Fibroblast growth factor 21 associating with serotonin and dopamine in the cerebrospinal fluid predicts impulsivity in healthy subjects.

BACKGROUND: Impulsivity is more commonly reported in subjects with mental disorders compared to healthy subjects, suggesting a potential application of impulsivity in predicting impulsivity-related mental disorders. However, no biomarker of impulsivity available so far. This study explored the association between cerebrospinal fluid (CSF) fibroblast growth factor 21 (FGF21), a key hormonal mediator of the stress response, and impulsivity in healthy subjects. METHODS: A total of 126 healthy persons subjected to surgery of anterior cruciate ligament were recruited in the present study. The impulsiveness of the subjects was evaluated by the Chinese version of the Barratt Impulsiveness Scale (BIS)-11 before surgery. CSF and blood samples of the subjects were collected before spinal anesthesia for surgery. The levels of FGF21, serotonin and dopamine in CSF and the level of FGF21 in blood of the subjects were measured by ELISA using commercial kits. RESULTS: Negative correlations were found between BIS-11 total score and either FGF21, serotonin or dopamine in CSF. However, BIS-11 total score was not correlated with FGF21 in blood. In addition, FGF21 was positively correlated with serotonin and dopamine in CSF, respectively. Multivariable linear regression models indicated that the decrease of FGF21 level associating with the decrease of serotonin and dopamine level in CSF contributed to the higher impulsivity. Furthermore, receiver operating characteristic curve (ROC) analysis indicated an important role of CSF FGF21 predicting high impulsivity. CONCLUSIONS: FGF21, serotonin and dopamine in CSF associate with impulsivity in opposite directions. The decrease of CSF FGF21 is related to higher impulsivity, and indicate that CSF FGF21 may predict impulsivity in healthy subjects.

De Winter syndrome may be an early electrocardiogram pattern of acute myocardial infarction, two cases report.

BACKGROUND: De Winter syndrome is an electrocardiogram (ECG) pattern related to acute occlusion of the anterior descending artery. The incidence rate of De Winter syndrome is rare, but still requires much attention from clinicians. METHODS: Two patients who finnaly diagnosed with De Winter syndrome were included in our study. RESULTS: A 55-year-old male farmer, who was previously healthy, came to the emergency room due to sudden pain in the precordial area for 6 hours, accompanied with back pain and sweating. The second ECG revealed De Winter syndrome. Emergency coronary angiography was taken, which showed a severe atrioventricular block; diffuse stenosis in the proximal and middle segments of the left anterior descending branch, with 90% stenosis in the severest region. Percutaneous coronary intervention (PCI) of the left anterior descending artery was performed. A 70-year-old man with a history of hypertension arrived at the Emergency Department with chest pain for 3 hours. The first ECG was performed, which was contacted with de winter syndrome. The second ECG demonstrated acute anterior Myocardial infarction. Emergency coronary angiography showed approximately 95% stenosis at the junction of the proximal and middle segments. PCI of the proximal and middle segments of the left anterior descending artery was performed. CONCLUSION: De Winter syndrome is a type of acute coronary syndrome, which may be an early ECG pattern in the development of acute ST-segment elevation myocardial infarction. Therefore, once De Winter syndrome is observed on the ECG, acute coronary syndrome, especially acute anterior descending occlusion should not be ignored.

Puerarin from Pueraria lobate attenuates ischemia-induced cardiac injuries and inflammation in vitro and in vivo: The key role of miR-130a-5p/HMGB2 pathway.

Acute myocardial infarction (AMI) is a common cardiovascular disease and puerarin (Pue) is an active compound from Pueraria lobate with cardio-protective potential. In the current study, the mechanism underlying the cardio-protective effects of Pue was explored by focusing miR-130a-5p/HMGB2 pathway. MiR expression profile was determined and myocardial infarction was induced in cardiomyocytes and rats, which was treated with Pue. The role of miR-130a-5p and downstream HMGB2/NF-κB axis in the cardio-protective effects of Pue was also explored. Pue increased viability and suppressed inflammation in OGD cardiomyocytes, which was associated with the deactivation of HMGB2/NF-κB pathway. After the suppression of miR-130a-5p, the cardio-protective effects of Pue were compromised. In rat models, Pue attenuated structure deterioration and inflammatory response in heart. At the molecular level, miR-130a-5p was up-regulated, and HMGB2 were down-regulated. It was demonstrated that Pue induced the expression of miR-130a-5p, which suppressed the activity of HMGB2/NF-κB, contributing to the attenuation of infarct heart tissues.

The interaction of persistent antiphospholipid antibodies positivity and cigarette smoking is associated with an increased risk of cardiovascular events: Cross-sectional and longitudinal analysis.

BACKGROUND: The antiphospholipid antibody (aPL)-positivity was suggested as a nontraditional risk of coronary artery disease (CAD) and it was associated with cigarette smoking. The co-occurrence of them was usually reported in individuals with cardiovascular diseases. This study was to demonstrate their interaction on the increasing risk of cardiovascular events. METHODS AND RESULTS: A total of 826 consecutive male individuals who underwent coronary angiography (CAG) /percutaneous coronary intervention (PCI) were prospectively followed and classified into three groups based on different smoking statuses. The current smoking subjects had the highest occurrence of aPL-positivity, including aCL IgM (20.1%) and aß2GP1 IgM (15.5%). IgM isotype positivity was an independent risk factor of CAD in the multivariate model, OR: 2.70 (1.52-4.80) for aCL IgM and OR:2.50 (1.35-4.63) for aß2GP1 IgM.The interaction of current smoking and IgM isotype positivity was significantly associated with increased risk of CAD, OR: 8.75(4.59-16.66) for aCL IgM and OR: 8.78(4.28-17.98) for aß2GP1 IgM. During about 3 years of follow-up, the smoking patients carrying persistent aPL positivity had the highest cumulative incidence of recurrent myocardial infarction and in-stent restenosis after CAD. CONCLUSION: The interaction of current smoking and IgM isotype positivity was significantly associated with the increased risk of CAD, including positive aCL IgM and aß2GP1 IgM. Cigarette smoking elevated the risk of subsequent cardiovascular events in the presence of IgM isotype positivity, including recurrent myocardial infarction and in-stent restenosis.

Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway.

Autophagy suppression plays key a role during myocardial fibrosis (MF) progression. Exosomes from stem cells attenuate MF. The current study aimed to explain the antifibrosis effects of exosomes by focusing on microRNAs (miRs). MF was induced in rats using transverse aortic constriction (TAC) method and handled with exosomes from bone mesenchymal stem cells (BMSCs). The results of in vivo assays were verified with H9c2 cells. MiR expression profile was determined using microarray detection. The influence of miR-199a-3p modulation in vivo and in vitro on the antifibrosis effect of exosomes then was assessed. Exosomes attenuated MF by inhibiting inflammation, improving tissue structure, and inhibiting fibrosis-related indicators in TAC rats, and the effects were associated with autophagy activation. In H9c2 cells, exosomes suppressed cell viability, induced cell apoptosis, inhibited fibrosis-related indicators, while and the inhibition of autophagy by 3-MA would block the effect of exosomes. Based on the microarray detection, miR-199a-3p level was selected as therapeutic target. The inhibition of miR-199a-3p impaired the antifibrosis effects of exosomes on H9c2 cells, which was associated with autophagy inhibition. Collectively, exosomes from BMSCs exerted antifibrosis effects via the distant transfer of miR-199a-3p to heart tissues, which induced autophagy by inhibiting mTOR.

Association of growth differentiation factor-15 level with adverse outcomes in patients with stable coronary artery disease: A meta-analysis.

Background and aims: Studies on the association between growth-differentiation factor-15 (GDF-15) level and adverse outcomes have yielded conflicting results in patients with stable coronary artery disease (CAD). This meta-analysis aimed to evaluate the association of baseline GDF-15 level with adverse outcomes in stable CAD patients. Methods: Two authors independently searched PubMed and Embase databases from inception to May 31, 2021 for available studies that investigated the association of baseline GDF-15 level with all-cause mortality, cardiovascular mortality, or major adverse cardiovascular events (MACEs) in stable CAD patients. Pooled multivariable adjusted hazard ratio (HR) with 95% confidence interval (CI) was calculated for the highest vs. the lowest GDF-15 level. Results: Seven studies that involved 28,765 stable CAD patients were identified and analyzed. The meta-analysis showed that the highest GDF-15 level was associated with higher risk of MACEs (HR 1.42; 95% CI 1.29-1.57; p < 0.001), cardiovascular mortality (HR 1.64: 95% CI 1.25-2.14; p < 0.001), and all-cause mortality (HR 2.01; 95% CI 1.67-2.42; p < 0.001) when compared the lowest GDF-15 level. Moreover, the values of GDF-15 level in predicting MACEs were consistently observed in each named subgroup. Conclusions: Elevated blood GDF-15 level is an independent predictor of MACEs, cardiovascular mortality, and all-cause mortality in stable CAD patients. The baseline GDF-15 level may play an important role in the risk stratification of stable CAD patients.

Clinical nursing pathway improves disease cognition and quality of life of elderly patients with hypertension and cerebral infarction.

OBJECTIVE: This study aimed to explore the application effect of clinical nursing pathway model in elderly patients with hypertension and cerebral infarction. METHODS: A total of 106 elderly patients with hypertension and cerebral infarction were recruited and divided into a control group (n=51) and a test group (n=55). Both groups of patients received conventional care, and the test group was given additional care if clinical nursing pathway. The blood pressure indexes, knowledge of stroke, nursing satisfaction, neurological deficit, and activity of daily living (ADL) of the two groups of patients were observed. RESULTS: After nursing care, the scores of Stroke Knowledge Questionnaire (SKQ) and Barthel index (BI) increased in both groups, and they were significantly higher in the test group than in the control group. The scores of systolic blood pressure (SBP), diastolic blood pressure (DBP) and National Institutes of Health Stroke Scale (NIHSS) decreased significantly in both groups after nursing, and they were lower in the test group than the control group. In addition, patients in the test group exhibited higher nursing satisfaction than the control group, as well as higher rates of blood pressure control at discharge, two months, four months and six months after discharge. CONCLUSION: The application of clinical nursing pathway can improve the disease cognition and quality of life of elderly patients with hypertension and cerebral infarction, and promote their recovery.