Translational perspectives on precision nutrition, microbiome modulation, and muscle remodeling in critical illness Open Access doi.org/10.59717/j.xinn-nutr…

Longitudinal study: cumulative average screen viewing time was associated with lower academic performance

Nutritional interventions slow coronary calcification, but do they improve clinical outcomes? Open Access doi.org/10.59717/j.xinn-nutr…

Reframing multidomain lifestyle intervention for dementia prevention through equity and implementation Open Access doi.org/10.59717/j.xinn-nutr…

Want to live longer? Don't just eat less, eat smarter! Optimizing macro balance beats strict caloric restriction for healthy aging & longevity. #HealthyAging #Longevity #NutritionScience #PrecisionDiet

Beyond dietary restriction: Towards next-generation precision diets for healthy aging Open Access doi.org/10.59717/j.xinn-nutr…

9/ Summary: Longevity isn't about deprivation, it’s about precision! Focus on high-quality plant foods, smart protein timing, rich fiber, and healthy fats. A proposed dietary and lifestyle pyramid for longevity:

7/ Age-Stratified Nutrition Optimal diets change as we age: • Midlife (36-64): Plant-rich, lower animal protein, high fiber (40-60g). • Older Adults (65+): Moderate-to-higher protein (15-20%) to fight sarcopenia and frailty.

6/ Dietary Fiber: The Longevity Hero High fiber intake (25-30g+ daily) reduces mortality by up to 23%. Fiber feeds gut microbes to produce Short-Chain Fatty Acids (SCFAs), suppressing systemic inflammation. Recommended fiber sources for a longevity die:

5/ Healthy Fats Are Vital Quality over elimination! Polyunsaturated fats (PUFAs) and plant MUFAs lower mortality risk. In contrast, saturated/trans fats & long-term ketogenic diets carry long-term health trade-offs. Recommended fat sources for a longevity diet:

4/ Protein & Amino Acid Balance In midlife, lower total/animal protein slows aging pathways like IGF-1/mTOR. Plant protein consistently lowers all-cause mortality! Restricting specific amino acids extends lifespan in preclinical models. Recommended protein sources:

3/ Carbs Matter Quality > Quantity Data across 400k+ individuals shows a U-shaped risk curve: moderate carbs (~50-55%) are best. Swap refined carbs for low-GI whole grains, legumes, and tubers. Recommended carbohydrate sources for a longevity diet

2/ Longevity is governed by nutrient-sensing pathways: mTOR, IIS, AMPK, and SIRTs. By tweaking macronutrient quality and balance, we can directly modulate these pathways to delay cellular aging. Nutritional signaling pathways involved in macronutrient regulation of aging

Can changing what you eat extend your healthspan as much as cutting calories? A newly published review in The Innovation Nutrition says: YES. Here is how "Precision Nutrition" is replacing severe restriction for healthy aging 🧵👇

Read 6 minutes. Stress reduced by 68%.

How do we sequence ADCs after EVP in advanced bladder cancer. @DrRosenbergMSK Switching payload appears more important than switching target. iZABREN (HER1/3 Topo1) vs platinum chemo and SACTMT (TROP2/TOPO1 vs taxane) in EVP resistant disease are enrolling #GuardSymposium2026

One CT. 18 organs. 146 findings. @ScienceMagazine RADAR: 425K exams, 15M anatomy pairs, no extra labels. Internal AUC 0.913; external 0.87–0.91. 4 cancers up to 0.984 (pathology). Unseen acute abdomen: 0.904. Beat most of 26 radiologists. +~10% sensitivity as a teammate.

Small cell carcinoma of the bladder: why ADC targets from conventional UC do not simply carry over, and what may work instead 🧵 New in @Histo_Journal: 88 SmCCB from Milan and Erlangen, 79 fully profiled by IHC for ASCL1, NEUROD1, POU2F3, YAP1, HNF4α, NE and tuft cell markers, plus 7 therapeutic targets and NECTIN4 FISH. 🔬 Two phenotypes 🟢 High-NE (57/79): ASCL1-driven, NEUROD1-driven or mixed, diffuse synaptophysin, chromogranin and CD56 🟠 Low-NE (22/79): POU2F3-driven, YAP1-driven or TF-negative, weak or absent NE markers, significantly associated with admixed urothelial, glandular or squamous histology 🎯 ADC and BiTE targets, one by one Nectin-4 (membranous) • Completely negative in 75% (60/80) • Median H-score 0, mean 11.6, max 220 • Higher in Low-NE than High-NE (median 1.5 vs 0, P<0.001), consistent with retained urothelial differentiation NECTIN4 amplification (FISH) • 16/73 (21.9%), a frequency comparable to conventional UC • No difference between High-NE and Low-NE (P=0.835) • No association with membranous protein (P=0.099) TROP2 • Completely negative across the cohort HER2, FOLR1, Claudin 18.2 • Rare and weak expression only DLL3 • Positive in 35/43 evaluable High-NE cases (81%) • Nearly absent in Low-NE (P<0.001) • Relevant for DLL3-directed BiTEs such as tarlatamab and for DLL3 ADCs in development SLFN11 • Median H-score 125, significantly higher in High-NE (P=0.006) • Supports testing DNA-damaging strategies in this group 💡 Key takeaways 1️⃣ High-NE SmCCB is largely Nectin-4 protein negative, yet carries NECTIN4 amplifications at rates similar to conventional UC. The amplification is present, the protein is not. 2️⃣ Our hypothesis: this points to NE transdifferentiation from a urothelial precursor that already harboured the amplification. The gene status is retained, while the urothelial protein program, including Nectin-4, is switched off during lineage change. The equal amplification rate in both phenotypes fits this model. It needs confirmation in paired and clonal analyses. 3️⃣ Practical consequence: NECTIN4 FISH alone should not be read as a surrogate for target presence in SmCCB. Gene status and membranous protein both need to be assessed. 4️⃣ Enfortumab vedotin benefit cannot be assumed in High-NE SmCCB. Low-NE tumours with residual urothelial features remain the more plausible candidates for UC-type ADCs. 5️⃣ High-NE SmCCB behaves biologically like SCLC: DLL3-high, SLFN11-high. This makes it a rational population for SCLC-directed strategies. 6️⃣ A tuft cell-like subset exists: POU2F3-driven tumours co-express POU2AF2 (11/16) and ChAT (13/16), with preclinical mSWI/SNF vulnerabilities. 7️⃣ A simple workflow (NE markers ± TF panel) can stratify SmCCB in routine diagnostics today. ⚠️ Limits: retrospective, TMA-based, no treatment or outcome annotation. Treatment-annotated and paired pre/post-therapy cohorts are the next step. Big shout out to Nazario Tenace from San Raffaele he drove this work as fellow. Bright future for this talented pathologist. Shout out also at great collaborators from Sann Raffaele @AndreaNecchi @Albert0Briganti @F_Montorsi and @mauriziocollechia @maurilioponzoni @claudiodoglioni and @UroMoschini Great collaboration between San Raffaele Milan and UK Erlangen, led by Nazario Tenace, with @andreanecchi 🔗 doi.org/10.1111/his.70284

Antibiotics are failing against C. diff! 🦠 Multi-target natural products (MTDLs) neutralise toxins & stop spores without killing gut microflora. A game-changer for superbugs! #PharmaTech #AntimicrobialResistance #GutHealth

26 radiologists. 14 hospitals. RADAR beat most of them on abdominal CT. Then they used it as a teammate: sensitivity +~10%. It also highlights where to look. This is the version of medical AI that actually helps in the reading room.