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Research Areas

Continuing to offer an assortment of products relevant to all your research interests. 

AIDS/HIV Allergy Angiogenesis/ Cardiovasular Apoptosis
Bone, Skeletal, Cartilage Cancer Cell Culture Chemotaxis
Diabetes/Weight Regulation FGF Superfamily Immune System Inflammation
Lipid Metabolism Neurobiology Proliferation Receptors
Stem Cells & Differentiation TGF-β Superfamily TNF Superfamily Transplantation
Wound Healing      


AIDS / HIV Research

The human immunodeficiency virus (HIV) targets the cells of an infected individual’s immune system to progressively damage and destroy the natural functions of immune defense.  Resulting in immunodeficiency, the retrovirus causes an increasing susceptibility to opportunistic infections and cancers, and, during the most advanced stages of HIV infection, progresses into acquired immunodeficiency syndrome (AIDS), or the simultaneous occurrence of more than 20 opportunistic infections and/or related cancers.  Current research concerning HIV infection and AIDS focuses upon developing improvements to modern methods of treatment and prevention, and the possible discovery of new methods for the treatment, prevention and vaccination of the retrovirus.

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Allergy Research
An allergy is a hypersensitivity disorder of the immune system in which exposure, either in the form of ingestion, inhalation or direct contact, to an antigen considered harmless under normal circumstances initiates the production of immune cells expressing sensitivity to that specific allergen, which upon subsequent instances of exposure results in an adverse reaction.  The occurrence of an allergic reaction is a distinct one in that following an initial instance of exposure, in which the mast cells and basophils of the immune system are sensitized to the allergen by the immunoglobulin E antibody, any subsequent exposure can result in the excessive activation of these immune cells leading to the secretion of histamine, along with other inflammatory factors. Histamine, which is commonly considered primarily responsible for the majority allergy related symptoms, is released from the activated mast cells and basophils during degranulation, a process in which the contents of cellular granules are voided into surrounding tissues.  Symptoms generally associated with an allergic reaction include vascular dilation, mucous secretion, smooth muscle contraction, nerve stimulation, and inflammation.  Largely dependent upon the specific sensitivity of an individual to a particular allergen, as well as the degree and mode of exposure, the severity of an allergic reaction can vary drastically from mild, typified by seasonal allergies such as hay fever, to potentially life-threatening, in some cases of exposure to environmental, dietary or pharmacologic allergens, and can result in an unpredictable inflammatory response of either localized or generalized proportions.

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Angiogenesis / Cardiovascular Research
Angiogenesis is the normal physiological process by which new blood vessels and capillary beds sprout from preexisting vessels, resulting in the creation or expansion of a vascular network within a region of tissue. The construction and maintenance of an architecture of blood vessels functions primarily to provide the hosting tissue, and those cells involved in its structure, with a means for importing those nutrients required for survival and maintenance, and removing unnecessary waste. Consequently, the angiogenic process is a fundamental component of embryonic growth and development, tissue repair and wound healing, the resolution of inflammatory responses, and the onset of neoplasia.  The expansion of a vascular network is a relatively fragile process governed by a delicate balance between stimulatory and inhibitory factors, and is, therefore, highly susceptible to instances of disruptive interference at several levels.  Occurrences of angiogenic perversion can result in pathological angiogenesis, which is characterized by the abnormally rapid and uncontrolled proliferation of blood vessels.  Pathological angiogenesis is critical to the transitioning of a tumor to malignancy, and a contributing factor to a multitude of other diseases, including ischemic chronic wounds, cardiovascular disease, diabetic retinopathy, rheumatoid arthritis, macular degeneration, and psoriasis.  Due to its involvement in such an array of diseases, the ability to manipulate angiogenesis through both natural and synthetic inhibitors and activators represents a promising prospect for the prevention and treatment of diseases characterized by abnormal vascularization. 

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Apoptosis Research
Apoptosis, or the process of programmed cell death by which individual cells are eliminated through highly controlled fragmentation into membrane-bound particles for phagocytosis by surrounding cells, is employed during normal physiological conditions to produce deliberate and orderly death of cells not destined to be present in the final tissue.  This rapid and efficient removal of cells, mediated by an intracellular cascade, circumvents those damaging consequences associated with cellular necrosis, allows for the recycling of the apoptotic cell’s organic components, and is characterized by the following cellular changes:  cell shrinkage resulting from dehydration, an increased permeability of the cellular membrane, both nuclear and cytoplasmic condensation, the endolytic cleavage of genomic material, and ultimately the formation of membrane-bound vesicles, or apoptotic bodies, containing intact ribosomes, mitochondria and nuclear material for absorption and removal by phagocytes.  The critical involvement of apoptosis within morphogenesis and tissue homeostasis, as well as the absence of normal apoptotic activity in cancer cells and some degenerative diseases, signify the importance of research concerning apoptosis and those cytokines involved in the activation or suppression of apoptotic events.

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Bone Skeletal Cartilage Research
Comprised of a complete networking of both individual and adjoined bones, along with the connective tissue responsible for their overall cohesion, the skeletal system functions to provide the structural framework essential for the support and protection of body’s major organs, and the scaffolding required for both the anchorage of the body’s musculature and the facilitation of movement.  The physical and mechanical characteristics of the body are largely influenced by the partnership of the skeletal and muscular systems, which are jointly referred to as the musculoskeletal system and together consist of 206 bones connected to more than four hundred muscles via tendons, as well as the temporary cartilage from which bone is ossified and the permanent cartilage found constructing the external ear and nose.  The skeletal system demonstrates a breadth of versatility through the remarkable capacity of connective tissue to assume a wide range of physical states; as is exemplified by the opposition between the strong rigid nature of the mineralized matrices from which bone is constructed, and the firm yet flexible infrastructure of protein fibers and protoglycans that makes up cartilage.  Given the involvement of a great many cell types and signaling pathways during bone growth and development, as well as the dynamic processes of preservation and remodeling that follow, disruption of these pathways has been implicated in instances of abnormality and disorders, such as osteoporosis, arthritis, and inheritable skeletal diseases, associated with defective processes of bone growth and maintenance.

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Cancer Research
Cellular proliferation represents an important element within a broad spectrum of physiological processes responsible for the assurance of normal development and maintenance, including fertilization and early development, population growth, and normal tissue maintenance and repair.  Therefore, a vast number of mechanisms have evolved to ensure the regulation and proper progression of the proliferation process.  Although corruption of normal cellular proliferation is minimized with the existence of these checkpoints and safeguards functioning to ensure the prevention, identification, and rectification of abnormal progression through the phases of cellular division, unmitigated proliferation can be provoked by instances of spontaneous genomic mutations, or those mutations resulting from a physical or chemical mutagen.  Unrestrained cell proliferation that defies the normal constraints of cellular division is the defining feature of cancer, which results from a culmination of mutations causing, among other attributes, decreased density-dependent growth inhibition, anchorage-independence, telomerase production, decreased dependence on external growth factors, inhibition of cell cycle control mechanisms, the inhibition of controlled apoptosis of damaged cells, and an excessive accumulation chromosomal abnormalities.  Although unrestricted proliferation is a defining feature of cancerous cells, it is not this defiance of normal cell cycle regulation, but rather the ability to evade immune responses and the possibility for those cells to spread invasively, that introduce the potential for malignancy.  Modern cancer research focuses on the comprehension of those pathways responsible for both normal and abnormal cellular proliferation, the significance of cell cycle regulators within these pathways, those mutations contributing to the evasion these constraints, those genomic errors and mutagens responsible for such mutations, and the pathways for the development and metastasis of cancerous cells, among numerous other aspects, for advancements in developing innovative methods of prevention and treatment.

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Cell Culture Research
Cell culture is the complex and delicate process of maintaining and/or growing dispersed cells, which have been isolated from either tissue or serum, under controlled conditions, generally outside of the respective natural environment, and more commonly upon the surface of a cell culture plate immersed in nutrient rich growth media.  With the exception of some primary cell lines that have been derived from tumor tissue, most primary cell cultures are incapable of indefinite expansion given that these cells tend to undergo only a finite number of population doublings before succumbing to senescence, at which point the general viability of the cells is retained but the ability to undergo further replications is lost.  Those tumor-derived primary cell lines that demonstrate the ability to avoid senescence and proliferate indefinitely, do so through the accumulation of either coincidental or manufactured mutations that cooperatively allow for unrestrained cell proliferation that defies the normal constraints of cellular division, such as telomerase production, decreased density-dependent growth inhibition and anchorage-independence.  The use of cell cultures, which can be maintained in states of both suspension and adherence in order to mimic the respective environments from which those cells were initially removed, has proven to be fundamental to advancements in the disciplines of  tissue culturing and engineering, the manufacturing of viral vaccines, and the production of both proteins and antibodies.

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Chemotaxis Research
The term chemotaxis is used to describe the movement of organisms or cells in response to the presence of a chemical or chemical gradient, whereby the orientation or movement of the organisms or cells is influenced in a positive or negative manner by the substance exhibiting chemical properties.  Chemoattractants and chemorepellents function to induce either positive or negative chemotaxis respectively.  Although both can include a number of organic and inorganic substances, the most commonly researched inducers of chemotaxis are chemokines, or cytokines secreted by cells for the purpose of driving cellular movement and activation.  Considering the significance of chemotaxis in cellular movement during a number of biological processes, including immune response and development, it is of no surprise that a relatively large amount of emphasis has been placed upon research concerning chemotaxis and, more specifically, the Chemokines functioning to direct cellular movement.

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Diabetes / Weight Regulation
Within the scope of evolutionary history, the maintenance of a healthy body weight, generally defined as the adequate relationship between the intake and expenditure of energy, represents a significant determinant for the survival of higher level organisms.  Generally speaking, the stability of a healthy body weight is a direct consequence of those autonomic pathways responsible for maintaining a relatively constant reservoir of energy while at the same time supplying the body with its energy and nutrition requirements.  Given the significance of normal energy consumption, conversion and dispersal, numerous pathways have evolved for the regulation of these processes, and instances of abnormal or dysfunctional weight regulation have been implicated as provoking, or being provoked by, a multitude of disorders and diseases.  Obesity, which is universally considered to be one of the leading causes of preventable death, is defined as the excessive accumulation of adipose tissue that adversely impacts the general health of an individual, and can drastically increase the affected individual’s risk of developing a slew of related health issues, such as cardiovascular disorders, type-2 diabetes, liver disease, osteoarthritis and thrombosis.  The onset of insulin resistance in overweight individuals and the susceptibility of weight gain associated with insulin resistance, have implicated obesity as both a cause and symptom for the development of type-2 diabetes, the metabolic syndrome in which an affected individual develops an inability to sufficiently produce or respond to insulin.  Although generally considered to be the direct consequence of a sustained combination of excessive caloric consumption and a noted lack of physical activity, the underlying causes of obesity, whether of a genetic, physiological, psychological, or social nature, are extremely complex and have yet to be fully explained.

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FGF Superfamily Research
The Fibroblast Growth Factor (FGF) Superfamily is comprised of multifunctional proteins that serve to regulate a number of complex biological processes related to the development, restoration and/or redistribution of prenatal and postnatal tissue as well as angiogenesis, wound healing, nerve regeneration, chronic inflammation, and cancer growth.  Members of the FGF Superfamily function through paracrine, autocrine and intracrine pathways to promote spatial and temporal integrations of several cell responses, such as proliferation, growth, differentiation, and migration, While proteins of the FGF family exhibit only a modest degree of primary sequence homology, they preserve the ability to signal through at least one of four tyrosine kinase receptors, which include FGFR1 through FGFR4, and interact with heparin sulphate proteoglycans (HSPGs). Given the significance of fibroblast growth factor involvement within such an array of biological processes, and the abundance of conditions associated with deviations from normal FGF production and activity, understanding normal and aberrant FGF function has become critical to current research concerning the prevention and treatment of FGF-associated diseases.

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Immune System Research
Representing a vast and complex network of cells, tissues, and organs, the immune system is comprised of several cell types, each having distinct and specialized functions such as engulfing bacteria, producing antibodies, and killing parasites, tumor cells and virally-infected cells, that collectively serve to protect the body from bacterial, fungal, and viral infections, as well as from the growth and dispersal of tumor cells.  Representing a duality of responsibilities, the immune system initiates the body’s quick and efficient response to alien agents, while also distinguishing these threats from the body’s healthy cells in order to avoid attacks against the host; a process known as autoimmunity. Lymphocytes and other cells from the immune system, such as macrophages and dendritic cells, produce a large array of cell signaling proteins that are collectively referred to as cytokines, which are responsible for the intercellular communications necessary for the accurate and efficient performance of both innate and adaptive immune responses.  Our understanding of the immune system has advanced significantly in recent years, and it has become evident that cytokines play a central role in the activation and regulation of the immune response.

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Inflammation Research
Inflammation is the fundamental process of adaptive, localized response of vascular tissues to instances of irritation, injury or abnormal stimulation resulting from invasive agents, whether of a physical, chemical, or biologic nature, serving to eradicate any such injurious stimuli and compromised tissue to reduce the amount of harm caused by the event.  The inflammatory response functions through a dynamic complex of cell signaling pathways to address such instances of invasion by triggering the orchestrated delivery of leukocytes to the affected area through dilation of surrounding blood vessels and a localized increase of blood flow.  If the inflammatory response successfully removes the initiating invasive agent and the injured tissue surrounding the site, then the signaling cascade is discontinued, inflammation withdraws and the tissue repair and recovery follows.  If, however, the inflammatory response fails to appropriately address the invasive agent and those affected tissues, such as in cases of accelerated tissue damage, then the inflammatory response can persist indefinitely and result in a chronic state of inflammation.  Damage caused by such occurrences of chronic inflammation generally accumulates progressively and, more often than not, asymptomatically over an extended period of time, and can ultimately result in instances of severe tissue deterioration.  Advances in related research have helped demonstrate the importance of regulation within the tightly controlled physiological pathways responsible for the inflammatory response in terms of preventing chronic states of inflammation, and implications of chronic inflammation as the underlying cause of severe diseases including Alzheimer's disease, cardiovascular disease, and colorectal cancer.

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Lipid Metabolism Research
Lipids, which include glycerides, phospholipids and sterols, constitute a broad spectrum of naturally occurring fatty molecules that are fundamental to the development and maintenances of both cells and tissues through their main biological functions within essential signaling pathways, the storage and transportation of energy, and as the precursors to more complex structures, such as those components constructing the cellular membrane.  More importantly, the process of metabolizing those dietary lipids that are normally ingested as complex triglycerides, sterols, and membrane phospholipids, represents the pathway by which these dietary lipids are degraded to free fatty acids that are then small enough to cross the intestinal barrier.  Following transportation across the intestinal barrier, these free fatty acids are manufactured into triglycerides that are then packaged for transport and released into the blood stream through the lymph system.  Upon delivery to the membranes of hepatocytes, adipocytes or muscle fibers, these triglycerides become the fundamental components of energy storage, accumulating within a region of tissue until energy is required and they are once again broken down into free fatty acids with the activation of the hormone-sensitive enzyme lipase.

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Neurobiology Research
The term neurobiology describes the scientific study of the nervous system within a purely biologic capacity, encompassing those scientific disciplines concerned with the development, molecular and cellular structure, chemistry, functionality, evolution, and pathology of the neural networks constructing the nervous system.  The nervous system, which in vertebrates is comprised of both the central and peripheral nervous systems, is a sophisticated networking of neural cells that function through the transmission of excitatory or inhibitory signaling to process information and orchestrate all bodily functions, including the capacity for motor and sensory function, cognition, and emotion.  Understanding the development and homeostasis of the nervous system, the many pathways responsible for maintaining and regulating its proper functionality, and the implications of nervous system dysfunction, remain poignant within research concerning the nervous system and neurodegenerative diseases

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Proliferation is defined as the highly regulated cascade of events responsible for cellular reproduction and maintenance of the relationship between rates of cellular death and division within an expanding population of similar cells.  Controlled and regulated proliferation of specific target cells is essential for a broad spectrum of physiological processes including fertilization, prenatal and postnatal development, and tissue maintenance and repair.  Numerous biological mechanisms have evolved to ensure proper regulation and progression of these processes.  Although these safeguards function to ensure the identification, prevention, and rectification of abnormal progression through the phases of cellular division, unmitigated proliferation can be provoked by instances of spontaneous genomic mutations or those mutations resulting from physical or chemical mutagens.  Unrestrained cell proliferation that defies the normal constraints of cellular division is one of the defining characteristics of cancer, in which a culmination of mutations or other aberrations of cellular processes ultimately lead to decreased density-dependent growth inhibition, anchorage-independence, telomerase production, decreased dependence on external growth factors, inhibition of cell cycle control mechanisms, the inhibition of controlled apoptosis of damaged cells, chromosomal abnormalities, along with the modification of other cellular attributes.  Increased knowledge of both normal and abnormal proliferative mechanisms is essential to the comprehensive understanding of cancer development as well as the functioning of normal developmental processes.

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Receptors Research
Within the disciplines of cellular biology, a receptor is a protein molecule found embedded in the plasma membrane of, or within the nucleus or cytoplasm of, a cell that functions as a primary initiator of intercellular communications by selective binding and responding to specific factors, including: cytokines, antigens, antibodies, hormones, neurotransmitters, and other cellular or immunological ligands.  In general, the cell’s ability to perceive and respond to its surrounding environment begins with external stimulation in the form of an extracellular signaling molecule that binds to a receptor protein, which, in turn, initiates a cascading sequence of biochemical events known as signal transduction.  These signaling pathways can also include the further participation of intracellular receptors found immersed within the cytoplasm or nucleus of the cell that bind secondary messenger molecules, and in turn enable a various cooperative interactions between multiple signaling pathways in order to achieve appropriate cellular responses to complex combinations of signaling stimuli.  Due to the intricate context of communication and reaction within essential cellular processes, including differentiation, proliferation, and apoptosis, there is a tremendous amount of complexity and specificity associated with the physiological and biochemical changes of a particular pathway and the signaling molecules involved.

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Stem Cells & Differentiation Research
The human body develops from a single diploid cell called a zygote and contains at adulthood an estimated 85 trillion cells, of which more than 150 billion turn over every day.  All of these cells originate from a tiny population of so-called “embryonic” and “adult” stem cells which uniquely possess a long-term self- renewal capacity and have the potential to differentiate into a variety of cell lineages.  “Embryonic Stem Cells (ESC)” is a term commonly used to refer to a distinct cluster of pluripotent stem cells found in the inner cell mass of mammalian blastocysts (early-stage embryos).  Their primary function is to give rise to cell lineages of all three germ layers.  On the other hand, “Adult Stem Cells (ASC)” is one of several terms used to describe a diverse group of multipotent stem cells clustered in various niches throughout the body, particularly in loci with high cell turnover such as bone marrow, skin, and intestine, but also in sites with low cell turnover such as brain and pancreas. ASC, also known as somatic or tissue-specific stem cells, serve as a renewable source of specialized cells for tissue development, maintenance, and repair.  Depending upon the prevailing conditions in their microenvironment, individual stem cells express distinct cell-surface proteins and display differentiation patterns which normally suit the needs of the tissue or organ in which they reside.  Such stem-cell specialization is enabled by a battery of epigenetic regulatory factors which provide the means not only to arrest and maintain a particular stem-cell behavior, but also to modify it in response to changes in the cell’s microenvironment.

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TGF-beta Superfamily Research
Encompassing a plethora of growth, differentiation and morphogenic factors, the Transforming Growth Factor-β (TGF-β) Superfamily is comprised of signaling proteins that have been universally conserved throughout the animal kingdom and presently consists of over forty members, the likes of which include:  TGF-β isoforms, bone morphogenetic proteins (BMPs), growth differentiation factors (GDFs), activins, and inhibins.  Considered vital to the modulation of cell proliferation, differentiation, matrix synthesis, and apoptosis, members of the TGF-β Superfamily are fundamental to prenatal development and the postnatal growth, remodeling, and maintenance of various tissues and organs.  Noted for activating Smad signaling cascades through interactions with a conserved family of cell surface serine/threonine-specific protein kinase receptors, the complexity of TGF-β signaling has been demonstrated through the additional regulation of physiological processes by TGF-β Superfamily Ligand through non-canonical pathways, and the activation of signaling molecules other than Smad proteins.  Given the intricacies and significance associated with the activities of TGF-β Superfamily proteins, the impairment of proper signaling has been understandably connected to a variety of clinical indications, such as tumor cell growth, fibrosis, skeletal defects, and autoimmune disease.  Therefore, understanding the regulatory mechanisms that control TGF-β signaling, as well as the identification and characterization of their molecular components, have become topics of intense investigation.

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TNF Superfamily Research
Recognized for their involvement in the regulation of a broad spectrum of biological processes, such as cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation, members of the Tumor Necrosis Factor (TNF) Superfamily were originally identified as necrosis-inducing, anti-tumor cytokines for their ability to cause cell death in sarcomas and other cancerous cells.  The members of the TNF Superfamily are responsible for the regulation of cellular differentiation, survival and death through the activation of multiple signal transduction pathways by ligand mediated trimerization and the resulting recruitment of several intracellular adaptors.  Although normal levels of activity can be pivotal in terms of cellular growth and regeneration, as well as regulated events of apoptosis and inflammatory response, accumulating evidence indicates that the uncontrolled synthesis of TNF Superfamily proteins can be linked to a number of human diseases and disorders of chronic inflammation, as well as autoimmune diseases, insulin resistance, and cancer.  Consequently, a great deal of interest surrounds the understanding of those pathways associated with the activity of TNF Superfamily cytokines and the development of therapeutic methods of inhibition and regulation of TNF activity, release, translation and transcription.

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Transplantation Research
The term transplantation is used to describe the procedure of implanting a tissue, a portion of tissue, or a complete organ taken from the body of a donor within the body of a recipient, or alternatively taken from a donor site for insertion at a recipient site within a single patient in instances of autographting, for the purpose of compensating for an absent or damaged organ.  Whereas transplantable organs, which presently include the heart, lungs, kidneys, liver, pancreas, small intestines and thymus, are generally sourced from living individuals or donors that have been pronounced “brain dead,” donor tissue, such as varying proportions of bone, tendon, corneal tissue, skin and veins, can be donated from the living or recently deceased and preserved for some time in storage in a process termed tissue banking.  Transplantation remains one of the most challenging and multifaceted disciplines of modern medicine due to the obvious intricacies implicated in those procedures of removal and insertion, as well as the looming possibility for transplant rejection following successful implantation.  Although the occurrence of transplant rejection, during which the recipient’s immune system reacts adversely to the transplanted tissue or organ and can ultimately result in body’s refusal of said transplant, diminishes greatly with the passage of time following the transplant procedure, precautions of tissue typing and immunosuppressant drug therapy remain enormously essential steps in the avoidance of rejection.

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Wound Healing Research
Wound healing is the complex, dynamic process of restoration by which cellular structure and tissue arrangement are re-established following an incident of injury through a complex and highly coordinated series of interconnected events.  Generally, the process of wound healing is divided into four sequential, yet overlapping phases: the hemostasis phase, the inflammatory phase, the proliferative phase and the remodeling phase.  Homeostasis, the initial phase of wound healing that begins immediately after infliction of an injury, is the process by which blood flow is arrested or stagnated through the aggregation of platelets and the development of a fibrin clot, which in turn provides the structural support for the cellular constituents of inflammation.  The subsequent inflammatory phase is initiated by the release of cytokines from these aggregating platelets, and entails the orchestrated delivery of leukocytes, and later macrophages, for the removal of any injurious stimuli and compromised tissue from the affected region.  This phase concludes with the secretion of numerous factors responsible for initiating the migration and division of those cells destined for involvement in the proliferative phase.  This third phase of wound healing is characterized by the formation of new blood vessels (angiogenesis), the excretion of collagen and fibronectin from a newly forming extracellular matrix, the proliferation and migration of epithelial cells, and wound contraction.  Wound healing concludes with the fourth and final phase of remodeling.  During remodeling, which can persist for many years following the initial incident of injury, the wound enters a state of constant alteration during which wound contraction progresses, superfluous cells are removed through apoptosis, and collagen is remodeled and deposited along tension lines.  Under normal circumstances wound healing progresses through these four stages in a predictable and timely manner, culminating in the removal of any harmful agents and the replacement of normal skin to once again form a protective barrier against the external environment.  However, the wound healing process is as fragile as it is complex, and it is therefore extremely susceptible to occurrences of dysfunction, which can result in instances of chronic wounds or pathological scarring.

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