Caffeic acid: A game changer in pine wood nematode overwintering survival.

Following the invasion by the pine wood nematode (PWN) into north-east China, a notable disparity in susceptibility was observed among Pinaceae species. Larix olgensis exhibited marked resilience and suffered minimal fatalities, while Pinus koraiensis experienced significant mortality due to PWN infection. Our research demonstrated that the PWNs in L. olgensis showed a 13.43% reduction in lipid content compared to P. koraiensis (p < 0.05), which was attributable to the accumulation of caffeic acid in L. olgensis. This reduction in lipid content was correlated with a decreased overwintering survival of PWNs. The diminished lipid reserves were associated with substantial stunting in PWNs, including reduced body length and maximum body width. The result suggests that lower lipid content is a major factor contributing to the lower overwintering survival rate of PWNs in L. olgensis induced by caffeic acid. Through verification tests, we concluded that the minimal fatalities observed in L. olgensis could be attributed to the reduced overwintering survival of PWNs, a consequence of caffeic acid-induced stunting. This study provides valuable insights into PWN-host interactions and suggests that targeting caffeic acid biosynthesis pathways could be a potential strategy for managing PWN in forest ecosystems.

Impact of Bivalirudin on Ischemia/Reperfusion Injury in Patients with Reperfused STEMI Assessed by Cardiac Magnetic Resonance.

Thrombin is an important ischemia/reperfusion injury (IRI) mediator in patients with ST-elevation myocardial infarction (STEMI). This study examines the use of bivalirudin, a direct thrombin inhibitor, in reducing IRI in STEMI patients. STEMI patients (n = 21) were treated with bivalirudin and compared to 21 patients treated with unfractionated heparin (UFH) from the EARLY Assessment of Myocardial Tissue Characteristics by CMR in STEMI (EARLY-MYO-CMR) registry (NCT03768453). Infarct size (IS) and left ventricular ejection fraction (LVEF) were comparable between the two groups at follow up. During the first cardiac magnetic resonance (CMR) scan within the first week after percutaneous coronary intervention (PCI), all patients in both the bivalirudin and UFH groups exhibited myocardial edema. However, the myocardium edema volume was significantly less in the bivalirudin group (p < 0.05). At the one-month follow-up, a smaller proportion of patients in the bivalirudin group than in the UFH group exhibited myocardial edema (4.7% vs. 33.3%, p < 0.05). At the three-month follow-up, myocardial edema had completely resolved in the bivalirudin group, while it persisted in two patients in the UFH group. The incidence and volume of microvascular obstruction (MVO) were significantly lower in the bivalirudin group during the acute phase. Additionally, the incidence of intramyocardial hemorrhage (IMH) was significantly lower in the bivalirudin group during both the acute and follow up (p < 0.05). These findings were corroborated by T2 and T1 mapping results. The study concluded that the use of bivalirudin for anticoagulation is associated with attenuated IRI in STEMI patients who receive primary PCI.

Clinical and genetic characteristics of catecholaminergic polymorphic ventricular tachycardia combined with left ventricular non-compaction.

BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia is an ion channelopathy, caused by mutations in genes coding for calcium-handling proteins. It can coexist with left ventricular non-compaction. We aim to investigate the clinical and genetic characteristics of this co-phenotype. METHODS: Medical records of 24 patients diagnosed with catecholaminergic polymorphic ventricular tachycardia in two Chinese hospitals between September, 2005, and January, 2020, were retrospectively reviewed. We evaluated their clinical and genetic characteristics, including basic demographic data, electrocardiogram parameters, medications and survival during follow-up, and their gene mutations. We did structural analysis for a novel variant ryanodine receptor 2-E4005V. RESULTS: The patients included 19 with catecholaminergic polymorphic ventricular tachycardia mono-phenotype and 5 catecholaminergic polymorphic ventricular tachycardia-left ventricular non-compaction overlap patients. The median age of onset symptoms was 9.0 (8.0,13.5) years. Most patients (91.7%) had cardiac symptoms, and 50% had a family history of syncope. Overlap patients had lower peak heart rate and threshold heart rate for ventricular tachycardia and ventricular premature beat during the exercise stress test (p < 0.05). Sudden cardiac death risk may be higher in overlap patients during follow-up. Gene sequencing revealed 1 novel ryanodine receptor 2 missense mutation E4005V and 1 mutation previously unreported in catecholaminergic polymorphic ventricular tachycardia, but no left ventricular non-compaction-causing mutations were observed. In-silico analysis showed the novel mutation E4005V broke down the interaction between two charged residues. CONCLUSIONS: Catecholaminergic polymorphic ventricular tachycardia overlapping with left ventricular non-compaction may lead to ventricular premature beat/ventricular tachycardia during exercise stress test at lower threshold heart rate than catecholaminergic polymorphic ventricular tachycardia alone; it may also indicate a worse prognosis and requires strict follow-up. ryanodine receptor 2 mutations disrupted interactions between residues and may interfere the function of ryanodine receptor 2.

Impact of Glycemic Control on Coronary Inflammation Evaluated by Computed Tomography Pericoronary Fat Attenuation Index in Patients with Acute Coronary Syndrome.

Background: Coronary inflammation causes significantly increased risk of cardiovascular disease (CVD) in diabetic patients. This study investigated the relationship between coronary local inflammation, detected by pericoronary fat attenuation index (FAI), and different blood glucose control levels in low-risk acute coronary syndrome (ACS) patients with or without diabetes. Methods: A total of 309 patients with low-risk ACS were classified into three groups: non-diabetes, well-regulated diabetes, and poorly regulated diabetes. Pericoronary FAI around the proximal or left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA), were evaluated by coronary computed tomography angiography (CCTA), and systemic inflammatory variables and other biochemical indicators were detected by flow cytometry. Results: Pericoronary FAI values around the proximal LAD, LCX, and RCA in poorly regulated diabetes were significantly higher than those in well-regulated diabetes and non-diabetes, whereas those in well-regulated diabetes were not statistically different from those in non-diabetes. Further, plasma glycated hemoglobin (HbA1c) level was positively correlated with the pericoronary FAI values in LAD, LCX, and RCA. However, no significantly increased systemic inflammatory mediators were found in diabetic patients with poor glycemic control. Conclusions: Diabetic patients with poor glycemic control may have higher coronary local inflammation as detected by pericoronary FAI surrounding the three major coronary arteries. Clinical Trial Registration: NCT05590858.

Mexiletine Shortened QT Interval and Reduced Ventricular Arrhythmias in a Pedigree of Type 2 Long QT Syndrome Combined with Left Ventricular Non-Compaction.

In this study, we present a case of a 22-year-old female with a family history of syncope, suffering from recurrent syncope since childhood. She had an obvious prolonged QTc interval of up to 651 ms, a bifid T wave pattern on electrocardiogram, and torsade de pointes, corresponding to a syncope episode. Additionally, her echocardiogram showed left ventricular non-compaction in the apex. After treatment with mexiletine, the QTc interval has been observed to shorten immediately, and the T wave morphology recovered. A similar effect was also observed in her mother and young sister. Administration of propranolol prolonged her QTc interval. Target sequencing of candidate genes revealed a missense mutation in the pore area of the hERG protein, coded by KCNH2. We diagnosed this as a case of type 2 long QT syndrome in which mexiletine could be effective in shortening the QTc interval.