The role of uromodulin in cardiovascular disease: a review.

Uromodulin, also referred to as Tamm Horsfall protein (THP), is a renal protein exclusively synthesized by the kidneys and represents the predominant urinary protein under normal physiological conditions. It assumes a pivotal role within the renal system, contributing not only to ion transport and immune modulation but also serving as a critical factor in the prevention of urinary tract infections and kidney stone formation. Emerging evidence indicates that uromodulin may serve as a potential biomarker extending beyond renal function. Recent clinical investigations and Mendelian randomization studies have unveiled a discernible association between urinary regulatory protein levels and cardiovascular events and mortality. This review primarily delineates the intricate relationship between uromodulin and cardiovascular disease, elucidates its predictive utility as a novel biomarker for cardiovascular events, and delves into its involvement in various physiological and pathophysiological facets of the cardiovascular system, incorporating recent advancements in corresponding genetics.

Roles of TSP1-CD47 signaling pathway in senescence of endothelial cells: cell cycle, inflammation and metabolism.

Endothelial cells (ECs) serve as a barrier with forming a monolayer lining in the surface of vascular system. Many mature cell types are post-mitotic like neurons, but ECs have the ability to grow during angiogenesis. Vascular endothelial growth factor (VEGF) stimulates growth of vascular ECs derived from arteries, veins, and lymphatics and induces angiogenesis. Senescence of ECs is regarded as a key contributor in aging-induced vascular dysfunction via evoking increase of ECs permeability, impairment of angiogenesis and vascular repair. Several genomics and proteomics studies on ECs senescence reported changes in gene and protein expression that directly correlate with vascular systemic disorder. CD47 functions as a signaling receptor for secreted matricellular protein thrombospondin-1 (TSP1) and plays an important role in several fundamental cellular functions, including proliferation, apoptosis, inflammation, and atherosclerotic response. TSP1-CD47 signaling is upregulated with age in ECs, concurrent with suppression of key self-renewal genes. Recent studies indicate that CD47 is involved in regulation of senescence, self-renewal and inflammation. In this review, we highlight the functions of CD47 in senescent ECs, including modulation of cell cycle, mediation of inflammation and metabolism by the experimental studies, which may provide CD47 as a potential therapeutic target for aging-associated vascular dysfunction.

The therapeutic effect of glucocorticoids on type II respiratory failure, heart failure, and massive pericardial effusion caused by hypothyroidism: A case report.

Background: Hypothyroidism is a disease commonly observed in outpatient clinics but can occasionally cause severe cardiovascular and respiratory diseases requiring hospitalization. Case report: The patient reported herein suffered from heart failure, massive pericardial effusion, type II respiratory failure, and hypothyroidism. There was no related basic diseases of respiratory and cardiovascular system in the past. She failed to be weaned from invasive ventilation multiple times after routine treatment and was finally successfully weaned on day five of receiving the combination therapy of a high-dose methylprednisolone intravenous drip and levothyroxine oral administration. Conclusion: This case report indicates that hypothyroidism may be a cause of type II respiratory failure, heart failure, and massive pericardial effusion without cardiac tamponade and that a combination of levothyroxine and corticosteroids could effectively treat the disease. Clinical workers should consider the role of thyroid function in diagnosis, and the admission team should include this aspect in the monitoring scope. Moreover, the role of hormones in the treatment of patients with severe hypothyroidism should not be ignored, and timely treatment should be provided.

Porous Fe5Si3 intermetallic anode for the oxygen evolution reaction in acidic electrolytes.

Here, we show that a reactive synthesis method of mixed elemental powders can be used to synthesize a porous electrode consisting of an intermetallic Fe5Si3 that exhibits catalytic activity towards oxygen evolution reaction (OER) in acidic solutions, which is capable of delivering 10 mA cm-2 at an overpotential of 0.73 V and a small Tafel slope of ~ 381.8 mV dec-1. The amorphous silica formed in the anode surface during the electrochemical process is multifunctional, as it protects the electrode substrate from corrosion and acts as electrocatalysts for OER. Remarkably, the Si-based intermetallics can be generalized to include other OER catalytic elements (Mn, Fe, Co), including Mn-Si and Co-Si intermetallics.

A Review of Prognosis Model Associated With Cardiogenic Shock After Acute Myocardial Infarction.

Objective: Cardiogenic shock seriously affects the survival rate of patients. However, few prognostic models are concerned with the score of cardiogenic shock, and few clinical studies have validated it. In order to optimize the diagnosis and treatment of myocardial infarction complicated with cardiogenic shock and facilitate the classification of clinical trials, the prognosis score model is urgently needed. Methods: Cardiogenic shock, severe case, prognosis score, myocardial infarction and external verification were used as the search terms to search PubMed, Embase, Web of Science, Cochrane, EBSCO (Medline), Scopus, BMC, NCBI, Oxford Academy, Science Direct, and other databases for pertinent studies published up until 1 August 2021. There are no restrictions on publication status and start date. Filter headlines and abstracts to find articles that may be relevant. The list of references for major studies was reviewed to obtain more references. Results and Conclusions: The existing related models are in urgent need of more external clinical verifications. In the meanwhile, with the development of molecular omics and the clinical need for optimal treatment of CS, it is urgent to establish a prognosis model with higher differentiation and coincidence rates.

Myocarditis combined with hypertrophic cardiomyopathy: a case report.

Myocarditis can cause ventricular wall thickening due to myocardial edema. If the condition improves, the ventricular wall thickening should gradually decrease; a persistent thickening of the patient's ventricular wall indicates the coexistence of hypertrophic cardiomyopathy (HCM) and myocarditis. A 30-year-old man was referred to our hospital with continuous chest pain accompanied by profuse sweating. He suffered from fever for two days (the maximum body temperature: 38 °C) and the conditions improved following the use of antipyretics as self-administered medication before admission. Electrocardiogram exhibited ST-segment elevation in leads I and avL, and ST-T wave changes in leads II, III, avF, and V1-V6. Marked elevation of cardiac troponin I was found on laboratory testing. Respiratory tract infection testing showed negative results. A TORCH screen revealed positive herpes simplex virus (HSV), rubella virus (RV), and cytomegalovirus (CMV) IgG but all with negative IgM titer. Ultrasonic echocardiography showed thickness of the interventricular septum (17 mm) and diffuse left ventricular (LV) hypokinesia, without LV outflow tract obstruction. After consultation with the cardiology team, a diagnosis of myocarditis with HCM was made. Patients with myocarditis should be alerted to the possibility of HCM when there is persistent ventricular wall thickening.

Construction of Charring-Functional Polyheptanazine towards Improvements in Flame Retardants of Polyurethane.

Nitrogen-containing flame retardants have been extensively applied due to their low toxicity and smoke-suppression properties; however, their poor charring ability restricts their applications. Herein, a representative nitrogen-containing flame retardant, polyheptanazine, was investigated. Two novel, cost-effective phosphorus-doped polyheptazine (PCN) and cobalt-anchored PCN (Co@PCN) flame retardants were synthesized via a thermal condensation method. The X-ray photoelectron spectroscopy (XPS) results indicated effective doping of P into triazine. Then, flame-retardant particles were introduced into thermoplastic polyurethane (TPU) using a melt-blending approach. The introduction of 3 wt% PCN and Co@PCN could remarkably suppress peak heat release rate (pHRR) (48.5% and 40.0%), peak smoke production rate (pSPR) (25.5% and 21.8%), and increasing residues (10.18 wt%→17.04 wt% and 14.08 wt%). Improvements in charring stability and flame retardancy were ascribed to the formation of P-N bonds and P=N bonds in triazine rings, which promoted the retention of P in the condensed phase, which produced additional high-quality residues.

Is Vascular Amyloidosis Intertwined with Arterial Aging, Hypertension and Atherosclerosis?

Vascular amyloidosis (VA) is a component of aging, but both VA and aging move forward together. Although, not all age-related molecules are involved with VA, some molecules are involved in a crosstalk between both of them. However, the cellular mechanism by which, vascular cells are phenotypically shifted to arterial remodeling, is not only involved in aging but also linked to VA. Additionally, patients with hypertension and atherosclerosis are susceptible to VA, while amyloidosis alone may provide fertile soil for the initiation and progression of subsequent hypertension and atherosclerosis. It is known that hypertension, atherosclerosis and amyloidosis can be viewed as accelerated aging. This review summarizes the available experimental and clinical evidence to help the reader to understand the advance and underlying mechanisms for VA involvement in and interaction with aging. Taken together, it is clear that VA, hypertension and atherosclerosis are closely intertwined with arterial aging as equal partners.

Successful treatment of a case of acute myocardial infarction due to type A aortic dissection by coronary artery stenting: A case report.

Acute type A aortic dissection (AD) has been recognized as a potentially life threatening condition, which sometimes involves the ostium of the coronary artery and may lead to acute myocardial infarction (AMI). In patients with acute type A AD presenting with clinical signs of AMI, it is crucial to establish the diagnosis rapidly in order to proceed with the correct treatment. The present study reports the diagnosis of a rare case of acute type A AD with the typical presentation of acute inferior MI and cardiogenic shock, which was accidentally diagnosed during catheterization and treated by right coronary ostial occlusion stenting, allowing for further surgical interventions.

An Association Study Identifies Two Single Nucleotide Polymorphisms on Chromosome 11q23.3 as a Risk Locus for Acute Myocardial Infarction in the Chinese Han Population.

BACKGROUND: To evaluate whether the Chinese Han population harbors genetic markers associated with risk of acute myocardial infarction (MI), which have previously been identified in other ethnic populations. METHODS: According to predefined criteria, 549 Chinese patients with acute MI and 551 Chinese subjects (controls) without a history of coronary artery disease (CAD) were selected for the study. Three prevalent single nucleotide polymorphisms (SNPs; rs1412444(LIPA), rs662799(APOA5) and rs964184(ZNF259)) associated with CAD and MI in other ethnic populations, were selected for sequence and association analyses within blood DNA of the Chinese Han population. RESULTS: Only two SNPs, rs662799 (APOA5) and rs964184 (ZNF259) found at two independent loci, were associated with risk of MI in the Chinese Han population. Using Bonferroni correction methods, significant differences in the association of these two SNPs (rs662799 (p = 0.0228) and rs964184 (p = 0.0060)) between Chinese patients with MI versus controls were revealed. CONCLUSIONS: We identified a significant association between two SNPs (rs964184 and rs662799) on chromosome 11q23.3 and MI risk in the Chinese Han population, which extends their clinical relevance to predicting the risk of MI in diverse ethnic populations.

High-resolution analysis of copy number variants in adults with simple-to-moderate congenital heart disease.

As patients with congenital heart disease (CHD) increasingly survive to childbearing age, it becomes important to understand the genetic origins of CHD. In children, CHD is frequently caused by chromosomal imbalances. We searched for submicroscopic imbalances in adults with CHD focusing on simple-to-moderate phenotypes, without associated dysmorphic features, a group not previously examined. A total of 100 Han Chinese adults with a diverse range of isolated CHD and 65 ethnically matched controls were screened using whole-genome array comparative genomic hybridization. Forty-five large (>100 kb) rare copy number variants (CNVs) were identified in 36/100 patients. These variants were not listed in the Database of Genomic Variants nor found in controls. In three of these genomic imbalances (22q11.2, 18q23, 3q21.3), genes that play an important role in cardiac development were implicated, including CRKL, NFATC1, PLXNA1, the latter has not been associated with human CHD before. This study detected a 0.7 Mb 22q11.2 deletion, which marginally overlapped the common 3 Mb 22q11.2 deletion, in one patient with a perimembranous ventricular septal defect without any extracardiac manifestation. Furthermore, we detected a novel inherited aberration dup (16q23.1). Although a causal relationship with CHD remains to be established, this CNVs profile provides a spectrum of genomic imbalances in this condition, and improves the CNV-phenotype correlations.