Antibiotics taken within the first year of life are linked to infant gut microbiome disruption and elevated atopic dermatitis risk.

Background: Atopic dermatitis (AD) is the most common chronic inflammatory skin disease in both pediatric and adult populations. The development of AD has been linked to antibiotic usage, which causes perturbation of the microbiome and has been associated with abnormal immune system function. However, imbalances in the gut microbiome itself associated with antibiotic usage have been inconsistently linked to AD.

CO hydrogenation over functional nanoporous polymers and metal-organic frameworks.

CO is one of the major environmental pollutants and its mitigation is attracting huge attention over the years due to continuous increase in this greenhouse gas emission in the atmosphere. Being environmentally hazardous and plentiful presence in nature, CO utilization as C1 resource into fuels and feedstock is very demanding from the green chemistry perspectives. To accomplish this CO utilization issue, functional organic materials like porous organic polymers (POPs), covalent organic frameworks (COFs) as well as organic-inorganic hybrid materials like metal-organic frameworks (MOFs), having characteristics of large surface area, high thermal stability and tunability in the porous nanostructures play significant role in designing the suitable catalyst for the CO hydrogenation reactions.

Loss of endothelial cell-specific autophagy-related protein 7 exacerbates doxorubicin-induced cardiotoxicity.

Doxorubicin (DOX) is an effective, broad-spectrum antineoplastic agent with serious cardiotoxic side effects, which may lead to the development of heart failure. Current strategies to diagnose, prevent, and treat DOX-induced cardiotoxicity (DIC) are inadequate. Recent evidence has linked the dysregulation and destruction of the vascular endothelium to the development of DIC.

Empagliflozin Reduces Myocardial Extracellular Volume in Patients With Type 2 Diabetes and Coronary Artery Disease.

Objectives: This study sought to evaluate the effects of empagliflozin on extracellular volume (ECV) in individuals with type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD).

Background: Empagliflozin has been shown to reduce left ventricular mass index (LVMi) in patients with T2DM and CAD. The effects on myocardial ECV are unknown.

Disruption of endothelial cell intraflagellar transport protein 88 exacerbates doxorubicin-induced cardiotoxicity.

Aims: Doxorubicin (DOX) is a potent anticancer drug with severe dose-dependent cardiotoxicity. To address this issue, previous research primarily focused on DOX-induced toxicity on cardiomyocytes. However, more recent research has looked into the endothelium as a therapeutic target due to the emerging role of endothelial cells in the support of cardiomyocyte survival and function.

The SGLT2 inhibitor empagliflozin reduces mortality and prevents progression in experimental pulmonary hypertension.

Pulmonary arterial hypertension (PAH) is a rare, but progressive and devastating vascular disease with few treatment options to prevent the advancement to right ventricular dysfunction hypertrophy and failure. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, enhances urinary glucose excretion as well as reduces cardiovascular events and mortality in individuals with type 2 diabetes. While empagliflozin has been reported to lower systemic hypertension due to increased diuresis, the effect of empagliflozin on PAH is unknown.

Recyclable Au/SiO-Shell/FeO-Core Catalyst for the Reduction of Nitro Aromatic Compounds in Aqueous Solution.

Highly stable gold nanoparticles immobilized on the surface of amine-functionalized nanocomposite microspheres possessing a magnetite (FeO) nanoparticle core and a silica (SiO) shell (Au/SiO-shell/FeO-core) were prepared. These gold nanocomposite catalysts were tested for 4-nitrophenol (4-NP) and 2-nitroaniline (2-NA) reduction in aqueous solution in the temperature range 293-323 K and in the presence of aqueous NaBH reducing agent. The magnetically recyclable gold catalyst showed high stability (∼3 months), efficient recyclability (up to 10 cycles), and high activity (∼100% conversion within 225 s, ∼700 ppm 4-NP or 2-NA).

Role of Endothelium in Doxorubicin-Induced Cardiomyopathy.

The clinical use of doxorubicin in cancer is limited by cardiotoxic effects that can lead to heart failure. Whereas earlier work focused on the direct impact of doxorubicin on cardiomyocytes, recent studies have turned to the endothelium, because doxorubicin-damaged endothelial cells can trigger the development and progression of cardiomyopathy by decreasing the release and activity of key endothelial factors and inducing endothelial cell death. Thus, the endothelium represents a novel target for improving the detection, management, and prevention of doxorubicin-induced cardiomyopathy.

A novel role of endothelial autophagy as a regulator of myocardial fatty acid oxidation.

Background: We sought to determine if endothelial autophagy affects myocardial energy metabolism.

Methods: We used isolated working mouse hearts to compare cardiac function, energy metabolism, and ischemic response of hearts from endothelial cell-specific ATG7 knockout (EC-ATG7) mice to hearts from their wild-type littermates. We also conducted gene analyses on human umbilical vein endothelial cells incubated with scrambled small interfering RNA or small interfering ATG7.

Role of endothelial primary cilia as fluid mechanosensors on vascular health.

Primary cilia are microtubule-based organelles that protrude from the cell surface of many mammalian cell types, including endothelial and epithelial cells, osteoblasts, and neurons. These antennal-like projections enable cells to detect extracellular stimuli and elicit responses via intracellular signaling mechanisms. Primary cilia on endothelial cells lining blood vessels function as calcium-dependent mechanosensors that sense blood flow.

Novel APC gene mutations associated with protein alteration in diffuse type gastric cancer.

Background: The role of adenomatous polyposis coli (APC) gene in mitosis might be critical for regulation of genomic stability and chromosome segregation. APC gene mutations have been associated to have a role in colon cancer and since gastric and colon tumors share some common genetic lesions, it is relevant to investigate the role of APC tumor suppressor gene in gastric cancer.

Methods: We investigated for somatic mutations in the Exons 14 and 15 of APC gene from 40 diffuse type gastric cancersamples.

Hyaluronidase 2 Deficiency Causes Increased Mesenchymal Cells, Congenital Heart Defects, and Heart Failure.

Background: Hyaluronan (HA) is required for endothelial-to-mesenchymal transition and normal heart development in the mouse. Heart abnormalities in hyaluronidase 2 (HYAL2)-deficient ( ) mice and humans suggested removal of HA is also important for normal heart development. We have performed longitudinal studies of heart structure and function in mice to determine when, and how, HYAL2 deficiency leads to these abnormalities.

Mutations in HYAL2, Encoding Hyaluronidase 2, Cause a Syndrome of Orofacial Clefting and Cor Triatriatum Sinister in Humans and Mice.

Orofacial clefting is amongst the most common of birth defects, with both genetic and environmental components. Although numerous studies have been undertaken to investigate the complexities of the genetic etiology of this heterogeneous condition, this factor remains incompletely understood. Here, we describe mutations in the HYAL2 gene as a cause of syndromic orofacial clefting.

Hyaluronidase 2 (HYAL2) is expressed in endothelial cells, as well as some specialized epithelial cells, and is required for normal hyaluronan catabolism.

Hyaluronidase 2 (HYAL2) is a membrane-anchored protein that is proposed to initiate the degradation of hyaluronan (HA) in the extracellular matrix. The distribution of HYAL2 in tissues, and of HA in tissues lacking HYAL2, is largely unexplored despite the importance of HA metabolism in several disease processes. Herein, we use immunoblot and histochemical analyses to detect HYAL2 and HA in mouse tissues, as well as agarose gel electrophoresis to examine the size of HA.

Ligand centered radical pathway in catechol oxidase activity with a trinuclear zinc-based model: synthesis, structural characterization and luminescence properties.

A new trinuclear zinc(II) complex, [Zn3(L)(NCS)2](NO3)2·CH3OH·H2O (1), of a (N,O)-donor compartmental Schiff base ligand (H2L=N,N'-bis(3-methoxysalicylidene)-1,3-diamino-2-propanol), has been synthesized in crystalline phase. The zinc(II) complex has been characterized by elemental analysis, IR spectroscopy, UV-Vis spectroscopy, powder X-ray diffraction study (PXRD), (1)H NMR, EI mass spectrometry and thermogravimetric analysis. PXRD revealed that 1 crystallizes in P-1 space group with a=9.

Growth arrest in the ribosomopathy, Bowen-Conradi syndrome, is due to dramatically reduced cell proliferation and a defect in mitotic progression.

Bowen-Conradi syndrome (BCS) is a ribosomopathy characterized by severe developmental delay and growth failure that typically leads to death by one year of age. It is caused by a c.257A>G, p.

Long-term correction of Sandhoff disease following intravenous delivery of rAAV9 to mouse neonates.

G(M2) gangliosidoses are severe neurodegenerative disorders resulting from a deficiency in β-hexosaminidase A activity and lacking effective therapies. Using a Sandhoff disease (SD) mouse model (Hexb(-/-)) of the G(M2) gangliosidoses, we tested the potential of systemically delivered adeno-associated virus 9 (AAV9) expressing Hexb cDNA to correct the neurological phenotype. Neonatal or adult SD and normal mice were intravenously injected with AAV9-HexB or -LacZ and monitored for serum β-hexosaminidase activity, motor function, and survival.

Murine hyaluronidase 2 deficiency results in extracellular hyaluronan accumulation and severe cardiopulmonary dysfunction.

Hyaluronidase (HYAL) 2 is a membrane-anchored protein that is proposed to hydrolyze hyaluronan (HA) to smaller fragments that are internalized for breakdown. Initial studies of a Hyal2 knock-out (KO) mouse revealed a mild phenotype with high serum HA, supporting a role for HYAL2 in HA breakdown. We now describe a severe cardiac phenotype, deemed acute, in 54% of Hyal2 KO mice on an outbred background; Hyal2 KO mice without the severe cardiac phenotype were designated non-acute.

In situ UV-vis and EPR study on the formation of hydroperoxide species during direct gas phase propylene epoxidation over Au/Ti-SiO(2) catalyst.

In recent years, there have been great experimental and theoretical advances in the understanding of the epoxidation of propylene by O(2) and H(2) over Au supported on titanium-containing oxidic supports; however, thus far spectroscopic evidence of reacting species for proposed mechanisms has been lacking. Hydroperoxide species have been postulated as an intermediate responsible for the epoxidation of propylene with O(2) and H(2). In order to obtain direct evidence for the different type of active oxygen species, in situ UV-vis and EPR measurements were carried out during the epoxidation of propylene with O(2) and H(2) over a Au/Ti-SiO(2) (Ti/Si = 3:100) catalyst.