Enhance citation management and literature review guidelines

- Updated SKILL.md in citation management to include best practices for identifying seminal and high-impact papers, emphasizing citation count thresholds, venue quality tiers, and author reputation indicators.
- Expanded literature review SKILL.md to prioritize high-impact papers, detailing citation metrics, journal tiers, and author reputation assessment.
- Added comprehensive evaluation strategies for paper impact and quality in literature_search_strategies.md, including citation count significance and journal impact factor guidance.
- Improved research lookup scripts to prioritize results based on citation count, venue prestige, and author reputation, enhancing the quality of research outputs.

scientific-skills/venue-templates/assets/examples/cell_summary_example.md

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+# Cell Press Summary, Highlights, and eTOC Examples
+
+Examples of Cell Press-specific elements including Summary (abstract), Highlights, and eTOC blurb.
+
+---
+
+## Complete Example 1: Senescence and Aging
+
+### Summary (150 words max)
+
+```
+Cellular senescence is a stress response that prevents damaged cell 
+proliferation but can drive tissue dysfunction through the senescence-
+associated secretory phenotype (SASP). How senescent cells resist 
+apoptosis despite expressing pro-apoptotic p53 has remained unclear. 
+Here, we identify FOXO4 as a pivotal mediator of senescent cell viability. 
+FOXO4 is highly expressed in senescent cells and directly interacts with 
+p53, retaining it in the nucleus and preventing p53-mediated apoptosis. 
+A cell-permeable peptide that disrupts FOXO4-p53 interaction selectively 
+induces p53 nuclear exclusion and apoptosis in senescent cells without 
+affecting proliferating cells. In vivo, this FOXO4 peptide neutralizes 
+doxorubicin-induced senescent cells and restores fitness, fur density, 
+and renal function in naturally aged mice. These findings establish 
+FOXO4-mediated p53 sequestration as a senescence-specific survival 
+pathway and demonstrate the therapeutic potential of targeted senescent 
+cell elimination.
+```
+
+### Highlights (≤85 characters each)
+
+```
+• FOXO4 is selectively upregulated in senescent cells and binds p53
+
+• FOXO4-p53 interaction retains p53 in the nucleus, preventing apoptosis
+
+• A FOXO4-targeting peptide induces apoptosis specifically in senescent cells
+
+• FOXO4 peptide treatment restores fitness and organ function in aged mice
+```
+
+### eTOC Blurb (30-50 words)
+
+```
+Baar et al. identify FOXO4 as a critical mediator of senescent cell survival 
+through p53 sequestration. A peptide disrupting FOXO4-p53 interaction 
+selectively eliminates senescent cells and restores tissue function in 
+aged mice, establishing proof-of-concept for targeted senolytic therapy.
+```
+
+### In Brief (1 sentence)
+
+```
+A FOXO4-targeting peptide selectively eliminates senescent cells by 
+releasing p53, restoring tissue function in aged mice.
+```
+
+---
+
+## Complete Example 2: Genome Organization
+
+### Summary (150 words max)
+
+```
+The three-dimensional organization of chromosomes within the nucleus 
+influences gene expression, DNA replication, and genome stability. 
+Phase separation has emerged as a potential mechanism for organizing 
+nuclear contents, but whether condensates can shape chromosome 
+structure in vivo remains unknown. Here, we show that the transcriptional 
+coactivator BRD4 forms liquid-like condensates at super-enhancers that 
+organize associated chromatin into hub structures. Optogenetic induction 
+of BRD4 condensates is sufficient to remodel chromosome topology and 
+activate transcription within minutes. Conversely, disruption of BRD4 
+condensates with the small molecule JQ1 dissolves chromatin hubs and 
+rapidly silences super-enhancer-controlled genes. Single-molecule 
+tracking reveals that condensate formation increases the local 
+concentration of transcription machinery 100-fold, explaining the 
+transcriptional potency of super-enhancers. These results establish 
+phase separation as a mechanism for chromatin organization and 
+transcriptional control with implications for understanding and 
+targeting oncogenic super-enhancers.
+```
+
+### Highlights
+
+```
+• BRD4 forms liquid condensates at super-enhancers in living cells
+
+• BRD4 condensates organize chromatin into transcriptionally active hubs
+
+• Optogenetic condensate induction rapidly remodels chromatin topology
+
+• Condensates concentrate transcription machinery 100-fold locally
+```
+
+### eTOC Blurb
+
+```
+Sabari et al. demonstrate that BRD4 forms phase-separated condensates 
+at super-enhancers that organize chromatin into hub structures and 
+concentrate transcription machinery. Optogenetic manipulation reveals 
+that condensate formation directly drives chromatin remodeling and 
+transcriptional activation.
+```
+
+---
+
+## Complete Example 3: Metabolism and Immunity
+
+### Summary (150 words max)
+
+```
+Immune cells undergo dramatic metabolic reprogramming upon activation, 
+switching from oxidative phosphorylation to aerobic glycolysis. This 
+metabolic shift is thought to support the biosynthetic demands of 
+rapid proliferation, but whether specific metabolites directly regulate 
+immune cell function remains largely unexplored. Here, we show that 
+the glycolytic metabolite phosphoenolpyruvate (PEP) sustains T cell 
+receptor signaling by inhibiting sarco/endoplasmic reticulum Ca²⁺-ATPase 
+(SERCA) activity. PEP accumulates in activated T cells and directly 
+binds SERCA, preventing calcium reuptake and prolonging store-operated 
+calcium entry. Genetic or pharmacological enhancement of PEP levels 
+augments T cell effector function and anti-tumor immunity in vivo. 
+Conversely, tumor-derived lactate suppresses PEP levels and impairs 
+T cell calcium signaling, contributing to tumor immune evasion. These 
+findings reveal an unexpected signaling role for a glycolytic 
+intermediate and suggest metabolic strategies to enhance T cell 
+responses in cancer immunotherapy.
+```
+
+### Highlights
+
+```
+• Phosphoenolpyruvate (PEP) accumulates during T cell activation
+
+• PEP directly binds and inhibits SERCA to sustain calcium signaling
+
+• Enhancing PEP levels augments anti-tumor T cell immunity
+
+• Tumor lactate suppresses T cell PEP levels and calcium signaling
+```
+
+### eTOC Blurb
+
+```
+Ho et al. discover that the glycolytic metabolite phosphoenolpyruvate 
+directly regulates T cell calcium signaling by inhibiting SERCA. This 
+metabolic-signaling link is exploited by tumors through lactate 
+secretion and offers new targets for cancer immunotherapy.
+```
+
+---
+
+## Graphical Abstract Description Examples
+
+### For Senescence Paper
+
+```
+"Graphical abstract for Cell paper on FOXO4 and senescence:
+
+Left panel: Senescent cell (enlarged, irregular shape) with FOXO4 (blue 
+oval) binding p53 (green oval) in nucleus, preventing apoptosis. Label: 
+'FOXO4 sequesters p53 → Senescent cell survival'
+
+Center panel: Same senescent cell with FOXO4 peptide (red wedge) 
+disrupting FOXO4-p53 interaction. p53 moves to mitochondria (orange 
+organelles). Label: 'FOXO4 peptide disrupts interaction'
+
+Right panel: Senescent cell undergoing apoptosis (fragmenting). Label: 
+'Selective senescent cell death'
+
+Bottom: Aged mouse (grey, hunched) → Treatment arrow → Rejuvenated mouse 
+(brown, active). Label: 'Restored fitness in aged mice'
+
+Color scheme: Blue for FOXO4, green for p53, red for peptide, grey 
+background for cells."
+```
+
+### For Chromatin Paper
+
+```
+"Graphical abstract for Cell paper on BRD4 condensates:
+
+Top row: Diagram showing BRD4 molecules (purple dots) clustering at 
+super-enhancer (yellow region on DNA strand), forming condensate 
+(purple droplet). Transcription factors (orange, green, blue small 
+circles) accumulate inside condensate.
+
+Middle: Chromatin fibers (grey) being pulled into hub structure around 
+condensate. Arrow showing '100× local concentration increase'
+
+Bottom: Two panels - Left shows 'JQ1' treatment dissolving condensate 
+and chromatin hub dispersing. Right shows 'Optogenetic activation' 
+creating new condensate with chromatin reorganization. Gene expression 
+indicators (up arrow, down arrow) for each condition."
+```
+
+---
+
+## Writing Tips for Cell Elements
+
+### Summary Tips
+
+1. **First sentence**: Establish the biological context
+2. **Second sentence**: State what was unknown (the gap)
+3. **"Here, we show/identify/demonstrate"**: Clear transition to your work
+4. **Middle sentences**: Key findings with mechanism
+5. **Final sentence**: Significance and implications
+
+### Highlights Tips
+
+- **Start with a noun or verb**: "FOXO4 forms..." or "Activation of..."
+- **One finding per bullet**: Don't combine multiple points
+- **Be specific**: Include the protein/gene/pathway name
+- **Check character count**: Strictly ≤85 characters including spaces
+- **Cover different findings**: Don't repeat the same point
+
+### eTOC Blurb Tips
+
+- **Start with author names**: "Smith et al. show that..."
+- **One or two sentences only**: Keep it punchy
+- **Include the key mechanism**: Not just the finding
+- **End with significance**: Why readers should care
+
+---
+
+## Character Counting for Highlights
+
+Use this to check your highlights:
+
+```
+• This highlight is exactly 52 characters long including sp
+  ↑ Count: 52 characters ✓ (under 85)
+
+• This highlight is getting close to the maximum allowed character limit
+  ↑ Count: 73 characters ✓ (under 85)
+
+• This highlight demonstrates what happens when you try to include way too much info
+  ↑ Count: 88 characters ✗ (over 85 - need to shorten)
+```
+
+---
+
+## See Also
+
+- `cell_press_style.md` - Comprehensive Cell Press writing guide
+- `nature_abstract_examples.md` - Compare with Nature abstract style
+