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Fulltext Percutaneous coronary intervention in Asians--are there differences in clinical outcome?

Koh AS, Khin LW, Choi LM, Sim LL, Chua TS, Koh TH, et al.

BMC Cardiovasc Disord, 2011;11:22.
PMID: 21605387 DOI: 10.1186/1471-2261-11-22

Ethnic differences in clinical outcome after percutaneous coronary intervention (PCI) have been reported. Data within different Asian subpopulations is scarce. We aim to explore the differences in clinical profile and outcome between Chinese, Malay and Indian Asian patients who undergo PCI for coronary artery disease (CAD).
Fulltext Triptolide inhibits epithelial-mesenchymal transition phenotype through the p70S6k/GSK3/β-catenin signaling pathway in taxol-resistant human lung adenocarcinoma

Tian Y, Li P, Xiao Z, Zhou J, Xue X, Jiang N, et al.

Transl Lung Cancer Res, 2021 Feb;10(2):1007-1019.
PMID: 33718039 DOI: 10.21037/tlcr-21-145

Background: Chemotherapy is one of the primary treatments for both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC), however, chemoresistance develops over time and is a bottleneck to effective chemotherapy worldwide. Therefore, the development of new potent therapeutic agents to overcome chemoresistance is of utmost importance. Triptolide is a natural component extracted from Tripterygium Wilfordii, a Chinese plant; our study aimed to evaluate its anti-tumor effects in taxol-resistant human lung adenocarcinoma and investigate its molecular mechanisms of chemoresistance.
Methods: Triptolide's inhibition of cell viability was detected by sulforhodamine B (SRB) assay. Cell cycle was measured by flow cytometry and cell apoptosis was assessed by flow cytometry and western blot. Expression of β-catenin was analyzed by western blot and immunofluorescence (IF). The anti-tumor effects of triptolide were determined using a subcutaneous in-vivo model. Cell proliferation and apoptosis were evaluated by immunohistochemistry (IHC) and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, respectively. The expression level of p-p70S6K and p-GSK-3α/β was evaluated by western blot and IHC.
Results: Triptolide inhibited cell proliferation, induced S-phase cell cycle arrest and apoptosis in taxol-resistant A549 (A549/TaxR) cells. Moreover, intraperitoneal injection of triptolide resulted in a significant delay of tumor growth without obvious systemic toxicity in mice. Additionally, triptolide reversed epithelial-mesenchymal transition (EMT) through repression of the p70S6K/GSK3/β-catenin signaling pathway.
Conclusions: Our study provides evidence that triptolide can reverse EMT in taxol-resistant lung adenocarcinoma cells and impairs tumor growth by inhibiting the p70S6K/GSK3/β-catenin pathway, indicating that triptolide has potential to be used as a new therapeutic agent for taxol-resistant lung adenocarcinoma.
Fulltext Lixisenatide treatment improves glycaemic control in Asian patients with type 2 diabetes mellitus inadequately controlled on metformin with or without sulfonylurea: a randomized, double-blind, placebo-controlled, 24-week trial (GetGoal-M-Asia)

Yu Pan C, Han P, Liu X, Yan S, Feng P, Zhou Z, et al.

Diabetes Metab Res Rev, 2014 Nov;30(8):726-35.
PMID: 24639432 DOI: 10.1002/dmrr.2541

BACKGROUND: This study assessed the efficacy and safety of the once-daily glucagon-like peptide-1 receptor agonist, lixisenatide, in Asian patients with type 2 diabetes mellitus inadequately controlled on metformin ± sulfonylurea.
METHODS: In this 24-week, double-blind, placebo-controlled, multinational study, patients were randomized to lixisenatide 20 µg once daily or placebo. The primary endpoint was absolute change in glycated haemoglobin (HbA1c ) from baseline to week 24.
RESULTS: A total of 391 patients were randomized. Lixisenatide significantly reduced HbA1c levels compared with placebo (LS mean difference: -0.36%, p = 0.0004). A significantly higher proportion of lixisenatide-treated patients achieved HbA1c targets of <7% (p = 0.003) and ≤6.5% (p = 0.001) versus placebo. Lixisenatide was associated with a statistically significant reduction in 2-h postprandial plasma glucose after a standardized breakfast versus placebo (LS mean difference: -4.28 mmol/L, p
Impact of age on the comparison between short-term vs 12-month dual antiplatelet therapy in patients with acute coronary syndrome treated with the COMBO dual therapy stent: 2-Year follow-up results of the REDUCE trial

Kedhi E, Verdoia M, Suryapranata H, Damen S, Camaro C, Benit E, et al.

Atherosclerosis, 2021 03;321:39-44.
PMID: 33639478 DOI: 10.1016/j.atherosclerosis.2021.02.006

BACKGROUND AND AIMS: The impact of advanced age on the optimal duration of dual antiplatelet therapy (DAPT) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary revascularization (PCI) is still greatly debated. Therefore, the aim of the present sub-analysis of the REDUCE trial was to assess the impact of age on the comparison between a short 3 months vs standard 12 months DAPT in ACS patients treated with the COMBO Dual Stent Therapy.
METHODS: The REDUCE trial is a prospective, multicenter, investigator-initiated study that randomized ACS patients undergoing PCI with the COMBO drug eluting stent to either 3 or 12 months of DAPT. The study population was divided according to age (
Oxidized phospholipids: evolution, signaling, cell death, and human diseases

Ouyang SH, Sun WY, Duan WJ, Wu YP, Lin XM, Gong HB, et al.

Sci Bull (Beijing), 2026 Oct 17.
PMID: 42977628 DOI: 10.1016/j.scib.2026.10.026

Oxidized phospholipids (OxPLs) represent a class of molecules generated during evolution that shift from fundamental membrane building-blocks to key signaling mediators, linking lipid metabolism, cellular redox homeostasis and multi-faceted cell-fate control. Generated by both enzymatic and non-enzymatic peroxidation events, OxPLs engage in extensive signaling crosstalk with lyso-phospholipids and oxylipins. The FerroLipid framework describes iron-lipid peroxidation crosstalk to contextualize iron-dependent lipid signaling. OxPLs govern diverse regulated cell-death programs: they act as lipid death signals in apoptosis and ferroptosis, tune ferroptotic outputs through intrinsic antioxidant systems, and exert context-specific modulatory effects on pyroptosis and other cell-death modalities. Beyond cell-death execution, OxPLs signal through pattern-recognition, scavenger and nuclear receptors to orchestrate inflammation, membrane remodeling, phagocytic clearance, autophagy, mitophagy and protein homeostasis. Threshold-dependent accumulation of OxPLs drives pathological processes across neurodegenerative, metabolic, cardiovascular, neoplastic and infectious diseases; their disease-specific molecular signatures confer potential as both diagnostic biomarkers and therapeutic targets. Redox phospholipidomics coupled with mass-spectrometry imaging enables accurate, species-resolved profiling of distinct OxPL species. Multiple pharmacological approaches and gene-editing interventions have demonstrated tangible translational prospects for OxPL-oriented therapy. This review synthesizes existing knowledge of OxPL biology from evolutionary origins and signaling mechanisms to disease relevance, analytical tools and therapeutic opportunities. It highlights major unresolved research bottlenecks and provides a solid conceptual foundation for advancing lipid-targeted treatments for complex human disorders.