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RISK / BOUNDARY

Prevalence, risk factors, and outcomes of refeeding-like syndrome in very low birth weight infants: A descriptive study.

Refeeding-like syndrome (RLS) occurs in very low birth weight (VLBW) (<1500 g) infants receiving parenteral nutrition. Little is known about prevalence, risk factors, or outcomes. We performed a single-center descriptive cohort study in 739 VLBW infants born between October 2016 and December 2023. The co-primary outcomes were RLS during the first week of life (any serum phosphate <4 mg/dL [<1.29 mmol/L]) and severe RLS (<2.5 mg/dL [<0.81 mmol/L]). We also examined clinical outcomes associated with RLS, as well as associations of infant gestation length, fetal growth, and maternal hypertensive disorders with RLS outcomes, as well as associations of RLS with infant outcomes, adjusting for covariates in logistic regression. Mean (standard deviation, SD) gestational age was 29.1 (2.8) weeks, 174 (23.5%) infants were small for gestational age (SGA), 36.6% had RLS, and 6.6% had severe refeeding-like syndrome (sRLS). Maternal hypertension was associated with higher odds of RLS (unadjusted odds ratio [OR] 1.8; 95% CI: 1.3, 2.4). Having gestational age <27 + 0 weeks (adjusted OR [aOR] 1.8; 95% CI: 1.2, 2.6) and being small for gestational age (aOR: 4.62; 95% CI: 3.2, 6.6) both increased the odds of RLS. Refeeding-like Syndrome was associated with higher odds of severe intraventricular hemorrhage and severe retinopathy of prematurity. Refeeding-like syndrome is common among VLBW infants, particularly those born with lower gestational age and impaired fetal growth, and may contribute to morbidities associated with VLBW infants. These findings support the importance of screening and preventive strategies.

Evidence boundary: 观察性队列可识别风险关联，不能自行推导具体营养处方或因果预防效果。

Source: PMID:42502881

WEEKEND OBSERVATION

Integrated multi-level transcriptomic and bioinformatics analysis identifies lipid metabolism-ubiquitination signatures and reveals ATG5, ASB4, LDLR, and CD36 as Candidate biomarkers in insulin resistance.

Observation and source date: 2026-07-26. This issue uses PubMed Date-Publication records; the same-day arXiv submitted-date window returned no relevant records.

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Insulin resistance (IR) is the core pathological basis of type 2 diabetes mellitus (T2DM). This study aimed to identify core lipid metabolism-ubiquitination-related feature genes in IR. Integrative transcriptomic and functional analysis screened differential genes via multiple machine learning models. Gene set enrichment analysis (GSEA), regulatory network prediction, and immune infiltration analysis were performed. C2C12 IR models were constructed, and ATG5 was knocked down to detect glucose-lipid metabolism, inflammation, and insulin signaling. Results showed that four feature genes were identified: Good genes Ankyrin Repeat And SOCS Box Containing 4 (ASB4)/ Low Density Lipoprotein Receptor (LDLR) and Bad genes ATG5/ CD36 molecule (CD36 blood group) (CD36). They were enriched in metabolism/inflammation pathways consistent with IR phenotypes. Regulatory network analysis predicted potential upstream microRNAs (miRNAs) and transcription factors (TFs) modulating these feature genes. IR/diabetes groups had lower ImmuneScores vs. insulin-sensitive groups. ATG5 was upregulated in IR models. Its knockdown inhibited autophagy, improved glucose and lipid metabolism, decreased inflammatory cytokines, and exerted no influence on cell viability. In conclusion, ASB4, LDLR, ATG5, and CD36 are potential IR biomarkers. ATG5 regulates IR via autophagy, insulin signaling, and metabolism, serving as a therapeutic target for metabolic diseases.

Evidence boundary: 细胞模型和计算筛选只能支持候选机制，不能据此把ATG5写成已证实的人体治疗靶点。

Source: PMID:42503036

Observation

2026-07-26

Asia/Shanghai · Sunday

Retrieved

PubMed Date-Publication

Selected

primary-source and boundary screen

Same-day arXiv

no older batch relabelled

METHOD / NEXT

Association between lifestyle and risk of early-onset cancer: Evidence from the European Prospective Investigation into Cancer and Nutrition and the UK Biobank.

The incidence of early-onset cancers (EOCs), defined as cancers diagnosed before 50 years of age, has risen globally over the past three decades. The association between modifiable lifestyle factors and EOC risk has been poorly investigated. Participants enrolled before age 50 in EPIC (39,459 men; 110,991 women) and the UK Biobank (52,188 men; 62,528 women) were analysed. We examined the association between smoking, alcohol consumption, body mass index (BMI), physical activity and diet, and risk of lifestyle-related EOCs - including cancer of the breast, lung, colorectum, stomach, liver, cervix, oesophagus, bladder, and others. Each risk factor was scored from 0 (most unfavourable) to 4 (most favourable). Cohort-specific hazard ratios (HR) with 95% confidence intervals (CI) were estimated in Cox regression models and pooled via a meta-analytic approach. We observed 361 lifestyle-related EOCs in men and 2618 in women, including 1765 breast cancers. In men, one-point increase in the smoking score, indicating less smoking, was inversely associated with risk of lifestyle-related EOC (HR 0.82, 95% CI: 0.76-0.88). In women, each one-point increase in smoking (less smoking), BMI (lower BMI), and physical activity (more active) scores was inversely associated with risk of lifestyle-related EOC excluding breast cancer (HRs: 0.89 [0.84-0.93], 0.93 [0.89-0.98], 0.95 [0.90-1.00], respectively). For breast cancer, only physical activity showed a statistically significant association (HR 0.95 [0.91-0.995]). Alcohol and diet showed no association. These findings support the importance of adopting a healthy lifestyle early in life to reduce cancer risk before the age of 50.

Evidence boundary: 这是观察性关联；饮酒和饮食未见总体关联，不能把相关结果简化成个体化因果承诺。

Source: PMID:42269246

Integrated multi-level transcriptomic and bioinformatics analysis identifies lipid metabolism-ubiquitination signatures and reveals ATG5, ASB4, LDLR, and CD36 as Candidate biomarkers in insulin resistance.

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