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Nitric oxide synthases (EC 1.14.13.39) (NOSs) are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. NO is an important cellular signaling molecule. It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural development.
When the enzyme adenosine deaminase is deficient in the body, the result is a toxic build-up of metabolites that impair lymphocyte development and function. [9] Many ADA deficient children with SCID have been treated with the polyethylene glycol-conjugated adenosine deaminase (PEG-ADA) enzyme.
The human SCD-1 gene structure and regulation is very similar to that of mouse SCD-1. Overexpression of SCD-1 in humans may be involved in the development of hypertriglyceridemia, atherosclerosis, and diabetes. [25] One study showed that SCD-1 activity was associated with inherited hyperlipidemia. SCD-1 deficiency has also been shown to reduce ...
The myosin-binding protein C, cardiac-type is a protein that in humans is encoded by the MYBPC3 gene. [5] This isoform is expressed exclusively in heart muscle during human and mouse development, [6] and is distinct from those expressed in slow skeletal muscle and fast skeletal muscle ().
A study using human uterine tissue found that a 1,000-fold excess of spironolactone (0.3–2 μM) resulted in no displacement of estradiol from the ER. [86] However, a subsequent study found that the medication did interact with the human ER at higher concentrations, albeit with very low affinity (K i = 20 μM). [15]
Major factors influencing cardiac output – heart rate and stroke volume, both of which are variable. [1]In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols , ˙, or ˙, [2] is the volumetric flow rate of the heart's pumping output: that is, the volume of blood being pumped by a single ventricle of the heart, per unit time (usually measured ...
Using a knock-in (KI) rat model, researchers found an AF-associated human variant in NPPA caused inflammation, fibroblast activation, atrial fibrosis, and AF in KI rats. [13] These findings suggest NPPA is a critical gene in cardiac development and dysfunction of this gene can lead to heart problems via altered ANP levels.
The angiotensin converting enzyme gene has more than 160 polymorphisms described as of 2018. [24] Studies have shown that different genotypes of angiotensin converting enzyme can lead to varying influence on athletic performance. [25] [26] However, these data should be interpreted with caution due to the relatively small size of the ...