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The labia are part of the female genitalia; they are the major externally visible portions of the vulva. In humans, there are two pairs of labia: the labia majora (or the outer labia) are larger and fattier, while the labia minora are folds of skin between the outer labia. The labia surround and protect the clitoris and the openings of the vagina and the urethra.
28 Nov 2022
Microbiome Metagenomics and Epigenomics on Gastric Cancer
The gut microbiome plays a pivotal role in the development and progression of gastric cancer. Similar microbes implicated in gastric cancer carcinogenesis have been detected in some of the risk factors of the disease, with microbial dysbiosis as a common root of concern as it promotes carcinogenesis through dysregulation of cancer immunosurveillance and induction of therapeutic resistance. The microbiome plays an important role in gastric cancer (GC) pathological phenotypes and should be taken into consideration when designing personalized cancer therapies.
21 Nov 2022
Plasma Membrane in Atherogenesis
Atherosclerotic cardiovascular diseases are an important medical problem due to their high prevalence, impact on quality of life and prognosis. The pathogenesis of atherosclerosis is an urgent medical and social problem, the solution of which may improve the quality of diagnosis and treatment of patients. Atherosclerosis is a complex chain of events, which proceeds and in which many cells in the bloodstream and the vascular wall are involved. A growing body of evidence suggests that there are complex, closely linked molecular mechanisms that occur in the plasma membranes of cells involved in atherogenesis. Lipid transport, innate immune system receptor function, and hemodynamic regulation are linked to plasma membranes and their biophysical properties. A better understanding of these interrelationships will improve diagnostic quality and treatment efficacy.
21 Nov 2022
Cell of Origin and Pathogenesis of FL Transformation
The gold standard for determining follicular lymphoma (FL) transformation is based on the histologically confirmed progression of grade 1, 2, or 3A FL to a high-grade lymphoma, consisting of a predominance of large cells and the loss of the follicular architecture. Histological transformation (HT) to a more aggressive disease–mostly diffuse large B-cell lymphoma–is considered one of the most dismal events in the clinical course of FL.
27 Oct 2022
Role of Liquid–Liquid Phase Separation in Cardiovascular Diseases
Liquid–liquid phase separation (LLPS) is a biochemical process in cells that can drive proteins, RNA, and other molecules to concentrate into droplets. These droplets do not have a lipid membrane but rather exist as distinct organelles relative to the surrounding environment, and act as biochemical reaction chambers. Significant progress has been made in the study of LLPS, especially in the neurodegenerative disease, cancer, and virology fields, but little is known about LLPS in cardiovascular disease (CVD).
18 Oct 2022
HMGB1 and Post-Aneurysmal Subarachnoid Hemorrhage
Aneurysmal subarachnoid hemorrhage (aSAH) is characterized by a robust sterile inflammatory response immediately after the subarachnoidal bleed. Several damage-associated molecular pattern molecules (DAMPs) are liberated upon injury of the brain cells from different intracellular compartments and have the capability to activate immune cells through the ligation of their cognizant receptors (pattern recognition receptors (PRRs)). Among them, high mobility group box-1 (HMGB1), which acts normally as a transcription factor, when released extracellularly upregulates inflammation due to its interaction with TLR-2, TLR-4 and RAGE during early brain injury after aSAH. However, recent investigations show that different isoforms of HMGB1 exist and may dominate during different phases of the brain injury with different consequences. Surprisingly, the oxidized isoform of HMGB1 plays an anti-inflammatory and pro-resovling role contrary to well accepted pro-inflammatory role of HMGB1 after aSAH.
17 Oct 2022
Matrix Vesicle-Mediated and Osteocytic Regulation of Bone Mineralization
Bone mineralization entails two mineralization phases: primary and secondary mineralization. Primary mineralization is achieved when matrix vesicles are secreted by osteoblasts, and thereafter, bone mineral density gradually increases during secondary mineralization. Nearby extracellular phosphate ions (PO43−) flow into the vesicles via membrane transporters and enzymes located on the vesicles’ membranes, while calcium ions (Ca2+), abundant in the tissue fluid, are also transported into the vesicles. The accumulation of Ca2+ and PO43− in the matrix vesicles induces crystal nucleation and growth. The calcium phosphate crystals grow radially within the vesicle, penetrate the vesicle’s membrane, and continue to grow outside the vesicle, ultimately forming mineralized nodules. The mineralized nodules then attach to collagen fibrils, mineralizing them from the contact sites (i.e., collagen mineralization). Afterward, the bone mineral density gradually increases during the secondary mineralization process.
28 Sep 2022
The Na+/H+ Exchangers in Cardiac Physiology Regulation
The Na+/H+ exchangers (NHEs) are membrane transporters that exchange one intracellular pro-ton for one extracellular Na+. The first discovered NHE isoform, NHE1, is expressed almost ubiquitously in all tissues, especially in the myocardium. During myocardial ische-mia-reperfusion, NHE1 catalyzes increased uptake of intracellular Na+, which in turn leads to Ca2+ overload and subsequently myocardial injury. Numerous preclinical research has shown that NHE1 is involved in cardiac hypertrophy and heart failure, but the exact molecular mecha-nisms remain elusive.
27 Sep 2022
Drugs Targeting Cancer Cells with Splicing Factor Mutations
Splicing factors are frequently mutated in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). These mutations are presumed to contribute to oncogenic transformation, but the underlying mechanisms remain incompletely understood. While no specific treatment option is available for MDS/AML patients with spliceosome mutations, novel targeting strategies are actively explored, leading to clinical trials of small molecule inhibitors that target the spliceosome, DNA damage response pathway, and immune response pathway.
05 Sep 2022
Neuroimaging-Based Assessments of OXPHOS-Related Complexes and Metabolites
In post-mortem studies, a significant dysregulation of electron transport chain (ETC) complexes was observed in patients with neurodegenerative diseases (NDs). These findings strongly implicate that mitochondrial dysfunction-linked alterations in oxidative phosphorylation (OXPHOS) can be considered a highly relevant molecular mechanism in different NDs. Histopathological examinations revealed decreased complex I level, preferentially in the substantia nigra (SN), in patients suffering from Parkinson’s disease (PD). These findings are consistent with the fact that inhibitors of complex I (such as the environmental toxins MPTP or rotenone) can cause parkinsonism in animal models and humans. Huntington’s disease (HD) has been associated with defects of complex II and, to a lesser extent, complex IV. The chronic administration of the complex II inhibitor 3-nitropropionic acid causes an HD-like phenotype in rodent and non-human primate models. In Alzheimer’s disease (AD), widespread cortical complex IV defects were identified in post-mortem brain tissue. The in vivo neuroimaging-based assessment of electron transport chain (ETC)-related metabolite levels could thus help elucidate the complex role of OXPHOS disturbances in NDs.
07 Jul 2022
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