Gene expression pattern in severely progressing covid-19 patients is related to diabetes mellitus type 1: A functional annotation analysis.

Aims: The aim of this study was to extract the signaling mediators or biological pathways that link covid-19 to other diseases such as type 1 diabetes mellitus (T1DM).

Methods: Microarray data of covid-19 (GSE164805) was extracted from Gene Expression Omnibus (GEO) and analyses were performed by R package and GEO2R. Functional enrichment analysis was done to extract enriched molecular pathways (MP), biological process (BP) and molecular function (MF).

Facile preparation of a novel biogenic silver-loaded Nanofilm with intrinsic anti-bacterial and oxidant scavenging activities for wound healing.

To eliminate the microbial infection from an injury site, various modalities have been developed such as dressings and human skin substitutes. However, the high amount of reactive oxygen species, microbial infection, and damaging extracellular matrix remain as the main challenges for the wound healing process. In this study, for the first time, green synthesized silver nanoparticles (AgNPs) using Teucrium polium extract were embedded in poly lactic acid/poly ethylene glycol (PLA/PEG) film to provide absorbable wound dressing, with antioxidant and antibacterial features.

Association of arginine vasopressin (AVP) promoter polymorphisms with preeclampsia.

Objectives: Preeclampsia (PE) is a disease of pregnancy characterized by early onset of maternal hypertension and proteinuria. New findings indicate that arginine vasopressin (AVP) may be a contributing factor to ignite PE. The aim of this study was to identify if there is any correlation between arginine vasopressin promoter polymorphisms and PE.

Reduced macrophage-dependent inflammation improves endothelin-1-induced vascular injury.

Transgenic mice with endothelium-specific endothelin-1 (ET-1) overexpression exhibit endothelial dysfunction and vascular remodeling, oxidative stress, and inflammation. We previously observed that monocytes/macrophages play a role in angiotensin II, aldosterone, and deoxycorticosterone acetate/salt-induced vascular remodeling, oxidative stress, and inflammation using a model with reduced monocytes/macrophages, the osteopetrotic (Op) mouse, which has a mutation in the macrophage colony stimulating factor (Csf1) gene. However, it is unknown whether monocytes/macrophages are implicated in adverse vascular effects of ET-1.

Potentiation of vascular oxidative stress and nitric oxide-mediated endothelial dysfunction by high-fat diet in a mouse model of estrogen deficiency and hyperandrogenemia.

Estrogen deficiency is associated with increased cardiovascular risk due, in part, to hypertension, endothelial dysfunction, obesity, and hypercholesterolemia. Underlying mechanisms for this remain unclear. Here, we investigated whether high-fat intake aggravates vascular dysfunction through oxidative stress and inflammation, which could predispose to cardiovascular injury in conditions of estrogen deficiency, such as menopause.

Deleterious combined effects of salt-loading and endothelial cell restricted endothelin-1 overexpression on blood pressure and vascular function in mice.

Background: We previously showed that young transgenic mice overexpressing preproendothelin-1 specifically in endothelial cells had hypertrophic remodeling, endothelial dysfunction, increased vascular NADPH oxidase activity, and inflammation in mesenteric small arteries without blood pressure (BP) elevation compared to nontransgenic wild-type littermates. To assess the consequences of salt-loading and the role of endothelin receptors, we investigated the effects of these on vascular structure, function, and oxidative stress in mesenteric arteries in salt-loaded transgenic mice treated with endothelin receptor antagonists.

Methods: Ten-month-old male transgenic and wild-type littermates were salt-loaded (4% NaCl) and treated with endothelin subtype A receptor antagonist (ET(A)RA, ABT-627, 5 mg/kg per day), endothelin subtype B receptor antagonist (ET(B)RA; A-192621, 30 mg/kg per day), or ET(A)/BRA (bosentan, 100 mg/kg per day) for 4 weeks.

Xanthine oxidase and mitochondria contribute to vascular superoxide anion generation in DOCA-salt hypertensive rats.

Vascular superoxide anion (O(2)(*-)) levels are increased in DOCA-salt hypertensive rats. We hypothesized that the endothelin (ET)-1-induced generation of ROS in the aorta and resistance arteries of DOCA-salt rats originates partly from xanthine oxidase (XO) and mitochondria. Accordingly, we blocked XO and the mitochondrial oxidative phosphorylation chain to investigate their contribution to ROS production in mesenteric resistance arteries and the aorta from DOCA-salt rats.

Effects of combined AT1 receptor antagonist/NEP inhibitor on vascular remodeling and cardiac fibrosis in SHRSP.

Background: The association of an angiotensin-converting enzyme inhibitor (ACEI) with a neutral endopeptidase inhibitor (NEPI) has potent blood pressure (BP) lowering action, but is associated with side-effects. We evaluated the effects of combining an angiotensin II type 1 (AT1) receptor blocker (ARB, valsartan) and a NEPI (CGS 25354) in comparison with a dual ACEI/NEPI (CGS 30440) in stroke-prone spontaneously hypertensive rats (SHRSP).

Methods And Results: Ten-week-old SHRSP were treated with valsartan (10 mg/kg per day), valsartan + CGS 25354 (100 mg/kg per day), CGS 25354, CGS 30440 (10 mg/kg per day) or hydralazine (25 mg/kg per day) for 10 weeks.

Increased blood pressure, vascular inflammation, and endothelial dysfunction in androgen-deficient follitropin receptor knockout male mice.

The relationship between testosterone, vascular function, and blood pressure remains unclear. Here we utilized a mouse model of andropause, follitropin receptor knockout (FORKO) male mice, which are testosterone-deficient, to investigate whether vascular function and structure are altered and whether this is associated with elevated blood pressure. Blood pressure was measured by radiotelemetry, and vascular function and structure were assessed in isolated pressurized mesenteric resistance arteries in wild-type (WT) and FORKO mice.

Resistance artery remodeling in deoxycorticosterone acetate-salt hypertension is dependent on vascular inflammation: evidence from m-CSF-deficient mice.

Deoxycorticosterone acetate (DOCA)-salt hypertension has an important endothelin-1 (ET-1)-dependent component. ET-1-induced vascular damage may be mediated in part by oxidative stress and vascular inflammation. Homozygous osteopetrotic (Op/Op) mice, deficient in macrophage colony-stimulating factor (m-CSF), exhibit reduced inflammation.

Early obesity and age-related mimicry of metabolic syndrome in female mice with sex hormonal imbalances.

Objective: To investigate the relationship of early obesity to metabolic syndrome during sex hormonal imbalances in mutant female mice at different ages.

Research Methods And Procedures: Hormonal imbalances, accumulation and nature of adipose tissue, food intake, glucose tolerance, and expression of candidate genes and markers of inflammation were studied by comparing wild-type, null, and haploinsufficient follitropin receptor knockout female mice at different ages.

Results: Follitropin receptor deletion in mice produced null females that are infertile and haploinsufficient mice that undergo accelerated biological aging.

Angiotensin II induces vascular dysfunction without exacerbating blood pressure elevation in a mouse model of menopause-associated hypertension.

Background: Follitropin-receptor knockout (FORKO) mice are estrogen-deficient, hyperandrogenic and exhibit features of menopause and elevated blood pressure (BP). Because the renin-angiotensin system has been implicated in menopause-associated hypertension, we questioned whether angiotensin II (Ang II) challenge would further increase BP in FORKO mice and whether this is associated with cardiovascular remodeling and inflammation.

Results: Ang II (400 ng/kg per min) increased BP, assessed by radiotelemetry, similarly in female FORKO and wild-type (WT) mice.

Angiotensin II-dependent chronic hypertension and cardiac hypertrophy are unaffected by gp91phox-containing NADPH oxidase.

The gp91phox-containing NADPH oxidase is the major source of reactive oxygen species (ROS) in the cardiovascular system and inactivation of gp91phox has been reported to blunt hypertension and cardiac hypertrophy seen in angiotensin (Ang) II-infused animals. In the current study, we sought to determine the role of gp91phox-derived ROS on cardiovascular outcomes of chronic exposure to Ang II. The gp91phox-deficient mice were crossed with transgenic mice expressing active human renin in the liver (TTRhRen).

Attenuated responses to angiotensin II in follitropin receptor knockout mice, a model of menopause-associated hypertension.

Activation of the renin-angiotensin system has been implicated in the development of hypertension in menopausal women. We investigated whether blood pressure is elevated and whether angiotensin II (Ang II)-induced vascular reactivity is increased in follitropin receptor knockout (FORKO) female mice. These mice are estrogen-deficient and have characteristics similar to postmenopausal women.

Superoxide production in the vasculature of lipopolysaccharide-treated rats and pigs.

Sepsis is associated with increased production of reactive oxygen species (ROS); however, the metabolic sources of increased ROS are not well understood. We hypothesized that the recently described nonphagocytic NAD(P)H oxidase system could be an important source of the ROS superoxide anion (O2-) during sepsis, and the interaction of O2- with nitric oxide (NO) may contribute to sepsis-induced vascular Injury. To evaluate this issue, we measured O2- production before and after treatment with lipopolysaccharide (LPS) in rats, who are Inducible NO synthase producers (NOSII) and in pigs, who do not produce NOSII.

Endocrine alterations and signaling changes associated with declining ovarian function and advanced biological aging in follicle-stimulating hormone receptor haploinsufficient mice.

Reproductive aging in female mammals is characterized by a progressive decline in fertility due to loss of follicles and reduced ovarian steroidogenesis. In this study we examined some of the endocrine and signaling parameters that might contribute to a decrease in ovulation and reproductive performance of mice with haploinsufficiency of the FSH receptor (FSH-R). For this purpose we compared ovarian changes and hormone levels in FSH-R heterozygous (+/-) and wild-type mice of different ages (3, 7, and 12 mo).

Molecular characterization of a superoxide-generating NAD(P)H oxidase in the ventilatory muscles.

The molecular sources of reactive oxygen species (ROS) in skeletal muscles are not well understood. We hypothesized that nonphagocyte NAD(P)H oxidase could be a source of ROS in muscle fibers. We thus investigated the existence, structure, and contribution of nonphagocyte NAD(P)H oxidase to ROS production in rat skeletal muscles.