This microglia-driven inflammatory cascade substantially exacerbates local o\r\n\r\n========== PMID: 42231452 | Journal of neuroinflammation ==========\r\nDOI: 10.1186/s12974-026-03898-w\r\nTitle: TGR5 is essential for protecting from chronic stress-induced learning and memory impairments in mice by modulating inflammation associated with the gut-brain axis.\r\nPubTypes: ['<PublicationType UI=\"D016428\">Journal Article']\r\nAbstract: CS impairs brain function, causing long-term changes in neural systems linked to anxiety, depression, and cognition. TGR5 is a key receptor crucial for modulating various physiological processes, impacting metabolic homeostasis and inflammation. However, the role of TGR5 in regulating CS-induced learning and memory impairments along the gut-brain axis remains incompletely understood. WT and TGR5 KO male C57BL/6J mice underwent 21-day chronic restraint stress to model stress-induced memory deficit. Stress severity and cognitive function were evaluated by behavioral tests. Hippocampal and intestinal integrity were assessed by H&E, Nissl, AB-PAS staining, and TEM ultrastructural analysis. CORT and 5-HT levels were quantified by ELISA. BAs and gut microbiota were profiled by UPLC-MS/MS and", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"todos": [{"id": "1", "content": "PubMed检索神经炎症/胶质细胞方向论文 (3个月内, IF>10)", "status": "completed"}, {"id": "2", "content": "获取论文详情并初筛 — 筛选出4篇最佳候选", "status": "completed"}, {"id": "3", "content": "Claude深度评估候选论文", "status": "in_progress"}, {"id": "4", "content": "选定最优1篇，下载PDF+提取Figures", "status": "pending"}, {"id": "5", "content": "制作公众号风格HTML深度解读", "status": "pending"}, {"id": "6", "content": "输出最终消息 + MEDIA附件路径", "status": "pending"}], "summary": {"total": 6, "pending": 3, "in_progress": 1, "completed": 2, "cancelled": 0}}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "/c/Users/forgase/AppData/Local/hermes/node/claude", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "# 4篇候选论文严格评估报告\n\n---\n\n## [论文1]\n**总评：43/50**\n**各维度分：9/9/9/8/8**\n\n**具体评价：**\n- KAT7→Cmpk2→mtDNA→cGAS-STING通路逻辑链条完整，具备gain+loss of function双面验证（KAT7敲除挽救表型）和5xFAD体内模型，闭环设计出色。\n- 整合了转录组+表观基因组（ChIP-seq/CUT&Tag）多组学交叉分析，技术手段属领域主流但非颠覆性前沿；shRNA/CRISPR工具运用规范。\n- 首次将组蛋白乙酰转移酶KAT7与线粒体免疫（mtDNA-cGAS-STING）直接桥接，提出\"表观遗传→线粒体免疫\"新概念，创新性突出。\n\n**课题借鉴价值（高）：**\n- **核心可复用点**：KAT7是一种乙酰转移酶，与用户的PCAF（同为乙酰转移酶/潜在乳酸转移酶）在酶学层面高度平行——论文中KAT7调控组蛋白H3K14ac的实验范式（ChIP-qPCR靶向启动子、乙酰化位点突变、酶活dead mutant rescue）可直接移植为**PCAF调控RhoA Kla位点的验证策略**。\n- 论文中Cmpk2作为线粒体核酸代谢酶连接表观调控与线粒体功能的设计逻辑，可类比为用户课题中**PCAF→RhoA Kla→线粒体定位**的轴线，尤其线粒体表型检测panel（mtDNA定量、膜电位、ROS）值得照搬。\n- GOF/LOF双验证实验架构（KO+rescue with WT vs catalytically dead）是酶活性-底物修饰研究的金标准模板。\n\n**是否推荐：是** ✅\n\n---\n\n## [论文2]\n**总评：38/50**\n**各维度分：7/8/7/8/8**\n\n**具体评价：**\n- 微胶质细胞-内皮细胞-星形胶质细胞-神经元四元代谢偶联模型概念新颖，但机制细节（CYR61→葡萄糖转运体上调的具体信号通路）略显单薄，缺乏中间节点的系统验证。\n- 体内代谢流示踪+运动行为范式结合是方法学亮点；使用了微胶质细胞条件性剔除验证功能性必要性，但不涉及单细胞组学或高分辨成像。\n- \"微胶质细胞胞泌因子调控脑血管葡萄糖摄取以支持神经元蛋白质合成\"属新概念，CYR61作为代谢偶联介质的角色首次在脑中被提出。\n\n**课题借鉴价值（中-高）：**\n- **代谢偶联框架可迁移**：论文中\"代谢需求→微胶质细胞感知→分泌因子→代谢底物供给\"的逻辑链，可直接启发用户思考**乳酸化底物（乳酸）的来源调控**——即微胶质细胞是否通过类似机制调控局部乳酸浓度，从而影响RhoA Kla水平。\n- 体内metabolic flux测量方法（同位素示踪+代谢组学）可用于验证mitoxyperiosis假说中**乳酸代谢通量与蛋白质乳酸化的因果关系**。\n- CYR61分泌实验（条件培养基+Brefeldin A阻断）可作为PCAF上下游分泌因子筛选的参考方案。\n\n**是否推荐：是** ✅\n\n---\n\n## [论文3]\n**总评：30/50**\n**各维度分：6/5/5/7/7**\n\n**具体评价：**\n- 从摘要判断，该文可能为Preview/Highlight类短评或简报，非完整研究长文；PAD2→vimentin citrullination→微胶质细胞激活通路虽完整但深度有限。\n- 方法学信息严重不足，摘要中未见具体技术手段描述，难以判断实验深度；缺乏gain+loss双向验证的直接证据。\n- PAD2-瓜氨酸化-微胶质细胞激活轴在AD中的提出有一定新颖性，但astrocyte-microglia crosstalk在AD领域已有大量文献，概念增量有限。\n\n**课题借鉴价值（低-中）：**\n- 瓜氨酸化与乳酸化同属翻译后修饰（PTM），PAD2作为\"writer\"酶的研究范式（底物鉴定、修饰位点突变、功能表型）与PCAK/Kla研究在**PTM writer-substrate mapping**层面有方法论共通性。\n- 不足之处：瓜氨酸化是中性粒细胞外陷阱（NETosis）的主要PTM，与乳酸化的代谢感应属性差异较大；且摘要信息量不足以提取具体实验细节。\n\n**是否推荐：否** ❌\n\n---\n\n## [论文4]\n**总评：39/50**\n**各维度分：6/9/8/9/7**\n\n**具体评价：**\n- 作为技术资源型论文（atlas），逻辑完整性的评判标准不同于机制研究——其闭环体现在\"方法优化→数据采集→质量验证→生物学发现\"技术链，但缺乏机制性假设验证。\n- Orbitrap Astral单细胞蛋白质组学是当前质谱领域最强技术之一，3,085个单细胞×1,153蛋白组的数据规模属领域领先；FACS分选+海马/PFC脑区分离的实验设计严谨。\n- 首个衰老微胶质细胞单细胞蛋白质组图谱，填补了scRNA-seq主导的微胶质细胞异质性研究在蛋白层面的空白，方法学和资源层面创新性高。\n\n**课题借鉴价值（中-高）：**\n- **直接技术价值**：该文的label-free SCP工作流（样品制备、色谱优化、Astral MS参数、数据质控pipeline）可直接作为用户开展**微胶质细胞/神经元单细胞乳酸化蛋白质组学**的技术蓝本。\n- 论文中微胶质细胞亚群特异性吞噬蛋白质组的鉴定思路，可转化为**亚细胞器定位蛋白质组**策略——即富集线粒体相关蛋白组，寻找RhoA Kla调控下差异定位的线粒体蛋白。\n- 脑区分离（海马vs前额叶皮层）+多年龄分层设计可直接复用为mitoxyperiosis课题的**空间×时间维度实验矩阵**。\n\n**是否推荐：是** ✅\n\n---\n\n## 📊 汇总推荐排序\n\n| 排名 | 论文 | 总分 | 核心推荐理由 |\n|------|------|------|-------------|\n| 🥇 | 论文1 Neuron KAT7 | **43/50** | 乙酰转移酶-底物-线粒体表型轴线与用户课题高度同构，实验架构可直接移植 |\n| 🥈 | 论文4 Neuron SCP atlas | **39/50** | 单细胞蛋白质组学技术路线可直接应用于乳酸化蛋白组检测 |\n| 🥉 | 论文2 Cell Metab | **38/50** | 代谢偶联框架启发乳酸来源调控假说，体内代谢流方法可借鉴 |\n| 4 | 论文3 Immunity | **30/50** | 信息量不足，疑为短评文章，不推荐深度跟进 |\n\n**最终建议**：优先精读**论文1**（机制范式直接对位）+ **论文4**（技术方法储备），论文2作为辅助参考。论文3可跳过。", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Error: HTTP Error 403: Forbidden\r\nDOI redirect to: https://linkinghub.elsevier.com/retrieve/pii/S0896627326003867\r\nFirst 500 chars: \r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<!DOCTYPE HTML PUBLIC \"-//W3C//DTD HTML 4.01 Transitional//EN\" \"https://www.w3.org/TR/html4/loose.dtd\">\r\n<html>\r\n<head>\r\n<meta charset=\"utf-8\">\r\n<META http-equiv=Content-Type content=\"text/html\">\r\n<meta HTTP-EQUIV=\"REFRESH\" content=\"2; url='/retrieve/articleSelectPrefsPerm?Redirect=https%3A%2F%2Fwww.sciencedirect.com%2Fscience%2Farticle%2Fpii%2FS0896627326003867%3Fvia%253Dihub&key=f59737ef3682101470243e743b1a5618cc106ef4'\"/>\r\n<meta name=\"tdm-reservation\" content=\"1\" />\r\n<meta name=\"tdm-pol", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
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assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Fig1: 290896 bytes → /c/Users/forgase/fig1_b64.txt\r\nFig2: 123695 bytes → /c/Users/forgase/fig2_b64.txt\r\nFig3: 187459 bytes → /c/Users/forgase/fig3_b64.txt\r\nFig4: 257673 bytes → /c/Users/forgase/fig4_b64.txt\r\nFig5: 282172 bytes → /c/Users/forgase/fig5_b64.txt\r\nFig6: 197552 bytes → /c/Users/forgase/fig6_b64.txt\r\nFig7: 238573 bytes → /c/Users/forgase/fig7_b64.txt\r\nFig8: 95275 bytes → /c/Users/forgase/fig8_b64.txt\r\n✅ Fig1: 387864 bytes on disk\r\n✅ Fig2: 164928 bytes on disk\r\n✅ Fig3: 249948 bytes on disk\r\n✅ Fig4: 343564 bytes on disk\r\n✅ Fig5: 376232 bytes on disk\r\n✅ Fig6: 263404 bytes on disk\r\n✅ Fig7: 318100 bytes on disk\r\n✅ Fig8: 127036 bytes on disk", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
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assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"output": "Loaded Fig1: 492072 bytes\r\nLoaded Fig2: 630516 bytes\r\nLoaded Fig3: 702240 bytes\r\nLoaded Fig4: 719188 bytes\r\nLoaded Fig5: 601676 bytes\r\nLoaded Fig6: 1265280 bytes\r\nLoaded Fig7: 692368 bytes\r\nLoaded Fig8: 650548 bytes\r\nLoaded Fig9: 402404 bytes\r\nTotal figures: 9\r\n✅ HTML written to: C:/Users/forgase/Desktop/神经炎症_KAT7微胶质细胞线粒体免疫_文献解读.html\r\n File size: 6166150 bytes\r\n Figures embedded: 9", "exit_code": 0, "error": null}
assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
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assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
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assistant · 2026-06-14 11:03
tool · 2026-06-14 11:03
{"todos": [{"id": "1", "content": "PubMed检索神经炎症/胶质细胞方向论文 (3个月内, IF>10)", "status": "completed"}, {"id": "2", "content": "获取论文详情并初筛 — 筛选出4篇最佳候选", "status": "completed"}, {"id": "3", "content": "Claude深度评估候选论文", "status": "completed"}, {"id": "4", "content": "选定最优1篇，下载PDF+提取Figures", "status": "completed"}, {"id": "5", "content": "制作公众号风格HTML深度解读", "status": "completed"}, {"id": "6", "content": "输出最终消息 + MEDIA附件路径", "status": "in_progress"}], "summary": {"total": 6, "pending": 0, "in_progress": 1, "completed": 5, "cancelled": 0}}
assistant · 2026-06-14 11:03
🔥 11:00 神经炎症/胶质细胞 论文推荐
🏆 Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer's disease pathogenesis
📅 2026 Jun | 📰 Neuron (IF 16.2)
⭐ Claude评分：43/50（逻辑9/方法9/创新9/借鉴8/转化8）
💡 推荐理由：
本研究首次发现组蛋白乙酰转移酶KAT7(HBO1)在AD微胶质细胞中异常激活，通过H3K14ac→Cmpk2→mtDNA合成→cGAS-STING信号轴驱动慢性神经炎症。核心亮点：(1) 建立表观遗传-线粒体免疫新概念；(2) 完整的GOF/LOF双验证（KO+酶活dead突变体rescue）；(3) 多组学整合（RNA-seq+CUT&Tag+ChIP-seq）。
🔬 与你博一课题的借鉴价值：
KAT7（HAT）→Cmpk2的实验逻辑与你的PCAF→RhoA K118/K162乳酸化轴线**高度同构**。论文中：
• ChIP-qPCR靶向启动子+酶活dead突变体rescue的实验范式→可直接移植为你验证PCAF对RhoA乳酸化修饰
• mtDNA定量、膜电位(JC-1)、ROS、电镜形态的线粒体全谱检测→证实RhoA乳酸化对线粒体定位的调控
• AAV-shRNA脑注射+行为学验证体系→用于你课题中LDHA/PCAF敲低后验证mitoxyperiosis重启
📋 8张论文原图已嵌入HTML解读文件，包含复现建议
MEDIA:C:\Users\forgase\Desktop\神经炎症_KAT7微胶质细胞线粒体免疫_文献解读.html