sk-claudecode 1.0.0

package/skills/scientific/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
+

package/skills/scientific/venue-templates/assets/examples/medical_structured_abstract.md

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+# Medical Journal Structured Abstract Examples
+
+Examples of structured abstracts for NEJM, Lancet, JAMA, and BMJ showing the labeled section format expected at medical journals.
+
+---
+
+## NEJM Style (250 words max)
+
+### Example 1: Clinical Trial
+
+```
+BACKGROUND
+Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce cardiovascular 
+events in patients with type 2 diabetes and established cardiovascular 
+disease. Whether these benefits extend to patients with heart failure and 
+reduced ejection fraction, regardless of diabetes status, is unknown.
+
+METHODS
+We randomly assigned 4,744 patients with heart failure and an ejection 
+fraction of 40% or less to receive dapagliflozin (10 mg once daily) or 
+placebo, in addition to recommended therapy. The primary outcome was a 
+composite of worsening heart failure (hospitalization or urgent visit 
+requiring intravenous therapy) or cardiovascular death.
+
+RESULTS
+Over a median of 18.2 months, the primary outcome occurred in 386 of 
+2,373 patients (16.3%) in the dapagliflozin group and in 502 of 2,371 
+patients (21.2%) in the placebo group (hazard ratio, 0.74; 95% confidence 
+interval [CI], 0.65 to 0.85; P<0.001). A first worsening heart failure 
+event occurred in 237 patients (10.0%) in the dapagliflozin group and 
+in 326 patients (13.7%) in the placebo group (hazard ratio, 0.70; 95% 
+CI, 0.59 to 0.83). Death from cardiovascular causes occurred in 227 
+patients (9.6%) and 273 patients (11.5%), respectively (hazard ratio, 
+0.82; 95% CI, 0.69 to 0.98). Effects were similar in patients with and 
+without diabetes. Serious adverse events were similar between groups.
+
+CONCLUSIONS
+Among patients with heart failure and a reduced ejection fraction, 
+dapagliflozin reduced the risk of worsening heart failure or 
+cardiovascular death, regardless of the presence of diabetes.
+```
+
+**Key Features**:
+- Four labeled sections (BACKGROUND, METHODS, RESULTS, CONCLUSIONS)
+- Background: 2 sentences (problem + gap)
+- Methods: Study design, population, intervention, primary outcome
+- Results: Primary outcome with HR and 95% CI, key secondary outcomes
+- Conclusions: Clear, measured statement of findings
+
+---
+
+### Example 2: Observational Study
+
+```
+BACKGROUND
+Long-term use of proton-pump inhibitors (PPIs) has been associated with 
+adverse outcomes in observational studies, but causality remains uncertain. 
+The relationship between PPI use and chronic kidney disease is unclear.
+
+METHODS
+We conducted a prospective cohort study using data from 10,482 participants 
+in the Atherosclerosis Risk in Communities study who were free of kidney 
+disease at baseline. PPI use was ascertained at baseline and follow-up 
+visits. The primary outcome was incident chronic kidney disease, defined 
+as an estimated glomerular filtration rate less than 60 ml per minute per 
+1.73 m² of body-surface area.
+
+RESULTS
+Over a median follow-up of 13.9 years, incident chronic kidney disease 
+occurred in 56.0 per 1000 person-years among PPI users and in 42.0 per 
+1000 person-years among non-users (adjusted hazard ratio, 1.50; 95% 
+confidence interval [CI], 1.14 to 1.96). The association persisted after 
+adjustment for potential confounders, including indication for PPI use 
+and baseline kidney function. Sensitivity analyses using propensity-score 
+matching yielded similar results. No association was observed for 
+histamine H2-receptor antagonist use (hazard ratio, 1.08; 95% CI, 0.87 
+to 1.34).
+
+CONCLUSIONS
+PPI use was associated with an increased risk of incident chronic kidney 
+disease in this community-based cohort. These findings warrant cautious 
+use of PPIs and further investigation to establish causality.
+```
+
+**Key Features**:
+- Appropriate hedging for observational study ("associated with")
+- Incidence rates provided (per 1000 person-years)
+- Sensitivity analyses mentioned
+- Negative control (H2-receptor antagonists)
+- Cautious conclusion acknowledging limitation
+
+---
+
+## Lancet Style (300 words max)
+
+### Example 3: Clinical Trial with Summary Box
+
+```
+BACKGROUND
+Dexamethasone has been shown to reduce mortality in hospitalized patients 
+with COVID-19 requiring respiratory support. We aimed to evaluate whether 
+higher doses of corticosteroids would provide additional benefit in 
+patients with severe COVID-19 pneumonia.
+
+METHODS
+In this randomized, controlled, open-label trial conducted at 18 hospitals 
+in Brazil, we assigned patients with moderate-to-severe COVID-19 (PaO2/FiO2 
+≤200 mm Hg) to receive high-dose dexamethasone (20 mg once daily for 5 
+days, then 10 mg once daily for 5 days) or standard dexamethasone (6 mg 
+once daily for 10 days). The primary outcome was ventilator-free days 
+at 28 days.
+
+FINDINGS
+Between June 17, 2020, and September 20, 2021, we enrolled 299 patients 
+(151 assigned to high-dose dexamethasone and 148 to standard 
+dexamethasone). The mean number of ventilator-free days at 28 days was 
+14·2 (SD 10·8) in the high-dose group and 15·5 (SD 10·4) in the standard 
+group (difference, −1·3 days; 95% CI, −3·9 to 1·3; P=0·32). There was 
+no significant difference in 28-day mortality (high dose 35·8% vs 
+standard 31·8%; hazard ratio 1·16; 95% CI, 0·79 to 1·70). Hyperglycemia 
+requiring insulin was more frequent with high-dose dexamethasone (66·0% 
+vs 53·4%; P=0·027).
+
+INTERPRETATION
+In patients with moderate-to-severe COVID-19 pneumonia, high-dose 
+dexamethasone did not improve ventilator-free days and was associated 
+with increased hyperglycemia compared with standard-dose dexamethasone. 
+These findings do not support the use of high-dose corticosteroids in 
+COVID-19.
+
+FUNDING
+Ministry of Health of Brazil.
+```
+
+**Key Features**:
+- Lancet uses "Findings" instead of "Results"
+- Lancet uses "Interpretation" instead of "Conclusions"
+- Includes funding statement in abstract
+- Decimal point (·) instead of period in numbers (Lancet style)
+
+---
+
+## JAMA Style (350 words max)
+
+### Example 4: Diagnostic Study
+
+```
+IMPORTANCE
+Lung cancer screening with low-dose computed tomography (CT) reduces 
+mortality but identifies many indeterminate pulmonary nodules, leading 
+to unnecessary invasive procedures. Improved risk prediction could 
+reduce harms while preserving benefits.
+
+OBJECTIVE
+To develop and validate a deep learning model for predicting malignancy 
+risk of lung nodules detected on screening CT.
+
+DESIGN, SETTING, AND PARTICIPANTS
+This retrospective cohort study included 14,851 participants with 
+lung nodules from the National Lung Screening Trial (NLST) for model 
+development and 5,402 participants from an independent multi-site 
+validation cohort (2016-2019). Data analysis was performed from 
+January to November 2022.
+
+EXPOSURES
+Deep learning model prediction of malignancy risk based on CT imaging.
+
+MAIN OUTCOMES AND MEASURES
+The primary outcome was lung cancer diagnosis within 2 years. Model 
+performance was assessed by area under the receiver operating 
+characteristic curve (AUC), sensitivity, specificity, and comparison 
+with radiologist assessments.
+
+RESULTS
+In the validation cohort (median age, 65 years; 57% male), 312 nodules 
+(5.8%) were diagnosed as lung cancer within 2 years. The deep learning 
+model achieved an AUC of 0.94 (95% CI, 0.92-0.96), compared with 0.85 
+(95% CI, 0.82-0.88) for the Lung-RADS categorization used by radiologists 
+(P<0.001). At 95% sensitivity, the model achieved 68% specificity compared 
+with 38% for Lung-RADS, corresponding to a 49% reduction in false-positive 
+nodules requiring follow-up. The model's performance was consistent across 
+subgroups defined by nodule size, location, and patient demographics.
+
+CONCLUSIONS AND RELEVANCE
+A deep learning model for lung nodule malignancy prediction outperformed 
+current clinical standards and could substantially reduce false-positive 
+findings in lung cancer screening, decreasing unnecessary surveillance 
+and invasive procedures.
+```
+
+**Key Features**:
+- JAMA-specific sections (IMPORTANCE, OBJECTIVE, DESIGN...)
+- "Importance" section required (2-3 sentences on why this matters)
+- Detailed design section
+- "Exposures" clearly stated
+- "Main Outcomes and Measures" explicit
+
+---
+
+## BMJ Style (300 words max)
+
+### Example 5: Cohort Study
+
+```
+OBJECTIVE
+To examine the association between statin use and risk of Parkinson's 
+disease in a large population-based cohort.
+
+DESIGN
+Prospective cohort study.
+
+SETTING
+UK Biobank, 2006-2021.
+
+PARTICIPANTS
+402,251 adults aged 40-69 years without Parkinson's disease at baseline.
+
+MAIN OUTCOME MEASURES
+Incident Parkinson's disease identified through hospital admissions, 
+primary care records, and death certificates. Hazard ratios were 
+estimated using Cox regression, adjusted for age, sex, education, 
+smoking, alcohol, physical activity, body mass index, and comorbidities.
+
+RESULTS
+Over a median follow-up of 12.3 years, 2,841 participants developed 
+Parkinson's disease (incidence rate 5.7 per 10,000 person-years). 
+Statin use at baseline was not associated with incident Parkinson's 
+disease (adjusted hazard ratio 0.95, 95% confidence interval 0.87 to 
+1.04). Results were consistent across analyses stratified by statin 
+type (lipophilic vs hydrophilic), dose, and duration of use, and in 
+sensitivity analyses accounting for reverse causation. No protective 
+association was observed in analyses restricted to participants with 
+high cardiovascular risk or in propensity-score matched cohorts.
+
+CONCLUSIONS
+In this large prospective cohort, statin use was not associated with 
+reduced risk of Parkinson's disease, contrary to findings from some 
+previous observational studies. The null findings were robust across 
+multiple sensitivity analyses. These results do not support a 
+neuroprotective effect of statins against Parkinson's disease.
+
+WHAT IS ALREADY KNOWN ON THIS TOPIC
+Previous observational studies have yielded inconsistent results 
+regarding statin use and Parkinson's disease risk.
+
+WHAT THIS STUDY ADDS
+This large prospective study with long follow-up found no evidence 
+that statin use protects against Parkinson's disease.
+```
+
+**Key Features**:
+- BMJ uses abbreviated section headers
+- Includes "What is already known" and "What this study adds" boxes
+- Design, Setting, and Participants as separate sections
+- Clear Main Outcome Measures section
+
+---
+
+## Key Differences Between Journals
+
+| Element | NEJM | Lancet | JAMA | BMJ |
+|---------|------|--------|------|-----|
+| **Word limit** | 250 | 300 | 350 | 300 |
+| **Results label** | RESULTS | FINDINGS | RESULTS | RESULTS |
+| **Conclusions label** | CONCLUSIONS | INTERPRETATION | CONCLUSIONS AND RELEVANCE | CONCLUSIONS |
+| **Unique sections** | — | Funding in abstract | IMPORTANCE | What is known/adds |
+| **Decimal style** | Period (.) | Centered dot (·) | Period (.) | Period (.) |
+
+---
+
+## Essential Elements for All Medical Abstracts
+
+### Background/Context
+- Disease burden or clinical problem (1 sentence)
+- Knowledge gap or rationale for study (1 sentence)
+
+### Methods
+- Study design (RCT, cohort, case-control)
+- Setting (number of sites, country/region)
+- Participants (N, key inclusion criteria)
+- Intervention or exposure
+- Primary outcome with definition
+
+### Results
+- Number enrolled and analyzed
+- Primary outcome with effect size and 95% CI
+- Key secondary outcomes
+- P-values for primary comparisons
+- Adverse events (if applicable)
+
+### Conclusions
+- Clear statement of main finding
+- Appropriate hedging based on study design
+- Clinical implication (optional, 1 sentence)
+
+---
+
+## Common Mistakes in Medical Abstracts
+
+❌ **Missing confidence intervals**: "HR 0.75, P=0.02" → include 95% CI
+❌ **Relative risk only**: Add absolute risk reduction, NNT
+❌ **Causal language for observational studies**: "PPIs cause kidney disease"
+❌ **Overstated conclusions**: Claims exceeding evidence
+❌ **Missing sample sizes**: Always include N for each group
+❌ **Vague outcomes**: "Improved outcomes" without specific definition
+
+---
+
+## See Also
+
+- `medical_journal_styles.md` - Comprehensive medical writing guide
+- `venue_writing_styles.md` - Style comparison across venues
+