Successful Long-Term Aspirin Desensitization in a Pilot With Aspirin-Exacerbated Respiratory Disease.

Aspirin-exacerbated respiratory disease (AERD) is a triad of asthma, chronic rhinosinusitis with nasal polyposis (CRSwNP), and adverse respiratory reactions to the ingestion of aspirin/non-steroidal anti-inflammatory drugs.1 Patients with AERD are frequently plagued with CRSwNP that is difficult to manage with systemic steroids, nasal steroids, and surgical polypectomy, often requiring multiple endoscopic sinus surgeries and frequent otolaryngology follow-up.2,3 There are an abundance of therapies to treat CRSwNP in the setting of AERD, all with varying costs, efficacies, and indications for treatment.

A Case of Trimethoprim-Sulfamethoxazole-Induced Aseptic Meningitis Masquerading as Septic Shock.

Trimethoprim-sulfamethoxazole-induced aseptic meningitis (TSIAM) is a rare adverse reaction to a commonly prescribed antibiotic. We describe a case of severe TSIAM which resembled septic shock. A 30-year-old male with relapsed Hodgkin's lymphoma 25 days status post autologous stem cell transplant presented to our clinic for evaluation of trimethoprim-sulfamethoxazole (TMP-SMX) hypersensitivity.

Severe Heart Failure in an Infant Born to a Mother Diagnosed With Influenza A Before Delivery.

Neonatal myocarditis and heart failure secondary to maternal infection with a myocarditis-associated virus in the weeks preceding delivery is rare. To our knowledge, this is the first report of an infant with myocarditis and heart failure in the setting of a maternal diagnosis of influenza A. Influenza is, however, known to be a cause of myocarditis in children, and several studies have shown vertical transmission of antibodies to influenza.

Electrospun Bimetallic NiCr Nanoparticles@Carbon Nanofibers as an Efficient Catalyst for Hydrogen Generation from Ammonia Borane.

In this study, we report on the fabrication and utilization of NiCr alloy nanoparticles (NPs)-decorated carbon nanofibers (CNFs) as efficient and competent non-precious catalysts for the hydrolytic dehydrogenation of ammonia borane (AB) at 25 ± 2 °C. The introduced NFs have been fabricated in one step using a high-temperature thermal decomposition of the prepared electrospun nanofiber mats (nickel acetate tetrahydrate, chromium acetate dimer, and polyvinyl alcohol) in an inert atmosphere. The chemical composition of the NFs with different proportions of NiCr (x = 0.

Discovery of an Experimental Model of Unicuspid Aortic Valve.

Background: The epithelial growth factor receptor family of tyrosine kinases modulates embryonic formation of semilunar valves. We hypothesized that mice heterozygous for a dominant loss-of-function mutation in epithelial growth factor receptor, which are mice, would develop anomalous aortic valves, valve dysfunction, and valvular cardiomyopathy.

Methods And Results: Aortic valves from mice and control mice were examined by light microscopy at 2.

Synthesis of Amorphous Co Nanoparticles Supported onto TiO₂ Nanofibers as a Catalyst for Hydrogen Generation from the Hydrolysis of Ammonia Borane.

Co0 nanoparticles supported on TiO2 nanofibers (nanocomposite) were prepared using a simple electrospinning technique and In-Situ chemical reduction. The synthesized nanocomposite was used to generate hydrogen from ammonia borane (AB). Standard characterization techniques revealed dense distribution of Co0 nanoparticles (Co NPs) onto the TiO2 nanofibers (TiO2 NFs) in the prepared nanocomposite.

Fibrotic Aortic Valve Stenosis in Hypercholesterolemic/Hypertensive Mice.

Objective: Hypercholesterolemia and hypertension are associated with aortic valve stenosis (AVS) in humans. We have examined aortic valve function, structure, and gene expression in hypercholesterolemic/hypertensive mice.

Approach And Results: Control, hypertensive, hypercholesterolemic (Apoe(-/-)), and hypercholesterolemic/hypertensive mice were studied.

Spontaneous Aortic Regurgitation and Valvular Cardiomyopathy in Mice.

Objective: We studied the mechanistic links between fibrocalcific changes in the aortic valve and aortic valve function in mice homozygous for a hypomorphic epidermal growth factor receptor mutation (Wave mice). We also studied myocardial responses to aortic valve dysfunction in Wave mice.

Approach And Results: At 1.

Aortic valve sclerosis in mice deficient in endothelial nitric oxide synthase.

Risk factors for fibrocalcific aortic valve disease (FCAVD) are associated with systemic decreases in bioavailability of endothelium-derived nitric oxide (EDNO). In patients with bicuspid aortic valve (BAV), vascular expression of endothelial nitric oxide synthase (eNOS) is decreased, and eNOS(-/-) mice have increased prevalence of BAV. The goal of this study was to test the hypotheses that EDNO attenuates profibrotic actions of valve interstitial cells (VICs) in vitro and that EDNO deficiency accelerates development of FCAVD in vivo.

Osteoprotegerin inhibits aortic valve calcification and preserves valve function in hypercholesterolemic mice.

Background: There are no rigorously confirmed effective medical therapies for calcific aortic stenosis. Hypercholesterolemic Ldlr (-/-) Apob (100/100) mice develop calcific aortic stenosis and valvular cardiomyopathy in old age. Osteoprotegerin (OPG) modulates calcification in bone and blood vessels, but its effect on valve calcification and valve function is not known.

Vascular function during prolonged progression and regression of atherosclerosis in mice.

Objective: Endothelial dysfunction is associated with atherosclerosis in mice, but it is difficult to reduce cholesterol levels enough to study regression of atherosclerosis in genetically modified mice. The goal of this study was to examine vascular structure and function before and after reducing elevated plasma lipid levels with a genetic switch in Reversa mice, and identify novel mechanisms contributing to structural and functional improvements in the vasculature after reduction of blood lipids.

Methods And Results: After 6 months of hypercholesterolemia, endothelial function (maximum relaxation to acetylcholine) in aorta was impaired and responses to nitric oxide were unaffected.

Pioglitazone attenuates valvular calcification induced by hypercholesterolemia.

Objective: Development of calcific aortic valve stenosis involves multiple signaling pathways, which may be modulated by peroxisome proliferator-activated receptor-γ). This study tested the hypothesis that pioglitazone (Pio), a ligand for peroxisome proliferator-activated receptor-γ, inhibits calcification of the aortic valve in hypercholesteremic mice.

Methods And Results: Low density lipoprotein receptor(-/-)/apolipoprotein B(100/100) mice were fed a Western-type diet with or without Pio (20 mg/kg per day) for 6 months.

Evidence for active regulation of pro-osteogenic signaling in advanced aortic valve disease.

Objective: To test the hypothesis that valvular calcium deposition, pro-osteogenic signaling, and function can be altered in mice with advanced aortic valve disease.

Methods And Results: "Reversa" mice were given a Western-type diet for 12 months and screened for the presence of aortic valve stenosis. Mice with advanced valve disease were assigned to 1 of 2 groups: (1) those with continued progression for 2 months and (2) those with regression for 2 months, in which lipid lowering was accomplished by a genetic switch.

MnSOD protects against COX1-mediated endothelial dysfunction in chronic heart failure.

Endothelial function is impaired by oxidative stress in chronic heart failure (HF). Mechanisms that protect against increases in oxidative stress in HF are not clear. The goal of this study was to determine whether manganese superoxide dismutase (MnSOD) plays a key role in protecting against endothelial dysfunction in HF.

Lowering plasma cholesterol levels halts progression of aortic valve disease in mice.

Background: Treatment of hyperlipidemia produces functional and structural improvements in atherosclerotic vessels. However, the effects of treating hyperlipidemia on the structure and function of the aortic valve have been controversial, and any effects could be confounded by pleiotropic effects of hypolipidemic treatment. The goal of this study was to determine whether reducing elevated plasma lipid levels with a "genetic switch" in Reversa mice (Ldlr-/-/Apob(100/100)/Mttp(fl/fl)/Mx1-Cre+/+) reduces oxidative stress, reduces pro-osteogenic signaling, and retards the progression of aortic valve disease.

Dysregulation of antioxidant mechanisms contributes to increased oxidative stress in calcific aortic valvular stenosis in humans.

Objectives: The aim of this study was to determine whether oxidative stress is increased in calcified, stenotic aortic valves and to examine mechanisms that might contribute to increased oxidative stress.

Background: Oxidative stress is increased in atherosclerotic lesions and might play an important role in plaque progression and calcification. The role of oxidative stress in valve disease is not clear.

Role of angiotensin II in endothelial dysfunction induced by lipopolysaccharide in mice.

Endotoxin [or lipopolysaccharide (LPS)] increases levels of superoxide in blood vessels and impairs vasomotor function. Angiotensin II plays an important role in the generation of superoxide in several disease states, including hypertension and heart failure. The goal of this study was to determine whether the activation of the renin-angiotensin system contributes to oxidative stress and endothelial dysfunction after endotoxin.

Effects of a common human gene variant of extracellular superoxide dismutase on endothelial function after endotoxin in mice.

A common gene variant in the heparin-binding domain (HBD) of extracellular superoxide dismutase (ECSOD) may predispose human carriers to ischaemic heart disease. We have demonstrated that the HBD of ECSOD is important for ECSOD to restore vascular dysfunction produced by endotoxin. The purpose of this study was to determine whether the gene variant in the HBD of ECSOD (ECSOD(R213G)) protects against endothelial dysfunction in a model of inflammation.

Gene transfer of extracellular superoxide dismutase improves relaxation of aorta after treatment with endotoxin.

Lipopolysaccharide (LPS) impairs vascular function, in part by generation of reactive oxygen species. One goal of this study was to determine whether gene transfer of extracellular SOD (ECSOD) improves vascular responsiveness in LPS-treated rats. A second goal was to determine whether effects of ECSOD are dependent on the heparin-binding domain of the enzyme, which facilitates binding of ECSOD to the outside of cells.