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Movements, leaders, victories and the continuing fight for equality.
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Pioneers, champions, Negro Leagues, records, activism and excellence.
Meet the people whose lives, choices and achievements shaped the journey.
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Moments that changed communities, movements, institutions and the nation.
In August 1908, a white mob attacked Springfield, Illinois’s Black community, destroying homes and businesses and lynching two Black men. National outrage over the violence helped spur the movement that created the NAACP the following year.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
Neuronal cell adhesion molecule is a protein that in humans is encoded by the NRCAM gene.[5][6]
Cell adhesion molecules (CAMs) are members of the immunoglobulin superfamily. This gene encodes a neuronal cell adhesion molecule with multiple immunoglobulin-like C2-type domains and fibronectin type-III domains. This ankyrin-binding protein is involved in neuron-neuron adhesion and promotes directional signaling during axonal cone growth. This gene is also expressed in non-neural tissues and may play a general role in cell-cell communication via signaling from its intracellular domain to the actin cytoskeleton during directional cell migration. Allelic variants of this gene have been associated with autism[7] and addiction vulnerability. Alternative splicing results in multiple transcript variants encoding different isoforms.[6]
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 | This article on a gene on human chromosome 7 is a stub. You can help Wikipedia by adding missing information. |
Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
Neuronal cell adhesion molecule is a protein that in humans is encoded by the NRCAM gene. Cell adhesion molecules (CAMs) are members of the immunoglobulin superfamily. This gene encodes a neuronal cell adhesion molecule with multiple immunoglobulin-like C2-type domains and fibronectin type-III domains. This ankyrin-binding protein is involved in neuron-neuron adhesion and promotes directional signaling during axonal cone growth. This gene is also expressed in non-neural tissues and may play a general role in cell-cell communication via signaling from its intracellular domain to the actin cytoskeleton during directional cell migration. Allelic variants of this gene have been associated with autism and addiction vulnerability. Alternative splicing results in multiple transcript variants encoding different isoforms.
The L1 family is a family of cell adhesion molecules that includes four different L1-like proteins. They are members of the immunoglobulin superfamily (IgSF CAM). The members of the L1-family in humans are called L1 or L1cam, CHL1 (close homologue of L1), Neurofascin and NRCAM (NgCAM related cell adhesion molecule). L1 family members are found on neurons, especially on their axons. Sometimes they are found on glia, such as Schwann cells, radial glia and Bergmann glia cells and, as such, are important for neural cell migration during development. L1 family members are expressed throughout the vertebrate and invertebrate kingdoms. L1 family members are able to bind to a number of other proteins. As cell adhesion molecules, they often bind "homophilically" to themselves; for example L1 on one cell binding to L1 on an adjacent cell. L1 family members also bind "heterophilically" to members of the contactin or CNTN1 family. L1 family members bind to many cytoplasmic proteins such as Ankyrins, ezrin-moesin-radixin (ERM) proteins, signaling molecules like src (src gene) and erk (Extracellular signal-regulated kinases) and proteins important in trafficking, such as AP-2. NrCAM and neurofascin both have class 1 PDZ domain binding motifs at their COOH termini. NrCAM can bind to SAP102 and other members of the MAGUK family.
Coronary artery disease (CAD), also called coronary heart disease (CHD), or ischemic heart disease (IHD), is a type of heart disease involving the reduction of blood flow to the cardiac muscle due to the presence of atheromatous plaques in the arteries of the heart. It is the most common of the cardiovascular diseases. CAD can cause stable angina, unstable angina, myocardial ischemia, and myocardial infarction. A common symptom is angina, which is chest pain or discomfort that may travel into the shoulder, arm, back, neck, or jaw. Occasionally, it may feel like heartburn. In stable angina, symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur, and sometimes no symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart failure or an abnormal heart rhythm. Risk factors include high blood pressure, smoking, diabetes mellitus, lack of exercise, obesity, high blood cholesterol, poor diet, depression, excessive alcohol consumption and a family history of premature cardiovascular disease. A number of tests may help with diagnosis including electrocardiogram, cardiac stress testing, coronary computed tomographic angiography and coronary angiogram, among others. Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking. Medications for diabetes, high cholesterol, or high blood pressure are sometimes used. Although primary prevention strategies involving statin medications reduce the incidence of the sequelae of CAD, there is limited evidence for the efficacy of early detection of CAD itself through screening of low-risk individuals who do not show symptoms. Treatment involves the same measures as prevention. Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended. Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease. In those with stable CAD it is unclear if PCI or CABG in addition to the other treatments improves life expectancy or decreases heart attack risk. In 2015, CAD affected 110 million people and resulted in 8.9 million deaths. It makes up 15.6% of all deaths, making it the most common cause of death globally. The risk of death from CAD for a given age decreased between 1980 and 2010, especially in developed countries. The number of cases of CAD for a given age also decreased between 1990 and 2010. In the United States in 2010, about 20% of those over 65 had CAD, while it was present in 7% of those 45 to 64, and 1.3% of those 18 to 45; rates were higher among males than females of a given age.
A retinal ganglion cell (RGC) is a type of neuron located near the inner surface (the ganglion cell layer) of the retina of the eye. It receives visual information from photoreceptors via two intermediate neuron types: bipolar cells and retina amacrine cells. Retina amacrine cells, particularly narrow field cells, are important for creating functional subunits within the ganglion cell layer and making it so that ganglion cells can observe a small dot moving a small distance. Retinal ganglion cells collectively transmit image-forming and non-image forming visual information from the retina in the form of action potential to several regions in the thalamus, hypothalamus, and mesencephalon, or midbrain. Retinal ganglion cells vary significantly in terms of their size, connections, and responses to visual stimulation but they all share the defining property of having a long axon that extends into the brain. These axons form the optic nerve, optic chiasm, and optic tract. A small percentage of retinal ganglion cells contribute little or nothing to vision, but are themselves photosensitive; their axons form the retinohypothalamic tract and contribute to circadian rhythms and pupillary light reflex, the resizing of the pupil.
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →Mae Jemison, aboard Space Shuttle Endeavour in 1992.
