query: primary neurulation begins in response to signals released by cells in the

pos: Neurulation and actin in the apical portion of the cell which constricts as they move. The variation in cell shapes is partially determined by the location of the nucleus within the cell, causing bulging in areas of the cells forcing the height and shape of the cell to change. This process is known as apical constriction. The result is a flattening of the differentiating neural plate which is particularly obvious in salamanders when the previously round gastrula becomes a rounded ball with a flat top. See Neural plate The process of the flat neural plate folding into the cylindrical neural tube

pos: Neural fold Neural fold The neural fold is a structure that arises during neurulation in the embryonic development of both birds and mammals among other organisms. This structure is associated with primary neurulation, meaning that it forms by the coming together of tissue layers, rather than a clustering, and subsequent hollowing out, of individual cells (known as secondary neurulation). In humans, the neural folds are responsible for the formation of the anterior end of the neural tube. The neural folds are derived from the neural plate, a preliminary structure consisting of elongated ectoderm cells. The folds give rise to neural crest cells,

pos: Neurulation model of how primary neural inductions was proposed in 2006. There has long been a general reluctance in the field to consider the possibility that primary neural induction might be initiated by mechanical effects. A full explanation for primary neural induction remains to be found. As neurulation proceeds after induction the cells of the neural plate become high-columnar and can be identified through microscopy as different from the surrounding presumptive epithelial ectoderm (epiblastic endoderm in amniotes). The cells move laterally and away from the central axis and change into a truncated pyramid shape. This pyramid shape is achieved through tubulin

pos: Neurula primary and secondary neurulation. Primary neurulation refers to the formation and inward folding of the neural plate upon itself to form the neural tube. In secondary neurulation, the neural tube forms via the merging of cavities in the medullary cord. In amphibians and reptiles, primary neurulation forms the whole neural tube, and the neural tube closes simultaneously along its length. Contrarily, in fish, secondary neurulation forms the neural tube. Both primary and secondary neurulation occur in birds and mammals, although with slight differences. Primary neurulation occurs in the cranial and upper spinal regions, which gives rise to the brain and

pos: Bone morphogenetic protein SMADs are important in the development of the heart, central nervous system, and cartilage, as well as post-natal bone development. They have an important role during embryonic development on the embryonic patterning and early skeletal formation. As such, disruption of BMP signaling can affect the body plan of the developing embryo. For example, BMP4 and its inhibitors noggin and chordin help regulate polarity of the embryo (i.e. back to front patterning). Specifically BMP-4 and its inhibitors play a major role in neurulation and the development of the neural plate. BMP-4 signals ectoderm cells to develop into skin cells, but the

pos: Neural plate cord development. This process as a whole is termed primary neurulation. Signaling proteins are also important in neural plate development, and aid in differentiating the tissue destined to become the neural plate. Examples of such proteins include bone morphogenetic proteins and cadherins. Expression of these proteins is essential to neural plate folding and subsequent neural tube formation. Generally divided into four steps, the process of primary neurulation involves the neural plate in the first three. The formation and folding of the neural plate is the first step in primary neurulation. This is followed by the refinement and growth of neural

pos: Neural plate create the neural tube. The figure demonstrates the development of the neural plate into the neural tube, which is where the neural crest cells are derived from as well. In primary neurulation, the layer of ectoderm divides into three sets of cells: the neural tube (future brain and spinal cord), epidermis (skin), and neural crest cells (connects epidermis and neural tube and will migrate to make neurons, glia, and skin cell pigmentation). During the stage of neural plate formation the embryo consists of three cell layers: the ectoderm that eventually forms the skin and neural tissues, the mesoderm that forms

pos: Neurulation Neurulation Neurulation refers to the folding process in vertebrate embryos, which includes the transformation of the neural plate into the neural tube. The embryo at this stage is termed the neurula. The process begins when the notochord induces the formation of the central nervous system (CNS) by signaling the ectoderm germ layer above it to form the thick and flat neural plate. The neural plate folds in upon itself to form the neural tube, which will later differentiate into the spinal cord and the brain, eventually forming the central nervous system. Different portions of the neural tube form by two

pos: Neurulation live births. Neurulation Neurulation refers to the folding process in vertebrate embryos, which includes the transformation of the neural plate into the neural tube. The embryo at this stage is termed the neurula. The process begins when the notochord induces the formation of the central nervous system (CNS) by signaling the ectoderm germ layer above it to form the thick and flat neural plate. The neural plate folds in upon itself to form the neural tube, which will later differentiate into the spinal cord and the brain, eventually forming the central nervous system. Different portions of the neural tube form

pos: Development of the nervous system notochord. Ectodermal cells overlying the notochord develop into the neural plate in response to a diffusible signal produced by the notochord. The remainder of the ectoderm gives rise to the epidermis (skin). The ability of the mesoderm to convert the overlying ectoderm into neural tissue is called neural induction. The neural plate folds outwards during the third week of gestation to form the neural groove. Beginning in the future neck region, the neural folds of this groove close to create the neural tube. The formation of the neural tube from the ectoderm is called neurulation. The ventral part of the

pos: Neurulation of the notochodral cells become incorporated into the center section neural plate to later form the floor plate of the neural tube. The notochord plate separates and forms the solid notochord. The folding of the neural tube to form an actual tube does not occur all at once. Instead, it begins approximately at the level of the fourth somite at Carnegie stage 9 (around Embryonic day 20 in humans). The lateral edges of the neural plate touch in the midline and join together. This continues both cranially (toward the head) and caudally (toward the tail). The openings that are formed

pos: Cerebral cortex develops from the most anterior part of the neural plate, a specialized part of the embryonic ectoderm. The neural plate folds and closes to form the neural tube. From the cavity inside the neural tube develops the ventricular system, and, from the epithelial cells of its walls, the neurons and glia of the nervous system. The most anterior (front, or cranial) part of the neural plate, the prosencephalon, which is evident before neurulation begins, gives rise to the cerebral hemispheres and its later cortex. Cortical neurons are generated within the ventricular zone, next to the ventricles. At first, this zone

pos: Neural plate plate cells. The third step of primary neurulation does not involve the neural plate per se, but rather the edges of the neural plate, which come together, turning the plate into the start of the neural tube. With the neural plate having folded into a tube, the neural folds come together to complete the fusion of the neural tube. This process is illustrated in the figure to the right, where the neural plate is shown in purple. The lime green marks the edges of the neural plate, which become the neural folds, involved in the folding of the plate to

pos: Neurulation tissue and close the tube. This change in expression stops the binding of the neural tube to the epidermis. Neural plate folding is a complicated step. The notochord plays an integral role in the development of the neural tube. Prior to neurulation, during the migration of epiblastic endoderm cells towards the hypoblastic endoderm, the notochordal process opens into an arch termed the notochordal plate and attaches overlying neuroepithelium of the neural plate. The notochordal plate then serves as an anchor for the neural plate and pushes the two edges of the plate upwards while keeping the middle section anchored. Some

pos: Human brain the fourth week in the neurulation stage the neural plate folds and closes to form the neural tube, bringing together the neural crest cells at the neural crest. The neural crest runs the length of the tube with cranial neural crest cells at the cephalic end and caudal neural crest cells at the tail. Cells detach from the crest and migrate in a craniocaudal (head to tail) wave inside the tube. Cells at the cephalic end give rise to the brain, and cells at the caudal end give rise to the spinal cord. The tube flexes as it grows, forming

neg: Neurulation points which then close up and down. In birds neural tube closure begins at one point of the midbrain and moves anteriorly and posteriorly. In secondary neurulation, the neural ectoderm and some cells from the endoderm form the medullary cord. The medullary cord condenses, separates and then forms cavities. These cavities then merge to form a single tube. Secondary neurulation occurs in the posterior section of most animals but it is better expressed in birds. Tubes from both primary and secondary neurulation eventually connect. The anterior portion of the neural tube forms the three main parts of the brain: the

neg: Ectoderm each give rise to a particular set of cells. The neural tube cells will become the central nervous system, neural crest cells will become the peripheral and enteric nervous system, along with melanocytes, facial cartilage and the dentin of teeth, and the epidermal cell region will give rise to epidermis, hair, nails, sebaceous glands, olfactory and mouth epithelium, as well as eyes. Neurulation proceeds by primary and secondary neurulation, both positioning neural crest cells between a superficial epidermal layer and a deep neural tube. During primary neurulation, the notochord cells of the mesoderm signal the adjacent, superficial ectoderm cells to

neg: Neural tube The neural tube develops in two ways: "primary neurulation" and "secondary neurulation". Primary neurulation divides the ectoderm into three cell types: Each organism uses primary and secondary neurulation to varying degrees. Mammalian neural tubes close in the head in the opposite order that they close in the trunk. Four neural tube subdivisions each eventually develop into distinct regions of the central nervous system by the division of neuroepithelial cells: the forebrain (prosencephalon), the midbrain (mesencephalon), the hindbrain (rhombencephalon) and the spinal cord. For a short time, the neural tube is open both cranially and caudally. These openings, called neuropores, close

neg: PTX3 control of autoimmunity. PTX3 Pentraxin-related protein PTX3 also known as TNF-inducible gene 14 protein (TSG-14) is a protein that in humans is encoded by the "PTX3" gene. Pentraxin 3 (ptx3) is a member of the pentraxin superfamily. This super family characterized by cyclic multimeric structure. PTX3 is rapidly produced and released by several cell types, in particular by mononuclear phagocytes, dendritic cells (DCs), fibroblasts and endothelial cells in response to primary inflammatory signals [e.g., toll-like receptor (TLR) engagement, TNFα, IL-1β]. PTX3 binds with high affinity to the complement component C1q, the extracellular matrix component TNFα induced protein 6 (TNFAIP6; also

neg: PTX3 PTX3 Pentraxin-related protein PTX3 also known as TNF-inducible gene 14 protein (TSG-14) is a protein that in humans is encoded by the "PTX3" gene. Pentraxin 3 (ptx3) is a member of the pentraxin superfamily. This super family characterized by cyclic multimeric structure. PTX3 is rapidly produced and released by several cell types, in particular by mononuclear phagocytes, dendritic cells (DCs), fibroblasts and endothelial cells in response to primary inflammatory signals [e.g., toll-like receptor (TLR) engagement, TNFα, IL-1β]. PTX3 binds with high affinity to the complement component C1q, the extracellular matrix component TNFα induced protein 6 (TNFAIP6; also called TNF-stimulated gene

neg: Development of the nervous system in humans folds of this groove close to create the neural tube (this form of neurulation is called primary neurulation). The ventral (front) part of the neural tube is called the basal plate; the dorsal (rear) part is called the alar plate. The hollow interior is called the neural canal. By the end of the fourth week of gestation, the open ends of the neural tube (the neuropores) close off. The spinal cord forms from the lower part of the neural tube. The wall of the neural tube consists of neuroepithelial cells, which differentiate into neuroblasts, forming the mantle layer (the gray

neg: Gendicine begins to over-express genes coding for the p53 protein needed to fight the tumour. Ad-p53 seems to act by stimulating the apoptotic pathway in tumour cells, which increases the expression of tumour suppressor genes and immune response factors (such as the ability of natural killer (NK) cells to exert "bystander" effects). It also decreases the expression of multi-drug resistance, vascular endothelial growth factor and matrix metalloproteinase-2 genes and blocking transcriptional survival signals. p53 mutation status of the tumour cells and response to Ad-p53 treatment are not closely correlated. Ad-p53 appears to act synergistically with conventional treatments such as chemo- and

neg: Epidermis calcium released from intracellular stores and another part comes from transmembrane calcium influx, through both calcium-sensitive chloride channels and voltage-independent cation channels permeable to calcium. Moreover, it has been suggested that an extracellular calcium-sensing receptor (CaSR) also contributes to the rise in intracellular calcium concentration. Epidermal organogenesis, the formation of the epidermis, begins in the cells covering the embryo after neurulation, the formation of the central nervous system. In most vertebrates, this original one-layered structure quickly transforms into a two-layered tissue; a temporary outer layer, the periderm, which is disposed once the inner basal layer or "stratum germinativum" has formed.

neg: Leishmania a role in resisting the complement system, inhibiting the oxidative burst response, inducing an inflammation response and preventing natural killer T cells recognising that the macrophage is infected with the "Leishmania" parasite. In order to avoid destruction by the immune system and thrive, the "Leishmania" 'hides' inside its host's cells. This location enables it to avoid the action of the humoral immune response (because the pathogen is safely inside a cell and outside the open bloodstream), and furthermore it may prevent the immune system from destroying its host through nondanger surface signals which discourage apoptosis. The primary cell types "Leishmania"

neg: Neurulation different processes, called primary and secondary neurulation, in different species. The concept of induction originated in work by Pandor in the 1817. The first experiments proving induction were attributed by Viktor Hamburger to independent discoveries of both Hans Spemann of Germany in 1901 and Warren Lewis of the USA in 1904. It was Hans Spemann who first popularized the term “primary neural induction” in reference to the first differentiation of ectoderm into neural tissue during neurulation. It was called "primary" because it was thought to be the first induction event in embryogenesis. The Nobel prize winning experiment was done by

neg: Pyroptosis replication niches and enhancing defensive responses through the release of proinflammatory cytokines and endogenous danger signals, in pathogenic inflammation, such as that elicited by HIV-1, this beneficial response does not eradicate the primary stimulus. In fact, it appears to create a pathogenic vicious cycle in which dying CD4 T cells release inflammatory signals that attract more cells into the infected lymphoid tissues to die and to produce chronic inflammation and tissue injury. It may be possible to break this pathogenic cycle with safe and effective caspase-1 inhibitors. These agents could form a new and exciting ‘anti-AIDS' therapy for HIV-infected subjects

neg: Neurulation proteins and growth factors have also been invoked as inducers including soluble growth factors such as bone morphogenetic protein, and a requirement for “inhibitory signals” such as noggin and follistatin. Even before the term induction was popularized several authors, beginning with Hans Driesch in 1894, suggested that primary neural induction might be mechanical in nature. A mechanochemical based model for primary neural induction was proposed in 1985 by Brodland &Gordon. An actual physical wave of contraction has been shown to originate from the precise location of the Spemann organizer which then traverses the presumptive neural epithelium and a full working

neg: Granule cell from the primary auditory cortex project directly on to the cochlear nucleus. This is important in the acoustic startle reflex, in which the pyramidal cells modulate the secondary orientation reflex and the granule cell input is responsible for appropriate orientation. This is because the signals received by the granule cells contain information about the head position. Granule cells in the dorsal cochlear nucleus play a role in the perception and response to sounds in our environment. Inhibition generated by granule cells, the most common GABAergic cell type in the olfactory bulb, plays a critical role in shaping the output of

neg: Neurogenesis cells. In the adult SVZ, the primary neural stem cells are SVZ astrocytes rather than RGCs. Most of these adult neural stem cells lie dormant in the adult, but in response to certain signals, these dormant cells, or B cells, go through a series of stages, first producing proliferating cells, or C cells. The C cells then produce neuroblasts, or A cells, that will become neurons. Significant neurogenesis also occurs during adulthood in the hippocampus of many mammals, from rodents to some primates, although its existence in adult humans is debated. The hippocampus plays a crucial role in the formation

neg: Polly Matzinger won universal acceptance. Some immunologists, following Janeway's ideas more directly, believe that the immune response is mainly fueled by innate evolutionarily conserved "pattern recognition receptors" which recognize patterns expressed by microbes such as bacteria, and do not see cell death in the absence of pathogens as a primary driver of immune responses. These ideas however, do not explain how the immune system rejects tumors, induce autoimmune diseases, or generate allergy and asthma. Seong and Matzinger have suggested that the "patterns" that the immune system recognizes on bacteria are not as different from the alarm signals released by damaged cells as

neg: Brain electric field sense of some types of fish. Each sensory system begins with specialized receptor cells, such as light-receptive neurons in the retina of the eye, or vibration-sensitive neurons in the cochlea of the ear. The axons of sensory receptor cells travel into the spinal cord or brain, where they transmit their signals to a first-order sensory nucleus dedicated to one specific sensory modality. This primary sensory nucleus sends information to higher-order sensory areas that are dedicated to the same modality. Eventually, via a way-station in the thalamus, the signals are sent to the cerebral cortex, where they are processed

neg: Neurulation limbs of the vertebrate ). Masses of tissue called the neural crest that are located at the very edges of the lateral plates of the folding neural tube separate from the neural tube and migrate to become a variety of different but important cells. Neural crest cells will migrate through the embryo and will give rise to several cell populations, including pigment cells and the cells of the peripheral nervous system. Failure of neurulation, especially failure of closure of the neural tube are among the most common and disabling birth defects in humans, occurring in roughly 1 in every 500

neg: Cochlea Corti, and determines the mechanical wave propagation properties of the cochlear system. The cochlea is filled with a watery liquid, the perilymph, which moves in response to the vibrations coming from the middle ear via the oval window. As the fluid moves, the cochlear partition (basilar membrane and organ of Corti) moves; thousands of hair cells sense the motion via their stereocilia, and convert that motion to electrical signals that are communicated via neurotransmitters to many thousands of nerve cells. These primary auditory neurons transform the signals into electrochemical impulses known as action potentials, which travel along the auditory nerve

neg: Neurulation rhombomeres generate many of the most essential neural circuits needed for life, including those that control respiration and heart rate, and produce most of the cranial nerves. Neural crest cells form ganglia above each rhombomere. The early neural tube is primarily composed of the germinal neuroepithelium, later called the ventricular zone, which contains primary neural stem cells called radial glial cells and serves as the main source of neurons produced during brain development through the process of neurogenesis. Paraxial mesoderm surrounding the notochord at the sides will develop into the somites (future muscles, bones, and contributes to the formation of

neg: Polly Matzinger cell death). The alarm signals released by these cells let the immune system know that there is a problem requiring an immune response. She argued that T cells and the immune response they orchestrate occurs not because of a neonatal definition of "self", as in the previous model, nor because of ancient definitions of pathogens, as in Janeway's argument, but because of a dynamic and constantly updated response to danger as defined by cellular damage. The danger model is broad, covering topics as diverse as transplantation, maternal/fetal immunity, autoimmunity, cancer treatments, and vaccines, but Matzinger points out that the original

neg: Neuroinflammation immune cells for an inflammatory response. Astrocytes are glial cells that are the most abundant cells in the brain. They are involved in maintenance and support of neurons and compose a significant component of the blood–brain barrier. After insult to the brain, such as traumatic brain injury, astrocytes may become activated in response to signals released by injured neurons or activated microglia. Once activated, astrocytes may release various growth factors and undergo morphological changes. For example, after injury astrocytes form the glial scar composed of a proteoglycan matrix that hinders axonal regeneration. Cytokines are a class of proteins that regulates

neg: Somatic evolution in cancer growth signals and thereby no longer rely on proliferation signals from the micro-environment. Normal cells are maintained in a nondividing state by antigrowth signals, which cancer cells learn to evade through genetic changes producing "insensitivity to antigrowth signals". A normal cell initiates programmed cell death (apoptosis) in response to signals such as DNA damage, oncogene overexpression, and survival factor insufficiency, but a cancer cell learns to "evade apoptosis", leading to the accumulation of aberrant cells. Most mammalian cells can replicate a limited number of times due to progressive shortening of telomeres; virtually all malignant cancer cells gain an ability to

neg: Merkel nerve ending functions as the enterochromaffin cell, the mechanosensory cell in the GI epithelium, which synthesizes 95% of the body's total serotonin or 5-HT. Like the cells responsible for the mechanotransduction in hearing, Merkel cells transduce mechanical forces into excitatory signals via ion conductance on mechanosensitive channels. of which Piezo2 is the Merkel cell´s primary mechanosensor. The Merkel cell´s somewhat rigid structure, and the fact that they are not encapsulated, causes them to have a sustained response in the form of action potentials or spikes) to mechanical deflection of the tissue. Because of their sustained response to pressure, Merkel nerve endings are

neg: Endocrine gland uptake and metabolism by most body cells. Somatostatin is released by Delta cells and act as an Inhibitor of GH, Insulin and Glucagon. The ovaries of the female, located in the pelvic cavity, release two main hormones. Secretion of estrogens by the ovarian follicles begins at puberty under the influence of FSH. Estrogens stimulate maturation of the female reproductive system and development of the secondary sexual characteristics. Progesterone is released in response to high blood levels of LH. It works with estrogens in establishing the menstrual cycle. The testes of the male begin to produce testosterone at puberty in response

neg: Pyroptosis Pyroptosis Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. In this process, immune cells recognize foreign danger signals within themselves, release pro-inflammatory cytokines, swell, burst and die. The released cytokines attract other immune cells to fight the infection and contribute to inflammation in the tissue. Pyroptosis promotes the rapid clearance of various bacterial and viral infections by removing intracellular replication niches and enhancing the host's defensive responses. However, in pathogenic chronic diseases, the inflammatory response does not eradicate the

neg: Psoriasis with psoriasis than in those without the infection. The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells, whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T cells. It is hypothesized that the diminished CD4+-T cell presence causes an overactivation of CD8+-T cells, which are responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy.

neg: Aphanomyces euteiches infected host plants. Oospores germinate as a response to chemical signals detected from the roots of new hosts plants. Germination can either be direct or indirect. Either way, infecting begins at the cell in the root tips of the host plant. In direct germination, the oospore produces hyphae which directly penetrate host cells at the plant’s root tips. In indirect germination, the oospore produces sporangia which release zoospores. The zoospores then encyst on the host plant cells, and germinate. After direct or indirect germination, coenocytic hyphae of "A. euteiches" colonize host tissue through inter- and intra-cellular growth. For sexual reproduction,

neg: Cell communication (biology) Cell communication (biology) Cell communication is the ability of cells to communicate with adjacent cells within an organism. Cells transmit and receive signals acquired from fellow cells or by the environment surrounding the cell. The signals are transmitted across the cell membrane to prompt a response. The signal can cross the membrane itself, or it can interact with receptor proteins that contact both the interior and exterior of a cell. The correct receptor needs to be present on the cells surface to be able to respond to the signal. Signals pass from protein to protein when the signal travels through

neg: Neurula in manipulating the neural groove into a V-shape, as well as in neural tube closure. The ECM does not play a major role in spinal neurulation due to the close-packed nature of the mesodermal cells in the spinal region, which allows little intercellular space. Additionally, actin-containing microfilaments are believed to be necessary in cranial neurulation. They may act as the mechanism for neural folding, or they may stabilize neural folds that have already formed; however, their exact role has not been determined. There is some evidence that growth factors, such as insulin or transferrin, also play a role in neurulation,

neg: Cell migration Cell migration Cell migration is a central process in the development and maintenance of multicellular organisms. Tissue formation during embryonic development, wound healing and immune responses all require the orchestrated movement of cells in particular directions to specific locations. Cells often migrate in response to specific external signals, including chemical signals and mechanical signals. Errors during this process have serious consequences, including intellectual disability, vascular disease, tumor formation and metastasis. An understanding of the mechanism by which cells migrate may lead to the development of novel therapeutic strategies for controlling, for example, invasive tumour cells. Due to the highly viscous

neg: Cell migration and retrograde flow. Cell migration Cell migration is a central process in the development and maintenance of multicellular organisms. Tissue formation during embryonic development, wound healing and immune responses all require the orchestrated movement of cells in particular directions to specific locations. Cells often migrate in response to specific external signals, including chemical signals and mechanical signals. Errors during this process have serious consequences, including intellectual disability, vascular disease, tumor formation and metastasis. An understanding of the mechanism by which cells migrate may lead to the development of novel therapeutic strategies for controlling, for example, invasive tumour cells. Due to

neg: Action potential potential, such as plant cells, muscle cells, and the specialized cells of the heart (in which occurs the cardiac action potential). However, the main excitable cell is the neuron, which also has the simplest mechanism for the action potential. Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma, a single axon and one or more axon terminals. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of ligand-gated

neg: Sex differences in sensory systems response to short, aggressive, "Co" notes in "E. coqui". Altogether, sex specific tuning differences in the primary auditory neurons of the basilar papilla and duration sensitive cells in the torus semicircularis of males suggest a mechanism to explain the sex specific response behavior observed in "E. coqui". Like sex differences in the olfactory system of "M. sexta", and in the visual system of Bibionids, sex differences in the auditory system of "E. coqui" benefit receivers at a functional level by maximizing sensitivity to aggressive or mate attraction signals based on the sex of the receiver and which signal is relevant.

neg: Retina photoceptor sends a proportional response synaptically to bipolar cells which in turn signal the retinal ganglion cells. The photoreceptors are also cross-linked by horizontal cells and amacrine cells, which modify the synaptic signal before it reaches the ganglion cells, the neural signals being intermixed and combined. Of the retina's nerve cells, only the retinal ganglion cells and few amacrine cells create action potentials. In the retinal ganglion cells there are two types of response, depending on the receptive field of the cell. The receptive fields of retinal ganglion cells comprise a central, approximately circular area, where light has one effect

neg: Cochlear implant sound into movements of hair cells in the cochlea; the inside-portion of these hair cells release potassium ions in response to the movement of the hairs, and the potassium in turn stimulates other cells to release the neurotransmitter, glutamate, which makes the cochlear nerve send signals to the brain, which creates the experience of sound. Instead, the devices pick up sound and digitize it, convert that digitized sound into electrical signals, and transmit those signals to electrodes embedded in the cochlea. The electrodes electrically stimulate the cochlear nerve, causing it to send signals to the brain. There are several systems

neg: Psoriasis interleukin-36γ, tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-22. These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate. One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10. Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of psoriasis. DNA released from dying cells acts as an inflammatory stimulus in psoriasis and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α. In response to these chemical messages from dendritic cells and

neg: Polly Matzinger molecular signals that initiate response or by a small set of cells (e.g., regulatory T cells) that shut it down. There is now a growing body of work on regulatory T cells which argues that immune activity is stopped by a special subset of T cells. These ideas challenge several of the key specifics of Matzinger's model. Matzinger argues that these cells are misinterpreted because their functions have not been explored enough. To date (with rare exceptions) these cells have been tested almost exclusively for their ability to suppress highly inflammatory immune response types. The exceptions are illustrative in that

neg: Cell communication (biology) on the exterior of the cell. Another response that the cell may have is the signal directs actin molecules to assemble into filament allowing the cell to change shape. A carrier protein delivers a signal to a nuclear pore where it can enter the nucleus and turn the gene on or off. Cells can assimilate multiple signals and every cell collects a multifaceted combination of signals that all require the cell to respond simultaneously transmitting different signals though different signaling pathways. The cell assimilates the data from the signal to multiple signaling pathways to obtain the proper response. Cells communicate

neg: Chloroplast is controversial. Plants lack specialized immune cells—all plant cells participate in the plant immune response. Chloroplasts, along with the nucleus, cell membrane, and endoplasmic reticulum, are key players in pathogen defense. Due to its role in a plant cell's immune response, pathogens frequently target the chloroplast. Plants have two main immune responses—the hypersensitive response, in which infected cells seal themselves off and undergo programmed cell death, and systemic acquired resistance, where infected cells release signals warning the rest of the plant of a pathogen's presence. Chloroplasts stimulate both responses by purposely damaging their photosynthetic system, producing reactive oxygen species. High

neg: Signal transduction site of an inflammatory response. In a similar manner, integrins at the cell membrane of circulating platelets are normally kept inactive to avoid thrombosis. Epithelial cells (which are non-circulating) normally have active integrins at their cell membrane, helping maintain their stable adhesion to underlying stromal cells that provide signals to maintain normal functioning. In plants, there are no bona fide integrin receptors identified to date; nevertheless, several integrin-like proteins were proposed based on structural homology with the metazoan receptors. Plants contain integrin-linked kinases that are very similar in their primary structure with the animal ILKs. In the experimental model plant

neg: Guard cell of genetics. Cytosolic and nuclear proteins and chemical messengers that function in stomatal movements have been identified that mediate the transduction of environmental signals thus controlling CO intake into plants and plant water loss. Research on guard cell signal transduction mechanisms is producing an understanding of how plants can improve their response to drought stress by reducing plant water loss. Guard cells also provide an excellent model for basic studies on how a cell integrates numerous kinds of input signals to produce a response (stomatal opening or closing). These responses require coordination of numerous cell biological processes in guard cells,

neg: Repetitive visual stimulus Repetitive visual stimulus Repetitive Visual Stimulus (RVS) is a visual stimulus that has a distinctive property (e.g., frequency or phase). The stimuli are simultaneously presented to the user when focusing his/her attention on the corresponding stimulus. For example, when the user focuses his/her attention on an RVS, an SSVEP is elicited which manifests as oscilliatory components in the user's EEG, especially in the signals from the primary visual cortex, matching the frequency or harmonics of that RVS. Repetitive visual stimuli (RVS) are said to evoke a lesser response in brain cells, specifically superior collicular cells, than moving stimuli. Habituation is

neg: Crosstalk (biology) by interacting with the mitogen-activated protein (MAP) kinase pathway. cAMP is a compound synthesized in cells by adenylate cyclase in response to a variety of extracellular signals. cAMP primarily acts as an intracellular second messenger whose major intracellular receptor is the cAMP-dependent protein kinase (PKA) that acts through the phosphorylation of target proteins. The signal transduction pathway begins with ligand-receptor interactions extracellularly. This signal is then transduced through the membrane, stimulating adenylyl cyclase on the inner membrane surface to catalyze the conversion of ATP to cAMP. ERK, a participating protein in the MAPK signaling pathway, can be activated or inhibited

neg: Exosome (vesicle) response markers in prostate cancer. Exosomes secreted from tumour cells can deliver signals to surrounding cells and have been shown to regulate myofibroblast differentiation. In melanoma, tumor-derived vesicles can enter lymphatics and interact with subcapsular sinus macrophages and B cells in lymph nodes. A recent investigation showed that exosome release positively correlates with the invasiveness of ovarian cancer. Exosomes released from tumors into the blood may also have diagnostic potential. Exosomes are remarkably stable in bodily fluids strengthening their utility as reservoirs for disease biomarkers. Patient blood samples stored in biorepositories can be used for biomarker analysis as colorectal cancer

neg: Chemokine and secreted without any need to stimulate their source cell(s). Some chemokines have roles in development; they promote angiogenesis (the growth of new blood vessels), or guide cells to tissues that provide specific signals critical for cellular maturation. Other chemokines are inflammatory and are released from a wide variety of cells in response to bacterial infection, viruses and agents that cause physical damage such as silica or the urate crystals that occur in gout. Their release is often stimulated by pro-inflammatory cytokines such as interleukin 1. Inflammatory chemokines function mainly as chemoattractants for leukocytes, recruiting monocytes, neutrophils and other effector

neg: Neurula and they undergo neurulation up to day 5. Reptiles, including crocodiles, lizards, and turtles, tend to spend a longer time in the neurula stage. A typical frog embryo, incubated at at 18 °C, is an early stage neurula by 50 hours post-fertilization and a late stage neurula by 67 hours. The mouse embryo begins neurulation on day 7.5 of gestation and remains in the neurula stage until day 9. The mesoderm of a vertebrate embryo in the neurula stage can be divided into five regions. Ventral to the neural tube is the chordamesoderm. Lateral to either side of the neural

neg: Bystander effect (radiobiology) the same as the "abscopal effect". The abscopal effect is a phenomenon where the response to radiation is seen in an organ/site distant to the irradiated organ/area, that is, the responding cells are not juxtaposed with the irradiated cells. T-cells and dendritic cells have been implicated to be part of the mechanism. In suicide gene therapy, the "bystander effect" is the ability of the transfected cells to transfer death signals to neighboring tumor cells. Bystander effect (radiobiology) The radiation-induced bystander effect (bystander effect) is the phenomenon in which unirradiated cells exhibit irradiated effects as a result of signals received from

neg: Biotic stress molecules released into plant cells by pathogens. Detection of these signals in infected cells leads to an activation of effector-triggered immunity (ETI), a type of innate immune response. Both the pattern recognition immunity (PTI) and effector-triggered immunity (ETI) result from the upregulation of multiple defense mechanisms including defensive chemical signaling compounds. An increase in the production of salicylic acid (SA) has been shown to be induced by pathogenic infection. The increase in SA results in the production of pathogenesis related (PR) genes which ultimately increase plant resistance to biotrophic and hemibiotrophic pathogens. Increases in jasmonic acid (JA) synthesis near the

neg: Nutritional neuroscience that deficiency in either vitamin can result in megaloblastic anemia, characterized by organic mental change. The process of neural tube transformation into structures that will eventually develop into the central nervous system is known as neurulation, the success of which is dependent on the presence of folate within the body. This process begins in the human approximately 21 days after conception, and is completed by 28 days. Thus, a woman may not even be aware of her pregnancy by the time the process of neurulation is complete, potentially causing severe consequences in the development of the fetus. Functional problems in

neg: Biochemical cascade belong to complex multicellular organisms, they need to communicate among themselves and work for symbiosis in order to give life to the organism. These communications between cells triggers intracellular signaling cascades, termed signal transduction pathways, that regulate specific cellular functions. Each signal transduction occurs with a primary extracellular messenger that binds to a transmembrane or nuclear receptor, initiating intracellular signals. The complex formed produces or releases second messengers that integrate and adapt the signal, amplifying it, by activating molecular targets, which in turn trigger effectors that will lead to the desired cellular response. Signal transduction is realized by activation of

neg: ACAMPs apoptotic cells in order to attract phagocytes (mostly macrophages and immature dendritic cells). Thanks to these markers, apoptotic cells, unlike necrotic cells, do not trigger the unwanted immune response. Eat-me signals mark the apoptotic cells for phagocytes which can subsequently engulf them and actively prevent the inflammation. Various molecular markers can serve as eat-me signals, particularly a change in composition of the cell membrane, modifications of molecules on the cell surface, changed charge on the plasma membrane, or indirectly the extracellular bridging molecules. Deposition of different phospholipids in the phospholipid bilayer of the cell membrane is strictly asymmetric. On a

neg: ACAMPs receptors signalling directs the proinflammatory response triggered by PAMPs). ACAMPs Apoptotic-cell associated molecular patterns (ACAMPs) are molecular markers present on cells which are going through apoptosis, i.e. programmed cell death (similarly, Pathogen-associated molecular patterns (PAMPs) are markers of invading pathogens and Damage-associated molecular patterns (DAMPs) are markers of damaged tissue). The term was used for the first time by C. D. Gregory in 2000. Recognition of these patterns by the pattern recognition receptors (PRRs) of phagocytes then leads to phagocytosis of the apoptotic cell. These patterns include eat-me signals on the apoptotic cells, loss of don’t-eat-me signals on viable cells

neg: Danger model tumor antigens because transformed cells do not send any danger signals which could activate dendritic cells and initiate an immune response. "Danger signals" are normal intracellular molecules that are not found in the extracellular space under physiological conditions. The danger model has evolved over the years. "Danger signals" include DNA, RNA, heat shock proteins (Hsps), hyaluronic acid, serum amyloid A protein, ATP, uric acid and also cytokines like interferon alfa, interleukin-1β, CD40L and so on. The "Danger model" suggests that, upon cellular necrosis, cryptic molecules in normal cells might be liberated from the cytoplasm into the tissue microenvironment, new molecules

neg: Immunity (medical) This type of transfer differs from a bone marrow transplant, in which (undifferentiated) hematopoietic stem cells are transferred. When B cells and T cells are activated by a pathogen, memory B-cells and T- cells develop, and the primary immune response results. Throughout the lifetime of an animal, these memory cells will "remember" each specific pathogen encountered, and can mount a strong secondary response if the pathogen is detected again. The primary and secondary responses were first described in 1921 by English immunologist Alexander Glenny although the mechanism involved was not discovered until later.This type of immunity is both active and

neg: Neurulation forms the dorsal portions, devoted mostly to sensory processing. The dorsal epidermis expresses BMP4 and BMP7. The roof plate of the neural tube responds to those signals to express more BMP4 and other transforming growth factor beta (TGF-β) signals to form a dorsal/ventral gradient among the neural tube. The notochord expresses SHH. The floor plate responds to SHH by producing its own SHH and forming a gradient. These gradients allows for the differential expression of transcription factors. Neural tube closure is not entirely understood. Closure of the neural tube varies by species. In mammals closure occurs by meeting at multiple

neg: Immunological memory to a potentially dangerous agent. The course of secondary immune response is similar to primary immune response. After the memory B cell recognizes the antigen it presents the peptide: MHC II complex to nearby effector T cells. That leads to activation of these cells and rapid proliferation of cells. After the primary immune response has disappeared the effector cells of the immune response are eliminated. However, there remain antibodies previously created in the body that represent the humoral component of immunological memory and comprise an important defensive mechanism in subsequent infections. In addition to the formed antibodies in the body

neg: HLA-F open conformers, but it does not bind peptide complexes. The expression patterns of HLA-F in T cells suggest that HLA-F is involved in the communication pathway between T reg and activated T cells, where HLA-F signals that the immune response has been activated. During this communication, either HLA-F invokes secretion of inhibitory cytokines by the regulatory T cells or it provides a simple inhibitory signal to the regulatory T cells, allowing a normal immune response to proceed. Viral proteins and other exogenous antigens decrease surface HLA-F expression because the exogenous proteins interact with HLA class I molecules at the same

neg: Ectoderm will become endoderm cells, is completely engulfed by the prospective ectoderm, as these top cells undergo epiboly, where the ectoderm cells divide in a way to form one layer. This creates a uniform embryo composed of the three germ layers in their respective positions. Once there is an embryo with three established germ layers, differentiation among these three layers proceeds. The next event that will take place within the ectoderm is the process of neurulation, which results in the formation of the neural tube, neural crest cells and the epidermis. It is these three components of the ectoderm that will

neg: NF-κB schizophrenia. Recently, NF-κB activation has been suggested as a possible molecular mechanism for the catabolic effects of cigarette smoke in skeletal muscle and sarcopenia. Research has shown that during inflammation the function of a cell depends on signals it activates in response to contact with adjacent cells and to combinations of hormones, especially cytokines that act on it through specific receptors. A cells’ phenotype within a tissue develops through mutual stimulation of feedback signals that coordinate its function with other cells; this is especially evident during reprogramming of cell function when a tissue is exposed to inflammation, because cells alter

neg: Endocrinology of reproduction of steroidogenic acute regulatory protein (StAR)-mediated cholesterol transport and the synthesis of progesterone in hESC. The production of progesterone at this time induces embryroid body (akin to blastulation) and rosette (akin to neurulation) formation in vitro. Progesterone induces the differentiation of pluripotent hESC to neural precursor cells. Suppression of P4 signaling following withdrawal of progesterone, or treatment with the progesterone receptor antagonist RU-486 (mifepristone), inhibits the differentiation of hESC colonies into embryoid bodies (blastulation) or rosettes (neurulation). RU-486, a drug commonly used to terminate pregnancy in its early stages, acts not only to abort the embryo, but also to inhibit

neg: Lens (anatomy) signals from the developing neural retina induces the cells closest to the posterior end of the lens vesicle begin to elongate toward the anterior end of the vesicle. These signals also induce the synthesis of crystallins. These elongating cells eventually fill in the lumen of the vesicle to form the primary fibers, which become the embryonic nucleus in the mature lens. The cells of the anterior portion of the lens vesicle give rise to the lens epithelium. Additional secondary fibers are derived from lens epithelial cells located toward the equatorial region of the lens. These cells lengthen anteriorly and posteriorly

neg: Pyroptosis in which the treatment targets the host instead of the virus. Of note, Caspase-1 deficient mice develop normally, arguing that inhibition of this protein would produce beneficial rather than harmful therapeutic effects in HIV patients. Pyroptosis Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. In this process, immune cells recognize foreign danger signals within themselves, release pro-inflammatory cytokines, swell, burst and die. The released cytokines attract other immune cells to fight the infection and contribute to inflammation in the

neg: Inflammation muscle growth, it has been theorized that a signal-to-noise model may best describe the relationship between inflammation and muscle growth. By keeping the "noise" of chronic inflammation to a minimum, the localized acute inflammatory response signals a stronger anabolic response than could be achieved with higher levels of chronic inflammation. Inflammation Inflammation (from ) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury,

neg: Polly Matzinger of danger signals. The self/non-self model, the predominant model in immunology since the 1950s, began to encounter problems in the late 1980s when immunologists began to recognize that T cells depend on other cells to pick up and then present the things to which they will respond — and that the T cell response depends on whether the other cell (known as antigen-presenting cells) is sending activation signals to the T cells. In 1989, drawing on the ideas of Thomas Kuhn, Charles Janeway proposed that the old immunological paradigm had reached the limits of its usefulness—or, as he described it,

neg: Induced stem cells for nearly a year to look for signs of tumor formation and reported finding none. The same researchers have turned scar-forming astrocytes into progenitor cells called neuroblasts that regenerated into neurons in the injured adult spinal cord. Without myelin to insulate neurons, nerve signals quickly lose power. Diseases that attack myelin, such as multiple sclerosis, result in nerve signals that cannot propagate to nerve endings and as a consequence lead to cognitive, motor and sensory problems. Transplantation of oligodendrocyte precursor cells (OPCs), which can successfully create myelin sheaths around nerve cells, is a promising potential therapeutic response. Direct lineage conversion

neg: G0 phase of the cell cycle. Quiescence refers to a reversible G state where subpopulations of cells reside in a 'quiescent' state before entering the cell cycle after activation in response to extrinsic signals. Quiescent cells are often identified by low RNA content, lack of cell proliferation markers, and increased label retention indicating low cell turnover. Senescence is distinct from quiescence because senescence is an irreversible state that cells enter in response to DNA damage or degradation that would make a cell's progeny nonviable. Such DNA damage can occur from telomere shortening over many cell divisions as well as reactive oxygen species

neg: Auxin have been shown to be important for its tissue development. As auxins contribute to organ shaping, they are also fundamentally required for proper development of the plant itself. Without hormonal regulation and organization, plants would be merely proliferating heaps of similar cells. Auxin employment begins in the embryo of the plant, where directional distribution of auxin ushers in subsequent growth and development of primary growth poles, then forms buds of future organs. Next, it helps to coordinate proper development of the arising organs, such as roots, cotyledons and leaves and mediates long distance signals between them, contributing so to the

neg: Microfold cell lack microvilli, they are characterized by their microfolds, and hence receive their commonly known name. These cells are far less abundant than enterocytes. These cells can also be identified by cytoskeletal and extracellular matrix components expressed at the edge of cells or on their cell surfaces, such as actin, villin, cytokeratin, and vimentin. Factors promoting the differentiation of M cells have yet to be elucidated, but they are thought to develop in response to signals from immune cells found in developing Peyer's patches. B cells have been implicated in the developmental of M cells, since they are also localized in

neg: Polyclonal B cell response place. When the memory cells get stimulated by the antigen to produce plasma cells (just like in the clone's primary response), and leave even more memory cells in the process, this is known as a "secondary immune response," which translates into greater numbers of plasma cells and faster rate of antibody production lasting for longer periods. The memory B cells produced as a part of secondary response recognize the corresponding antigen faster and bind more strongly with it (i.e., greater affinity of binding) owing to affinity maturation. The soluble antibodies produced by the clone show a similar enhancement in antigen

neg: B cell T cell-independent (TI) antigens and include foreign polysaccharides and unmethylated CpG DNA. They are named as such because they are able to induce a humoral response in organisms that lack T cells. B cell response to these antigens is rapid, though antibodies generated tend to have lower affinity and are less functionally versatile than those generated from T cell-dependent activation. As with TD antigens, B cells activated by TI antigens need additional signals to complete activation, but instead of receiving them from T cells, they are provided either by recognition and binding of a common microbial constituent to toll-like receptors

neg: Pericyte characterized by negative expression for nestin (PDGFRβ+CD146+Nes-) and type-2 characterized by positive expression for nestin (PDGFRβ+CD146+Nes+). While both types are able to proliferate in response to glycerol or BaCl2-induced injury, type-1 pericytes give rise to adipogenic cells only in response to glycerol injection and type-2 become myogenic in response to both types of injury. The extent to which type-1 pericytes participate in fat accumulation is not known. Pericytes are also associated with allowing endothelial cells to differentiate, multiply, form vascular branches (angiogenesis), survive apoptotic signals and travel throughout the body. Certain pericytes, known as microvascular pericytes, develop around the walls

neg: Lipoxygenase Lipoxygenase Lipoxygenases () are a family of (non-heme), iron-containing enzymes most of which catalyze the dioxygenation of polyunsaturated fatty acids in lipids containing a cis,cis-1,4- pentadiene into cell signaling agents that serve diverse roles as autocrine signals that regulate the function of their parent cells, paracrine signals that regulate the function of nearby cells, and endocrine signals that regulate the function of distant cells. The lipoxygenases are related to each other based upon their similar genetic structure and dioxygenation activity. However, one lipoxygenase, ALOXE3, while having a lipoxygenase genetic structure, possesses relatively little dioxygenation activity; rather its primary activity appears

neg: Diabetic hypoglycemia as the adrenomedullary epinephrine response) causes the clinical syndrome of hypoglycemia unawareness — loss of the largely neurogenic warning symptoms of developing hypoglycemia. If a person has frequent episodes of hypoglycemia (even mild ones), the brain becomes "used to" the low glucose and no longer signals for epinephrine to be released during such times. More specifically, there are glucose transporters located in the brain cells (neurons). These transporters increase in number in response to repeated hypoglycemia (this permits the brain to receive a steady supply of glucose even during hypoglycemia). As a result, what was once the hypoglycemic threshold for

neg: Intrinsically photosensitive retinal ganglion cells able to isomerize "all-trans-"retinal into "11-cis-"retinal when stimulated with light without help from additional cells. The two isoforms of melanopsin differ in their spectral sensitivity, for the "11-cis"-retinal isoform is more responsive to shorter wavelengths of light, while the "all-trans" isoform is more responsive to longer wavelengths of light. ipRGCs are both pre- and postsynaptic to dopaminergic amacrine cells (DA cells) via reciprocal synapses, with ipRGCs sending excitatory signals to the DA cells and the DA cells sending inhibitory signals to the ipRGCs. These inhibitory signals are mediated through GABA which is co-released from the DA cells along with dopamine.

neg: Floor plate Nodal signaling is required for differentiation of medial floor plate cells whereas Shh is expendable. These data may indicate that the floor plate induction mechanism in amniotes and anamniotes differs. To reconcile these differences, a dual-mode induction model has been proposed in chick. In this model, exclusively ectodermal cells are induced to become medial floor plate during gastrulation by prechordal mesoderm, possibly through Nodal signaling. Later in development during neurulation, extended contact and interaction between notochord and fated floor plate cells causes differentiation, suggesting a cooperative effect between Nodal and Shh signaling. In the development of the central nervous system,

neg: DNA vaccination to be important for a full primary immune response. IM and ID DNA delivery initiate immune responses differently. In the skin, keratinocytes, fibroblasts and Langerhans cells take up and express antigens and are responsible for inducing a primary antibody response. Transfected Langerhans cells migrate out of the skin (within 12 hours) to the draining lymph node where they prime secondary B- and T-cell responses. In skeletal muscle striated muscle cells are most frequently transfected, but seem to be unimportant in immune response. Instead, IM inoculated DNA “washes” into the draining lymph node within minutes, where distal dendritic cells are transfected

neg: Autoimmune retinopathy is more commonly diagnosed in females (approximately 60% of diagnosed patients are females) in the age range of 50-60. A division of AIR, cancer-associated retinopathy is a paraneoplastic syndrome, which is a disorder caused by an immune system response to an abnormality. Autoimmune antibodies target proteins in retinal photoreceptor cells. The proteins targeted as antigenic are recoverin, "α"‐enolase and transducin. This autoimmune response leads to photoreceptor cell death. It causes progressive vision loss that can lead to blindness. CAR is typically associated with the anti-recoverin antibody. Retinal bipolar cells (cells in retina that transmit signals) react with the antibodies, leading

neg: Memory B cell only by a larger initial number of antigen-specific B1 clones. Memory B cell Memory B cells are a B cell sub-type that are formed within germinal centers following primary infection and are important in generating an accelerated and more robust antibody-mediated immune response in the case of re-infection (also known as a "secondary immune response"). During an initial infection (or primary immune response) involving a T-dependent antigen, naive follicular B cells are activated in the presence of T cells within the follicles of secondary lymphoid organs (i.e. spleen and lymph nodes) and undergo clonal expansion to produce a foci of

neg: Neuroanatomy and glial cells come in many types (see, for example, the nervous system section of the list of distinct cell types in the adult human body). Neurons are the information-processing cells of the nervous system: they sense our environment, communicate with each other via electrical signals and chemicals called neurotransmitters across synapses, and produce our memories, thoughts and movements. Glial cells maintain homeostasis, produce myelin, and provide support and protection for the brain's neurons. Some glial cells (astrocytes) can even propagate intercellular calcium waves over long distances in response to stimulation, and release gliotransmitters in response to changes in calcium

neg: Tumor microenvironment the similarity of the original and secondary tumor sites. Its role in blunting an immune attack awaited the discovery of adaptive cellular immunity. In 1960, Klein and colleagues found that in mice, primary methylcholanthrene-induced sarcomas exhibited an antitumor immune response mediated by lymph node cells to cancer cells derived from the primary tumor. This immune response did not however affect the primary tumor. The primary tumor instead established a microenvironment that is functionally analogous to that of certain normal tissues, such as the eye. Later, mice experiments by Halachmi and Witz showed that for the same cancer cell line, greater

neg: P14arf basal levels of Arf are usually low. Knocking down ARF with siRNA to exon 1β results in increased rRNA transcripts, rRNA processing, and ribosome nuclear export. The unrestrained ribosome biogenesis seen when NPM is not bound to ARF does not occur if NPM is also absent. Although the induction of ARF in response to oncogenic signals is considered to be of primary importance, the low levels of ARF seen in interphase cells also has a considerable effect in terms of keeping cell growth in check. Therefore, the function of basal level ARF in the NPM/ARF complex appears to be to

neg: CD19 mutations in CD21 and CD81 can also underlie primary immunodeficiency due to their role in the CD19/CD21 complex formation. These mutations can lead to hypogammaglobulinaemia as a result of poor response to antigen and defective immunological memory. Researchers found changes in the constitution of B lymphocyte population and reduced amounts of switched memory B cells with high terminal differentiation potential in patients with Down Syndrome. CD19 has also been implicated in autoimmune diseases, including rheumatoid arthritis and multiple sclerosis, and may be a useful treatment target. Mouse model research shows that CD19 deficiency can lead to hyporesponsiveness to transmembrane signals

neg: OPN1LW LWS cone cells into horizontal cells, bipolar cells, amacrine cells, and finally ganglion cells before continuing to the brain via the optic nerve. Ganglion cells compile the signal from the LWS cones with all other cone signals that occurred in response to the light that was seen, and pass the overall signal into the optic nerve. The cones themselves do not process colour, it is the brain that decides what colour is being seen by the signal combination it receives from the ganglion cells. Before humans evolved to be a trichromatic species, our vision was dichromatic and consisted of only

neg: Genetics tumor that grows and invades various tissues of the body. Normally, a cell divides only in response to signals called growth factors and stops growing once in contact with surrounding cells and in response to growth-inhibitory signals. It usually then divides a limited number of times and dies, staying within the epithelium where it is unable to migrate to other organs. To become a cancer cell, a cell has to accumulate mutations in a number of genes (three to seven). A cancer cell can divide without growth factor and ignores inhibitory signals. Also, it is immortal and can grow indefinitely,

neg: DNA repair reversion of previously-inhibited defects. It has become apparent over the past several years that the DNA damage response acts as a barrier to the malignant transformation of preneoplastic cells. Previous studies have shown an elevated DNA damage response in cell-culture models with oncogene activation and preneoplastic colon adenomas. DNA damage response mechanisms trigger cell-cycle arrest, and attempt to repair DNA lesions or promote cell death/senescence if repair is not possible. Replication stress is observed in preneoplastic cells due to increased proliferation signals from oncogenic mutations. Replication stress is characterized by: increased replication initiation/origin firing; increased transcription and collisions of transcription-replication

neg: Danger model important for stimulation of immune response are normal tissues. When tissue cells are distressed because of injury, infection and so on, they start to secrete or express on their surface so called "Danger signals". "Danger signals" are also thrown out to extracellular space in the case that stressed cell dies by immunologic not-silent cell death such as necrosis or pyroptosis (as opposed to apoptosis, controlled cell death). This model also dictates that despite their potential immunogenicity tumors do not induce significant immune responses which could destroy malignant cells. According to the danger model, the immune surveillance system fails to detect