Background: Glucose metabolism disorder is a common feature in cancer.Cancer cells generate much energy through anaerobic glycolysis, which promote the development of tumors. However, long non-coding RNA may play an important role in this process. Our aim is to explore a prognostic risk model based on the glucose metabolism-related lncRNAs which provides clues that lncRNAs predict a clinical outcome through glucose metabolism in breast cancer.Methods: 1222 RNA-seq were extracted from the TCGA database, and 74 glucose metabolism-related genes were loaded from the GSEA website. Then, 7 glucose metabolism-related lncRNAs risk score model was developed by univariate, Lasso, and multivariate regression analysis. The lncRNA risk model showed that highrisk patients predict a poor clinical outcome with high reliability (P=2.838×10-6).Univariate and multivariate independent prognostic analysis and ROC curve analysis proved that the risk score was an independent prognostic factor in breast cancer with an AUC value of 0.652. Finally, Gene set enrichment analysis showed that cell cycle-related pathways were significantly enriched in a high-risk group. Results: Our results showed that glucose metabolism-related lncRNAs can affect breast cancer progression. 7 glucose metabolism-related lncRNAs prognostic signature was established to evaluate the OS of patients with breast cancer. PICSAR, LINC00839, AP001505.1, LINC00393 were risk factors and expressed highly in the high-risk group. A Nomogram was made based on this signature to judge patients' living conditions and prognosis. Conclusion: 7 glucose metabolism-related lncRNAs risk score model had a high prognostic value in breast cancer. PICSAR, LINC00839, AP001505.1, LINC00393 were risk factors. AP001505.1 expression was increased in most triple-negative breast cancer cells treated with high glucose, which may also take part in breast cancer progression and potential therapeutic targets K E Y W O R D S breast cancer, glucose metabolism, lncRNA, lncRNA risk model

Objectives. Insulin resistance is associated with the prognosis of heart failure (HF) patients. The triglyceride glucose (TyG) index is a simple marker of insulin resistance. However, it remains unclear whether the TyG index is associated with the incidence of readmission in patients with HF. Methods. We enrolled 901 patients with completed records on serum triglyceride and glucose in our study. The TyG index was calculated as log (fasting triglycerides (mg/dL) x fasting glucose (mg/dL)/2). There were 310 cases of readmission and the average TyG index was 7.8 ± 0.7. Restricted cubic spline was fitted to explore the linearity of TyG index associating with 6-month readmission of HF patients. Logistic regression analysis was performed to explore the association between TyG index quartile and the incidence of 6-month readmission. Results. Only the 6-month readmission was significantly different among TyG quartiles, and it was the highest (41.9%) in the lowest quartile (ranging 6.17∼7.36). the TyG index was nonlinearly associated with 6-month readmission ( p for nonlinearity = 0.009), with the lower level of TyG index increasing the risk of 6-month readmission. Besides, multivariable logistic analysis showed that the lowest TyG quartile was associated with a higher incidence of 6-month readmission in the unadjusted model (odds ratio [OR] 1.74, 95% confidence interval [CI] 1.18–2.57; p = 0.005 ), partially adjusted model (OR 1.82, 95%CI 1.22–2.72; p = 0.004 ), and fully-adjusted model (OR 1.65, 95%CI 1.09–2.45; p = 0.024 ). The association was consistent across gender and diabetes group. Conclusion. A lower TyG index independently increased the risk of 6-month readmission in HF patients, which could be a prognostic factor in heart failure.

Pulmonary arterial hypertension (PAH) is a pathophysiological state of abnormally elevated pulmonary arterial pressure caused by drugs, inflammation, toxins, viruses, hypoxia, and other risk factors. We studied the therapeutic effect and target of tetramethylpyrazine (tetramethylpyrazine [TMP]; ligustrazine) in the treatment of PAH and we speculated that dramatic changes in myocardin levels can significantly affect the progression of PAH. In vivo, the results showed that administration of TMP significantly prolonged the survival of PAH rats by reducing the proliferative lesions, right ventricular systolic pressure (RVSP), mean pulmonary arterial pressure (mPAP), and the Fulton index in the heart and lung of PAH rats. In vitro, TMP can regulate the levels of smooth muscle protein 22‐alpha (SM22‐α), and myocardin as well as intracellular cytokines such as NO, transforming growth factor beta (TGF‐β), and connective tissue growth factor (CTGF) in a dose‐dependent manner (25, 50, or 100 μM). Transfection of myocardin small interfering RNA (siRNA) aggravated the proliferation of pulmonary artery smooth muscle cells (PSMCs), and the regulatory effect of TMP on α‐smooth muscle actin (α‐SMA) and osteopontin (OPN) disappeared. The application of 10 nM estrogen receptor alpha (ERα) inhibitor MPP promoted the proliferation of PSMCs, but it does not affect the inhibition of TMP on PSMCs proliferation. Finally, we found that TMP promoted the nucleation of myocardin‐related transcription factor‐A (MRTF‐A) and combined it with myocardin. In conclusion, TMP can inhibit the transformation of PSMCs from the contractile phenotype to the proliferative phenotype by promoting the formation of the nuclear (MRTF‐A/myocardin) transcription complex to treat PAH.