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Topic Review
Type I Interferon
Together with type III IFNs, Type I Interferons (IFNs-I) represent the first line of immune defense against viral infections. In the case of RNA viruses, after recognition of viral products by pattern recognition receptors (PRRs), such as the main cytosolic receptors RNA helicases retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), the signal converges on the activation of the mitochondrial antiviral signaling protein (MAVS), that, in turns, activates the TANK-binding kinase 1 (TBK1), leading to the phosphorylation and activation of IFN-regulatory factors 3 and 7 (IRF3, IRF7) [6,7]. IRFs then translocate to the nucleus and induce the production of IFNs-I (IFNα, IFNβ, IFNε, IFNτ, IFNκ, IFNω, IFNδ and IFNζ).
  • 559
  • 07 Sep 2021
Topic Review
Type I IFNs in Long-Haul COVID Syndrome
Interferons (IFNs) are pleiotropic cytokines originally identified for their antiviral activity. IFN-α and IFN-β are both type I IFNs that have been used to treat neurological diseases such as multiple sclerosis. Microglia, astrocytes, as well as neurons in the central and peripheral nervous systems, including spinal cord neurons and dorsal root ganglion neurons, express type I IFN receptors (IFNARs). Type I IFNs play an active role in regulating cognition, aging, depression, and neurodegenerative diseases. Notably, by suppressing neuronal activity and synaptic transmission, IFN-α and IFN-β produced potent analgesia.
  • 703
  • 06 Dec 2022
Topic Review
Type I Collagen
Type I collagen, the predominant protein of vertebrates, assembles into fibrils that orchestrate the form and function of bone, tendon, skin, and other tissues. Collagen plays roles in hemostasis, wound healing, angiogenesis, and biomineralization, and its dysfunction contributes to fibrosis, atherosclerosis, cancer metastasis, and brittle bone disease.
  • 1.5K
  • 26 Jan 2021
Topic Review
Type A Insulin Resistance Syndrome
Type A insulin resistance syndrome is a rare disorder characterized by severe insulin resistance, a condition in which the body's tissues and organs do not respond properly to the hormone insulin.
  • 447
  • 23 Dec 2020
Topic Review
Type A Influenza Vaccine
Type A influenza vaccine is for the prevention of infection of influenza A virus and also the influenza-related complications. Different monovalent type A influenza vaccines have been developed for different subtypes of influenza A virus including H1N1 and H5N1. Both intramuscular injection or intranasal spray are available on market. Unlike the seasonal influenza vaccines which are used annually, they are usually used during the outbreak of certain strand of subtypes of influenza A. Common adverse effects includes injection site reaction and local tenderness. Incidences of headache and myalgia were also reported with H1N1 whereas cases of fever has also been demonstrated with H5N1 vaccines. It is stated that immunosuppressant therapies would reduce the therapeutic effects of vaccines and that people with egg allergy should go for the egg-free preparations. There are different methods in developing the vaccines. Traditionally, inactivated viral vaccine and live attenuated virus vaccine have been approved. Inactivated viral vaccine is primary used parentally and the live attenuated vaccine is used intranasally. Development of new technologies including the recombinant hemagglutinin technology have widely been studied. Influenza A virus was successfully identified and isolated by Wilson Smith, Christopher Andrewes, and Patrick Laidlaw in the 1930s and the first inactivated monovalent influenza A vaccine was made after a decade. The first H5N1 vaccine was approved in 2007. It was intentionally developed to prepare for the possible H5N1 outbreak in the future. Moreover, in view of the H1N1 outbreak in 2009, H1N1 monovalent vaccines, targeting only H1N1 virus, was produced. Influenza A exists in many subtypes including H5N1, H1N1 and H3N2. Different formulations of monovalent vaccines have been developed over the years to cater different needs and antigens identified.
  • 187
  • 11 Oct 2022
Topic Review
Type 3 Diabetes
The exact connection between Alzheimer’s disease (AD) and type 2 diabetes is still in debate. However, poorly controlled blood sugar may increase the risk of developing Alzheimer’s. This relationship is so strong that some have called Alzheimer’s “diabetes of the brain” or “type 3 diabetes (T3D)”. Given more recent studies continue to indicate evidence linking T3D with AD, this state-of-the-art aimed to demonstrate the relationship between T3D and AD based on the fact that both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ are attributed to impaired insulin signaling, and that insulin resistance mediates the dysregulation of bioenergetics and progress to AD. 
  • 5.8K
  • 29 Oct 2020
Topic Review
Type 2 Transglutaminase in Coeliac Disease
Coeliac disease (CD) is a multifactiorial enteropathy that affects the small intestine of genetically predisposed individuals. A condition of partial to total atrophy, together with crypt hyperplasia and consistent lymphocytic infiltration, characterises the intestinal mucosa of affected patients. The main environmental trigger is a heterogenic proteic component of some dietary cereals, commonly known as gluten. A strong immune response against gluten, both cellular and humoral, is mounted in CD, accompanied by a humoral autoimmune response against self-proteins, in particular type 2 transglutaminase (TG2).
  • 726
  • 22 Jul 2022
Topic Review
Type 2 Diabetes: Beta Cell Compensation and Death
Type 2 diabetes (T2D) has become a worldwide epidemic, primarily driven by obesity from overnutrition and sedentariness. Physiologically, T2D manifests as an inability of the pancreatic beta cells to produce and secrete a sufficient bolus of insulin to elicit a response in target cells to transport glucose from the blood and properly regulate glucose levels. Insulin is synthesized in the endoplasmic reticulum (ER) of pancreatic beta cells where it undergoes a series of post-translational modifications to form mature insulin. Insulin resistance requires more insulin to be produced by beta cells to compensate for these desensitized cells. Consequently, this compensation causes additional strain on beta cells. This stress primarily originates from the ER and can also trigger oxidative stress. These cellular stresses can lead to beta cell decompensation, manifested by dysfunction and eventually a loss of beta cell mass.
  • 193
  • 04 Mar 2024
Topic Review
Type 2 Diabetes Optimal Treatment
Insulin, via a series of kinase activations and transductions, causes the glucose type 4 transporter channels to become embedded in the cellular membrane, allowing an exponential increase of glucose entry into the cell. T2D is characterized by failure of the insulin receptors to respond to insulin, thus preventing glucose uptake from the bloodstream. Later in the disease, the production of insulin by pancreatic islet cells is also curtailed. The vast preponderance of diabetes cases (95%) in the United States constitute T2D.
  • 517
  • 02 Jun 2021
Topic Review
Type 2 Diabetes Mellitus and COVID-19
Type 2 diabetes mellitus (T2DM) is one of the world’s leading causes of death and life-threatening conditions. Researchers shed light on the single-cell-based technologies and multi-omics approaches that have reached breakthroughs in the understanding of the pathomechanism of T2DM. Hyperglycemia initiates a pathobiochemical cascade that results in increased mortality in SARS-CoV-2-infected diabetic patients. The underlying molecular mechanisms are responsible for the worsening of both metabolic and hemodynamic conditions. 
  • 418
  • 21 Sep 2022
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