How is FOLIO Different from Its Predecessors?

FOLIO is a future-oriented library service platform. Enlightened by the results of the 2021 International Survey of Library Automation, the author shared thoughts on how FOLIO meets librarians’ expectations, why it’s a good time to get involved in the FOLIO project and what challenges FOLIO is facing at the current development stage

Cardioneuroablation for successful treatment of symptomatic bradycardia in a 12-year-old child after a 6-month follow-up

BackgroundCardioneuroablation (CNA) is recognized as a promising therapeutic option for adults with severe symptomatic bradycardia caused by excessive vagal tone. However, no pediatric cases have been reported to date. Therefore, the aim of this study is to evaluate the feasibility and efficacy of CNA in children.MethodsA 12-year-old male patient was hospitalized with symptoms of fatigue, palpitations, and syncope for more than 2 months, and was definitively diagnosed with functional sinoatrial node dysfunction by using a 12-lead electrocardiogram, 24-h Holter monitoring, loading dose of atropine test (0.04 mg/kg), and treadmill exercise test. Simultaneously, whole-exome sequencing was performed on the child and his core family members. After completing the preoperative examination and signing the informed consent form, the child underwent CNA therapy.ResultsFirst, the electroanatomic structures of both atria were mapped out by using the Carto 3 system, according to the protocol of purely anatomy-guided and local fractionated intracardiac electrogram–guided CNA methods. Then, the local fractionated intracardiac electrograms of each cardiac ganglionated plexus (GP), including the GP between the aortic root and the medial wall of the superior vena cava, the GP between the posterior wall of the coronary sinus ostium and the left atrium, the GP between the anterior antrum of the right superior pulmonary vein and the superior vena cava, the GP in the superolateral area around the root of the left superior pulmonary vein, the GP around the root of the right inferior pulmonary vein, and the GP around the root of the left inferior pulmonary vein, were used as targets for ablation at a power of 30 W with an ablation index of 350–400. At a 6-month follow-up, the child's heart rhythm saw a complete restoration to sinus rhythm and clinical symptoms disappeared.ConclusionThe first application of CNA in a child with symptomatic sinus bradycardia was achieved with better clinical outcomes. CNA can be carried out cautiously in children under suitable indications

A Case of Pediatric Heart Failure Caused by Anomalous Origin of the Left Coronary Artery from the Pulmonary Artery: Case Report and Literature Review

A female patient aged 3 months and 10 days was admitted to the cardiology department because of symptoms of heart failure. According to the echocardiography results, the patient received a diagnosis of primary endocardial fibroelastosis and was treated with γ-globulin, prednisone, digoxin, and diuretics. Coronary computed tomographic angiography and coronary angiography were performed as there was no improvement after 2 months of treatment. Finally, the patient received a diagnosis of anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). ALCAPA is a rare congenital heart defect that can cause severe heart failure during infancy, and is easily misdiagnosed clinically. In this report, we show the process of misdiagnosis of the case and consult the relevant literature, hoping to improve the understanding and early diagnosis of ALCAPA. </p

An eIF3a gene mutation dysregulates myocardium growth with left ventricular noncompaction via the p-ERK1/2 pathway

Left ventricular noncompaction (LVNC) is a heterogeneous disorder with unclear genetic causes and an unknown mechanism. eIF3a, an important member of the Eukaryotic translation initiation factor 3 (eIF3) family, is involved in multiple biological processes, including cell proliferation and migration during myocardial development, suggesting it could play a role in LVNC development. To investigate the association between a novel variant (c.1145 A- > G) in eIF3a and LVNC, and explore potential mechanisms that could lead to the development of LVNC. A novel eIF3a variant, c.1145 A- > G, was identified by whole-exome sequencing in a familial pedigree with LVNC. Adenovirus vectors containing wild-type eIF3a and the mutated version were constructed and co-infected into H9C2 cells. Cell proliferation, apoptosis, cell migration, and differentiation, as well as phosphorylation of ERK1/2 were studied and were measured by proliferation assays, flow cytometry, real-time PCR and Western blot, respectively. The eIF3a mutation inhibited the proliferation of H9C2 cells, induced apoptosis, promoted cell migration, and inhibited the differentiation of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). The effect of the eIF3a mutation may be attributed to a decrease in expression of p-ERK1/2. A novel eIF3a gene mutation disrupted the p-ERK1/2 pathway and caused decreased myocardium proliferation, differentiation, accelerated migration.This finding may provide some insight into the mechanism involved in LVNC development

An EGLN1 mutation may regulate hypoxic response in cyanotic congenital heart disease through the PHD2/HIF-1A pathway

Cyanotic congenital heart disease (CCHD), a term describing the most severe congenital heart diseases are characterized by the anatomic malformation of a right to left shunt. Although the incidence of CCHD are far less than the that of congenital heart diseases (CHD), patients with CCHD always present severe clinical features such as hypoxia, dyspnea, and heart failure. Chronic hypoxia induces hypoxemia that significantly contributes to poor prognosis in CCHD. Current studies have demonstrated that the prolyl-4-hydroxylase2 (PHD2, encoded by EGLN1)/hypoxia-inducible factor-1A (HIF-1A) pathway is a key regulator of hypoxic response. Thus, we aim to assess the associations of single polymorphisms (SNPs) of the EGLN1 gene and hypoxic response in CCHD. A missense variant of EGLN1 c.380G>C (rs1209790) was found in 46 patients (46/126), with lower hypoxia incidence and higher rate of collateral vessel formation, compared with the wild type (P C showed improved response to hypoxia compared with the wild-type counterparts. The EGLN1 c.380G>C mutation improves hypoxic response through the PHD2/HIF-1A pathway, which may provide a molecular mechanism for hypoxic response in CCHD. The effects of the EGLN1 c.380G>C mutation on CCHD prognosis deserve further investigation. Keywords: Cyanotic congenital heart disease, EGLN1, Hypoxic response, Mutation, Polymorphis

Assessment of Building Physical Vulnerability in Earthquake-Debris Flow Disaster Chain

Abstract Large earthquakes not only directly damage buildings but also trigger debris flows, which cause secondary damage to buildings, forming a more destructive earthquake-debris flow disaster chain. A quantitative assessment of building vulnerability is essential for damage assessment after a disaster and for pre-disaster prevention. Using mechanical analysis based on pushover, a physical vulnerability assessment model of buildings in the earthquake-debris flow disaster chain is proposed to assess the vulnerability of buildings in Beichuan County, China. Based on the specific sequence of events in the earthquake-debris flow disaster chain, the seismic vulnerability of buildings is 79%, the flow impact and burial vulnerabilities of damaged buildings to debris flow are 92% and 28% respectively, and the holistic vulnerability of buildings under the disaster chain is 57%. By comparing different vulnerability assessment methods, we observed that the physical vulnerability of buildings under the disaster chain process is not equal to the statistical summation of the vulnerabilities to independent hazards, which implies that the structural properties and vulnerability of buildings have changed during the disaster chain process. Our results provide an integrated explanation of building vulnerability, which is essential for understanding building vulnerability in earthquake-debris flow disaster chain and building vulnerability under other disaster chains

Cardiomyocyte Differentiation of Rat Bone Marrow Multipotent Progenitor Cells Is Associated with Downregulation of Oct-4 Expression

This study was to determine if bone marrow multipotent adult progenitor cells (MAPCs) underwent cardiac specification and Oct-4 expression during their cardiomyocyte differentiation in vitro. MAPCs were isolated from rat bone marrow, treated with 5-azacytidine (5-aza, 1 muM) for 24 h, and cultured in a serum-free medium for cardiac differentiation for up to 35 days. The cells started to express early cardiac-specific genes Nkx2.5 and GATA-4 with a significant increase in their mRNA level within 24 h after 5-aza treatment. Western blotting analysis and immunofluorescence staining revealed that the cardiac-specific proteins connexin-43 and troponin I were expressed in the cells 7 days after 5-aza treatment. Flow cytometry analysis demonstrated that over 37% of the cells were positive for troponin I by 35 days of differentiation, although the cells did not display spontaneous contraction. On the other hand, the undifferentiated MAPCs expressed a significant level of the stem-cell-specific marker Oct-4 that was dramatically decreased in the cells shortly after the initiation of cardiomyocyte differentiation as evaluated using real-time (RT)-polymerase chain reaction, Western blotting, immunofluorescence staining, and flow cytometry. These data indicated that MAPCs were able to effectively differentiate into cardiomyocyte-like cells after 5-aza induction in association with downregulation of Oct-4 expression.status: publishe

Age-Related Differences in the Association between Plasma High-Sensitivity C-Reactive Protein and Noncalcified or Mixed Coronary Atherosclerotic Plaques

Background. Previous studies have demonstrated that plasma high-sensitivity C-reactive protein (hsCRP) was the predictor for unstable coronary plaque. Patients with noncalcified plaque (NCP) or mixed plaque (MP) have a higher risk of poor outcomes. However, the association between hsCRP and the presence of NCP or MP (NCP/MP) in old adults remains unclear, and if present, whether there exist differences between young and old adults remain unknown. Thus, the aim of this study was to investigate the role of hsCRP in predicting the presence of NCP/MP and evaluate whether age has any impact on this association. Methods. A total of 951 subjects were included in this study. Complete clinical and laboratory data were collected. According to the characteristics of the most stenotic plaque, we divided them into 2 groups: calcified plaque (CP) and NCP/MP. Subjects with no plaque were classified as the control group (CR). Subjects with age≥60 years were defined as older adults, and those with age2.70 mg/L group in older adults. Multiple logistic regression analysis showed that hsCRP was an independent risk factor for the presence of NCP/MP (odds ratio OR=1.093, 95% CI 1.032–1.157, P=0.001) only in older adults. Conclusions. hsCRP is independently associated with the presence of NCP/MP in older adults but not in nonelderly people. These results suggest the potential significance of hsCRP-lowering regimens in older adults with NCP/MP

Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol

Background: We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy in vitro via one of its G protein-coupled receptor subtypes, LPA3. In this study, we examined the role of LPA3 in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction.Methods:In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to LPA3 knocked-down, or pretreated with a β-adrenergic receptor (β-AR) antagonist (propranolol) before LPA/ISO treatment. Cardiomyocyte size and hypertrophic gene (ANP, BNP) mRNA levels were determined. In vivo, LPA3-/- and wild-type mice were implanted subcutaneously with an osmotic mini-pump containing ISO or vehicle for 2 weeks; echocardiography was performed to determine the heart weight/body weight ratio, cardiomyocyte cross-sectional area, and level of ANP mRNA expression. LPA3-/- and wild-type mice were subjected to permanent coronary artery ligation or sham surgery for 4 weeks; cardiac function, including the degree of hypertrophy and infarction size, was determined.Results:In vitro, we found that knocked-down LPA3 in NRCMs did not attenuate ISO-induced hypertrophy, and propranolol was unable to abolish LPA-induced hypertrophy. In vivo, chronic ISO infusion caused cardiac hypertrophy in wild-type mice, while hypertrophic responses to ISO infusion were not attenuated in LPA3-/- mice. However, in a myocardial infarction (MI) model, LPA3-/- mice exhibited reduced cardiac hypertrophy compared to wild-type mice at 4 weeks post-MI, which was associated with reduced cardiac function and increased infarct size.Conclusions: Our data show that LPA3 appears to play a protective role in myocardial hypertrophy post-MI, but does not appear to be involved in the hypertrophy that occurs in response to β-AR stimulation in vivo and in vitro. These results implicate LPA-LPA3 lipid signaling in cardiac hypertrophy occurring after pathological insults like MI, which presents a new variable in β-AR-independent hypertrophy. Thus, modulation of LPA3 signaling might represent a new strategy for preventing the stressed myocardium from ischemia injury