@synsci/cli-darwin-x64 1.1.97 → 1.1.99

package/bin/skills/venue-templates/assets/examples/cell_summary_example.md

@@ -1,247 +0,0 @@
-# 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/bin/skills/venue-templates/assets/examples/medical_structured_abstract.md

@@ -1,313 +0,0 @@
-# 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
-