Objective. Ribonucleotide reductase M2 (RRM2) as an enzyme that catalyzes the deoxyreduction of nucleosides to deoxyribonucleoside triphosphate (dNTP) has been extensively studied, and it plays a crucial role in regulating cell proliferation. However, its role in ischemia-reperfusion injury (I/RI) is still unclear. Methods. SD rats were used as the research object to detect the expression of RRM2 in the myocardium by constructing an I/RI model. At the same time, primary SD neonatal rat cardiomyocytes were extracted, and hypoxia/reoxygenation (H/R) treatment simulated the I/RI model. Using transfection technology to overexpress RRM2 in cardiomyocytes, quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of RRM2, Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability, and immunofluorescence staining was used to detect Ki67 and EdU-positive cells. Western blot (WB) technology was used to detect YAP and its phosphorylation expression. Results. qRT-PCR results indicated that the expression of RRM2 was inhibited in the model group, and cardiomyocytes overexpressing RRM2 can obviously promote the proliferation of primary cardiomyocytes and improve the damage of cardiac structure and function caused by I/R. At the same time, RRM2 can promote the increase of YAP protein expression and the increase of Cyclin D1 mRNA expression. Conclusion. RRM2 expression was downregulated in myocardial tissue with I/R. After overexpression of RRM2, cardiomyocyte proliferation was upregulated and the Hippo-YAP signaling pathway was activated.

Purpose. To investigate the changes in thromboelastography (TEG) in patients with dyslipidemia to study its effect on the blood coagulation status. Methods. 131 patients hospitalized in Fujian Provincial Jinshan Hospital from January 2018 to December 2020 were selected, and 64 cases in the hyperlipidemia (HL) group and 67 cases in the non-HL group were set according to whether their blood lipids were abnormal. By measuring the changes of each parameter of TEG in patients, the relevant parameters R value, K value, α angle, and MA value were calculated. And routine blood coagulation (PT, APTT, INR, FIB, and TT) and routine blood (platelet count) tests were performed on all study subjects to analyze the changes of each index of the coagulation function and each parameter of TED in both groups and explore the clinical value of TEG on HL diseases. Results. Compared with the non-HL group, R and K values decreased, and angle and MA values increased in the HL group ( P < 0.05 ). PT, APTT, and INR values decreased, and FIB values increased in the HL group compared with the nonhyperlipidemic group ( P < 0.05 ). The TT levels were similar in the non-HL group and the HL group ( P > 0.05 ). Compared with the non-HL group, PLT values decreased, and PDW and MPV values increased in the HL group ( P < 0.05 ). R value was positively correlated with APTT, r= 0.373, P = 0.002 . K value was negatively correlated with PLT, r= −0.399, P = 0.002 . α angle and MA values were positively correlated with PLT, r= 0.319/0.475, P = 0.010 / P < 0.001 . The rest of the indexes did not correlate with each parameter of TEG significant correlation. Conclusion. TEG can predict the hypercoagulability and hypocoagulability of blood by the changes of R value, K value, α angle, and MA to evaluate the effect of hyperlipidemia on the coagulation status, which is important for guiding the adjustment of lipid-lowering, antithrombotic, and anticoagulation programs in patients with atherosclerosis combined with hyperlipidemia or postsurgery combined with hyperlipidemia.

Purpose: To evaluate the prognostic value of ghrelin, a growth hormone-releasing peptide, for mortality and readmission in elderly patients with acute heart failure (AHF). Patients and Methods: We measured plasma ghrelin and pro B-type natriuretic peptide (NT-proBNP) levels upon emergency admission in 241 prospectively recruited elderly AHF patients (61.0% men). The outcomes were all-cause mortality and/or readmission due to heart failure (HF). Multivariate Cox proportional hazards regression analyses were used to evaluate the prognostic value of ghrelin. Discrimination, calibration, and reclassification indices were compared between models, with or without ghrelin. Results: During 1.2 years of follow-up, we observed 90 events (57 deaths and 33 readmissions due to HF). Plasma ghrelin levels were significantly elevated in elderly AHF patients, when compared to healthy control subjects (P < 0.001). Patients with events had significantly higher baseline ghrelin levels, when compared to those without (P < 0.001). Ghrelin levels were positively correlated with NT-proBNP levels and HF severity, whereas they were negatively correlated with nutritional status (all P < 0.05). Log transformed ghrelin levels were independently associated with AHF events (hazard ratio = 2.64, 95% confidence interval = 1.11-6.25, P = 0.028). The incorporation of ghrelin into the reference model, or reference with the NT-proBNP model, both improved C-statistics (from 0.742-0.780 and 0.836-0.857; P = 0.074 and 0.044, respectively), resulting in an improvement in net reclassification index (14.42% and 10.45%, P = 0.020 and 0.025, respectively), and integrated discrimination index (5.64% and 3.60%, both P < 0.001). Patients who displayed the above NT-proBNP and ghrelin median levels had a markedly higher risk of AHF adverse events (P < 0.001). Conclusion: Plasma ghrelin is an independent predictor of adverse events in elderly AHF patients. Ghrelin may provide additional value to clinical parameters or NT-proBNP for prognostic risk stratification in AHF.

Objective: Von Hippel-Lindau syndrome (VHL), a rarely inherited disease with autosomal-dominant transmission, can be characterized by pheochromocytoma complicated with various clinical manifestations, such as paroxysmal hypertension, myocardial infarction, arrhythmia, and heart failure. The related case reports are rare, especially referring to myocardial infarction. However, it is important to obtain such a clinical case, since it may facilitate diagnose by utilization of genetic testing and prognosis by early surgical treatment. Design and method: A 53-year-old male patient presented with recurrent and progressive chest pain, hypertension, sweating and palpitation, associated with significant 15-year history of hypertension. Although these symptoms persisted 8 months, he did not receive any treatment before first hospitalization. Transthoracic echocardiography revealed left ventricular enlargement, left ventricular wall thickening, and the decrease of ejection fraction. Blood tests showed significant troponin I, catecholamine, and 24 hours urinary vanilla mantellic acid. ECG showed sinus tachycardia with ischemic changes. Besides, abdominal computed tomography scan revealed a tumor of 5.3 cm in diameter in the right adrenal gland. Thus, the patient was required to remove the tumor after 6 months. However, he hospitalized again due to those deteriorating symptoms. Coronary angiography revealed the left anterior descending stenosis 70%. Then he was admitted to intensive care unit and died of cardiogenic shock. Results: A diagnosis of this VHL syndrome was finally confirmed by genetic pedigree of the family and genetic testing. Gene tests showed that the patient and his daughter carried VHL gene c.G250C heterozygous missense mutation (VHL: p.V84L het), but the elder son without mutation in the same site. VHL type 2C, a subtype of VHL, is characterized by presenting as pheochromocytoma complicated with myocardial damage, myocardial infarction and heart failure. Conclusions: Test of the VHL gene mutation is necessary for the patients presenting as pheochromocytoma with myocardial infarction and their asymptomatic family members. Moreover, early surgical excision of pheochromocytoma may improve the prognosis of this disease.