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Wound healing

Wound healing refers to a living organism's replacement of destroyed or damaged tissue by newly produced tissue.

In undamaged skin, the epidermis (surface, epithelial layer) and dermis (deeper, connective layer) form a protective barrier against the external environment. When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. This process is divided into predictable phases: blood clotting (hemostasis), inflammation, tissue growth (cell proliferation), and tissue remodeling (maturation and cell differentiation). Blood clotting may be considered to be part of the inflammation stage instead of a separate stage.

The wound-healing process is not only complex but fragile, and it is susceptible to interruption or failure leading to the formation of non-healing chronic wounds. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease, infection, and metabolic deficiencies of old age.

Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection. Depending on each patient's needs, it can range from the simplest first aid to entire nursing specialties such as wound, ostomy, and continence nursing and burn center care.

Stages

 * Hemostasis (blood clotting): Within the first few minutes of injury, platelets in the blood begin to stick to the injured site. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting. This results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding.
 * Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. This happens through the process of phagocytosis, where white blood cells engulf debris and destroy it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.
 * Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur. In angiogenesis, vascular endothelial cells form new blood vessels. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin. Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue. In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells. When the cells' roles are close to complete, unneeded cells undergo apoptosis.
 * Maturation (remodeling): During maturation and remodeling, collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.

Timing and re-epithelialization
Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; If the epithelization of a wounded area is fast, the healing will result in regeneration.

Early vs cellular phase
Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase:

The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation.

The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. Subdivisions of the cellular phase are:
 * 1) Macrophages and inflammatory components (within 1–2 days)
 * 2) Epithelial-mesenchymal interaction: re-epithelialization (phenotype change within hours, migration begins on day 1 or 2)
 * 3) Fibroblasts and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14)
 * 4) Endothelial cells and angiogenesis (begins on day 4)
 * 5) Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size).

Inflammatory phase
Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or the stopping of blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.

Clotting cascade
When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass.

Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss. This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited. Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

Platelets, the cells present in the highest numbers shortly after a wound occurs, release mediators into the blood, including cytokines and growth factors. Growth factors stimulate cells to speed their rate of division. Platelets release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine, which serve several purposes, including increasing cell proliferation and migration to the area and causing blood vessels to become dilated and porous. In many ways, extravasated platelets in trauma perform a similar function to tissue macrophages and mast cells exposed to microbial molecular signatures in infection: they become activated, and secrete molecular mediators – vasoactive amines, eicosanoids, and cytokines – that initiate the inflammatory process.

Vasoconstriction and vasodilation
Immediately after a blood vessel is breached, ruptured cell membranes release inflammatory factors like thromboxanes and prostaglandins that cause the vessel to spasm to prevent blood loss and to collect inflammatory cells and factors in the area. This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at about 20 minutes post-wounding. Vasodilation is the result of factors released by platelets and other cells. The main factor involved in causing vasodilation is histamine. Histamine also causes blood vessels to become porous, allowing the tissue to become edematous because proteins from the bloodstream leak into the extravascular space, which increases its osmolar load and draws water into the area. Increased porosity of blood vessels also facilitates the entry of inflammatory cells like leukocytes into the wound site from the bloodstream.

Polymorphonuclear neutrophils
Within an hour of wounding, polymorphonuclear neutrophils (PMNs) arrive at the wound site and become the predominant cells in the wound for the first two days after the injury occurs, with especially high numbers on the second day. They are attracted to the site by fibronectin, growth factors, and substances such as kinins. Neutrophils phagocytise debris and kill bacteria by releasing free radicals in what is called a respiratory burst. They also cleanse the wound by secreting proteases that break down damaged tissue. Functional neutrophils at the wound site only have life-spans of around two days, so they usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages.

Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability. T cells also increase the activity of macrophages.

Macrophages
One of the roles of macrophages is to phagocytize other expended phagocytes, bacteria and damaged tissue, and they also debride damaged tissue by releasing proteases.

Macrophages function in regeneration and are essential for wound healing. They are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis and they also stimulate cells that reepithelialize the wound, create granulation tissue, and lay down a new extracellular matrix. By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury.

The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue. Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls. Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days. These factors attract cells involved in the proliferation stage of healing to the area.

In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility. Macrophages may restrain the contraction phase. Scientists have reported that removing the macrophages from a salamander resulted in failure of a typical regeneration response (limb regeneration), instead bringing on a repair (scarring) response.

Decline of inflammatory phase
As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. These changes indicate that the inflammatory phase is ending and the proliferative phase is underway. In vitro evidence, obtained using the dermal equivalent model, suggests that the presence of macrophages actually delays wound contraction and thus the disappearance of macrophages from the wound may be essential for subsequent phases to occur.

Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. However, inflammation can lead to tissue damage if it lasts too long. Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus, if the individual's immune system is compromised and is unable to clear the debris from the wound and/or if excessive detritus, devitalized tissue, or microbial biofilm is present in the wound, these factors may cause a prolonged inflammatory phase and prevent the wound from properly commencing the proliferation phase of healing. This can lead to a chronic wound.

Proliferative phase
About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended. As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time.

Angiogenesis
Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound. Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration. The tissue in which angiogenesis has occurred typically looks red (is erythematous) due to the presence of capillaries.

Angiogenesis occurs in overlapping phases in response to inflammation:
 * 1) Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area. Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix.
 * 2) Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli.
 * 3) Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.
 * 4) Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venules can divide and migrate chemotactically towards the wound, laying down new vessels in the process. Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment, as hypoxia stimulates the endothelial transcription factor, hypoxia inducible factor (HIF) to transactivate angiogenic genes such as VEGF and GLUT1. Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks.
 * 5) Vascular maturation: the endothelium of vessels mature by laying down new endothelial extracellular matrix, followed by basal lamina formation. Lastly the vessel establishes a pericyte layer.

Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels.

Endothelial cells are attracted to the wound area by fibronectin found on the fibrin scab and chemotactically by angiogenic factors released by other cells, e.g. from macrophages and platelets when in a low-oxygen environment. Endothelial growth and proliferation is also directly stimulated by hypoxia, and presence of lactic acid in the wound. For example, hypoxia stimulates the endothelial transcription factor, hypoxia-inducible factor (HIF) to transactivate a set of proliferative genes including vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1).

To migrate, endothelial cells need collagenases and plasminogen activator to degrade the clot and part of the ECM. Zinc-dependent metalloproteinases digest basement membrane and ECM to allow cell migration, proliferation and angiogenesis.

When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. Thus, when tissue is adequately perfused, migration and proliferation of endothelial cells is reduced. Eventually blood vessels that are no longer needed die by apoptosis.

Fibroplasia and granulation tissue formation
Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site. Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding. By the end of the first week, fibroblasts are the main cells in the wound. Fibroplasia ends two to four weeks after wounding.

As a model the mechanism of fibroplasia may be conceptualised as an analogous process to angiogenesis (see above) - only the cell type involved is fibroblasts rather than endothelial cells. Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound. The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia. The deposited fibroblastic connective tissue matures by secreting ECM into the extracellular space, forming granulation tissue (see below). Lastly collagen is deposited into the ECM.

In the first two or three days after injury, fibroblasts mainly migrate and proliferate, while later, they are the main cells that lay down the collagen matrix in the wound site. Origins of these fibroblasts are thought to be from the adjacent uninjured cutaneous tissue (although new evidence suggests that some are derived from blood-borne, circulating adult stem cells/precursors). Initially fibroblasts utilize the fibrin cross-linking fibers (well-formed by the end of the inflammatory phase) to migrate across the wound, subsequently adhering to fibronectin. Fibroblasts then deposit ground substance into the wound bed, and later collagen, which they can adhere to for migration.

Granulation tissue functions as rudimentary tissue, and begins to appear in the wound already during the inflammatory phase, two to five days post wounding, and continues growing until the wound bed is covered. Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional extracellular matrix (ECM). The provisional ECM is different in composition from the ECM in normal tissue and its components originate from fibroblasts. Such components include fibronectin, collagen, glycosaminoglycans, elastin, glycoproteins and proteoglycans. Its main components are fibronectin and hyaluronan, which create a very hydrated matrix and facilitate cell migration. Later this provisional matrix is replaced with an ECM that more closely resembles that found in non-injured tissue.

Growth factors (PDGF, TGF-β) and fibronectin encourage proliferation, migration to the wound bed, and production of ECM molecules by fibroblasts. Fibroblasts also secrete growth factors that attract epithelial cells to the wound site. Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring.

Collagen deposition
One of fibroblasts' most important duties is the production of collagen.

Collagen deposition is important because it increases the strength of the wound; before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot, which does not provide much resistance to traumatic injury. Also, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts.

Type III collagen and fibronectin generally begin to be produced in appreciable amounts at somewhere between approximately 10 hours and 3 days, depending mainly on wound size. Their deposition peaks at one to three weeks. They are the predominating tensile substances until the later phase of maturation, in which they are replaced by the stronger type I collagen.

Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain. This homeostasis signals the onset of the later maturation phase. Granulation gradually ceases and fibroblasts decrease in number in the wound once their work is done. At the end of the granulation phase, fibroblasts begin to commit apoptosis, converting granulation tissue from an environment rich in cells to one that consists mainly of collagen.

Epithelialization
The formation of granulation tissue into an open wound allows the reepithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebaceous (oil) glands are the main cells responsible for the epithelialization phase of wound healing. They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. In healing that results in a scar, sweat glands, hair follicles and nerves do not form. With the lack of hair follicles, nerves and sweat glands, the wound, and the resulting healing scar, provide a challenge to the body with regards to temperature control.

Keratinocytes migrate without first proliferating. Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue. Thus the time of onset of migration is variable and may occur about one day after wounding. Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration.

If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes. If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges.

Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide. Before they begin to migrate, cells must dissolve their desmosomes and hemidesmosomes, which normally anchor the cells by intermediate filaments in their cytoskeleton to other cells and to the ECM. Transmembrane receptor proteins called integrins, which are made of glycoproteins and normally anchor the cell to the basement membrane by its cytoskeleton, are released from the cell's intermediate filaments and relocate to actin filaments to serve as attachments to the ECM for pseudopodia during migration. Thus keratinocytes detach from the basement membrane and are able to enter the wound bed.

Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles. Actin filaments and pseudopodia form. During migration, integrins on the pseudopod attach to the ECM, and the actin filaments in the projection pull the cell along. The interaction with molecules in the ECM through integrins further promotes the formation of actin filaments, lamellipodia, and filopodia.

Epithelial cells climb over one another in order to migrate. This growing sheet of epithelial cells is often called the epithelial tongue. The first cells to attach to the basement membrane form the stratum basale. These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well. The more quickly this migration occurs, the less of a scar there will be.

Fibrin, collagen, and fibronectin in the ECM may further signal cells to divide and migrate. Like fibroblasts, migrating keratinocytes use the fibronectin cross-linked with fibrin that was deposited in inflammation as an attachment site to crawl across.

As keratinocytes migrate, they move over granulation tissue but stay underneath the scab, thereby separating the scab from the underlying tissue. Epithelial cells have the ability to phagocytize debris such as dead tissue and bacterial matter that would otherwise obstruct their path. Because they must dissolve any scab that forms, keratinocyte migration is best enhanced by a moist environment, since a dry one leads to formation of a bigger, tougher scab. To make their way along the tissue, keratinocytes must dissolve the clot, debris, and parts of the ECM in order to get through. They secrete plasminogen activator, which activates plasminogen, turning it into plasmin to dissolve the scab. Cells can only migrate over living tissue, so they must excrete collagenases and proteases like matrix metalloproteinases (MMPs) to dissolve damaged parts of the ECM in their way, particularly at the front of the migrating sheet. Keratinocytes also dissolve the basement membrane, using instead the new ECM laid down by fibroblasts to crawl across.

As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more cells for the advancing sheet. Proliferation behind migrating keratinocytes normally begins a few days after wounding and occurs at a rate that is 17 times higher in this stage of epithelialization than in normal tissues. Until the entire wound area is resurfaced, the only epithelial cells to proliferate are at the wound edges.

Growth factors, stimulated by integrins and MMPs, cause cells to proliferate at the wound edges. Keratinocytes themselves also produce and secrete factors, including growth factors and basement membrane proteins, which aid both in epithelialization and in other phases of healing. Growth factors are also important for the innate immune defense of skin wounds by stimulation of the production of antimicrobial peptides and neutrophil chemotactic cytokines in keratinocytes.

Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating. When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane. Cells reverse the morphological changes they underwent in order to begin migrating; they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane. Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin.

Contraction
Contraction is a key phase of wound healing with repair. If contraction continues for too long, it can lead to disfigurement and loss of function. Thus there is a great interest in understanding the biology of wound contraction, which can be modelled in vitro using the collagen gel contraction assay or the dermal equivalent model.

Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts. In full thickness wounds, contraction peaks at 5 to 15 days post wounding. Contraction can last for several weeks and continues even after the wound is completely reepithelialized. A large wound can become 40 to 80% smaller after contraction. Wounds can contract at a speed of up to 0.75 mm per day, depending on how loose the tissue in the wounded area is. Contraction usually does not occur symmetrically; rather most wounds have an 'axis of contraction' which allows for greater organization and alignment of cells with collagen.

At first, contraction occurs without myofibroblast involvement. Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction. Myofibroblasts contain the same kind of actin as that found in smooth muscle cells.

Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges. They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen. Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size. In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part.

As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis. The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating. These events signal the onset of the maturation stage of wound healing.

Maturation and remodeling
When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun. During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen. Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. The onset of the maturation phase may vary extensively, depending on the size of the wound and whether it was initially closed or left open, ranging from approximately three days to three weeks. The maturation phase can last for a year or longer, similarly depending on wound type.

As the phase progresses, the tensile strength of the wound increases. Collagen will reach approximately 20% of its tensile strength after three weeks, increasing to 80% after 12 months. The maximum scar strength is 80% of that of unwounded skin. Since activity at the wound site is reduced, the scar loses its red appearance as blood vessels that are no longer needed are removed by apoptosis.

The phases of wound healing normally progress in a predictable, timely manner; if they do not, healing may progress inappropriately to either a chronic wound such as a venous ulcer or pathological scarring such as a keloid scar.

Factors affecting wound healing
Many factors controlling the efficacy, speed, and manner of wound healing fall under two types: local and systemic factors.

Local factors

 * Moisture; keeping a wound moist rather than dry makes wound healing more rapid and with less pain and less scarring
 * Mechanical factors
 * Oedema
 * Ionizing radiation
 * Faulty technique of wound closure
 * Ischemia and necrosis
 * Foreign bodies. Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, "frequently, an innocent skin wound disguises the extensive nature of the injuries beneath". First-degree nerve injury requires a few hours to a few weeks to recover. If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry. A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection.
 * Low oxygen tension
 * Perfusion

Systemic factors

 * Inflammation
 * Diabetes – Individuals with diabetes demonstrate reduced capability in the healing of acute wounds. Additionally, diabetic individuals are susceptible to developing chronic diabetic foot ulcers, a serious complication of diabetes which affects 15% of people with diabetes and accounts for 84% of all diabetes-related lower leg amputations. The impaired healing abilities of diabetics with diabetic foot ulcers and/or acute wounds involves multiple pathophysiological mechanisms. This impaired healing involves hypoxia, fibroblast and epidermal cell dysfunction, impaired angiogenesis and neovascularization, high levels of metalloproteases, damage from reactive oxygen species and AGEs (advanced glycation end-products), decreased host immune resistance, and neuropathy.
 * Nutrients – Malnutrition or nutritional deficiencies have a recognizable impact on wound healing post trauma or surgical intervention. Nutrients including proteins, carbohydrates, arginine, glutamine, polyunsaturated fatty acids, vitamin A, vitamin C, vitamin E, magnesium, copper, zinc and iron all play significant roles in wound healing. Fats and carbohydrates provide the majority of energy required for wound healing. Glucose is the most prominent source of fuel and it is used to create cellular ATP, providing energy for angiogenesis and the deposition of new tissues. As the nutritional needs of each patient and their associated wound are complex, it is suggested that tailored nutritional support would benefit both acute and chronic wound healing.
 * Metabolic diseases
 * Immunosuppression
 * Connective tissue disorders
 * Smoking – Smoking causes a delay in the speed of wound repair notably in the proliferative and inflammatory phases. It also increases the likelihood of certain complications such as wound rupture, wound and flap necrosis, decrease in wound tensile strength and infection. Passive smoking also impairs a proper wound healing process.
 * Age – Increased age (over 60 years) is a risk factor for impaired wound healing. It is recognized that, in older adults of otherwise overall good health, the effects of aging causes a temporal delay in healing, but no major impairment with regard to the quality of healing. Delayed wound healing in patients of increasing age is associated with altered inflammatory response; for example delayed T-cell infiltration of the wound with alterations in the production of chemokines, and reduced macrophage phagocytic capacity.
 * Alcohol – Alcohol consumption impairs wound healing and also increases the chances of infection. Alcohol affects the proliferative phase of healing. A single unit of alcohol causes a negative effect on re-epithelialization, wound closure, collagen production and angiogenesis.

In the 2000s there arose the first Mathematical models of the healing process, based on simplified assumptions and on a system of differential equations solved through MATLAB. The models show that the "rate of the healing process" appears to be "highly influenced by the activity and size of the injury itself as well as the activity of the healing agent."

Research and development
Up until about 2000, the classic paradigm of wound healing, involving stem cells restricted to organ-specific lineages, had never been seriously challenged. Since then, the notion of adult stem cells having cellular plasticity or the ability to differentiate into non-lineage cells has emerged as an alternative explanation. To be more specific, hematopoietic progenitor cells (that give rise to mature cells in the blood) may have the ability de-differentiate back into hematopoietic stem cells and/or transdifferentiate into non-lineage cells, such as fibroblasts.

Stem cells and cellular plasticity
Multipotent adult stem cells have the capacity to be self-renewing and give rise to different cell types. Stem cells give rise to progenitor cells, which are cells that are not self-renewing, but can generate several types of cells. The extent of stem cell involvement in cutaneous (skin) wound healing is complex and not fully understood. Stem cell injection leads to wound healing primarily through stimulation of angiogenesis.

It is thought that the epidermis and dermis are reconstituted by mitotically active stem cells that reside at the apex of rete ridges (basal stem cells or BSC), the bulge of hair follicles (hair follicular stem cell or HFSC), and the papillary dermis (dermal stem cells). Moreover, bone marrow may also contain stem cells that play a major role in cutaneous wound healing.

In rare circumstances, such as extensive cutaneous injury, self-renewal subpopulations in the bone marrow are induced to participate in the healing process, whereby they give rise to collagen-secreting cells that seem to play a role during wound repair. These two self-renewal subpopulations are (1) bone marrow-derived mesenchymal stem cells (MSC) and (2) hematopoietic stem cells (HSC). Bone marrow also harbors a progenitor subpopulation (endothelial progenitor cells or EPC) that, in the same type of setting, are mobilized to aid in the reconstruction of blood vessels. Moreover, it is thought that extensive injury to skin also promotes the early trafficking of a unique subclass of leukocytes (circulating fibrocytes) to the injured region, where they perform various functions related to wound healing.

Wound repair versus regeneration
An injury is an interruption of morphology and/or functionality of a given tissue. After injury, structural tissue heals with incomplete or complete regeneration. Tissue without an interruption to the morphology almost always completely regenerates. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin. Non-injured skin has a continued replacement and regeneration of cells which always results in complete regeneration.

There is a subtle distinction between 'repair' and 'regeneration'. Repair means incomplete regeneration. Repair or incomplete regeneration, refers to the physiologic adaptation of an organ after injury in an effort to re-establish continuity without regards to exact replacement of lost/damaged tissue. True tissue regeneration or complete regeneration, refers to the replacement of lost/damaged tissue with an 'exact' copy, such that both morphology and functionality are completely restored. Though after injury mammals can completely regenerate spontaneously, they usually do not completely regenerate. An example of a tissue regenerating completely after an interruption of morphology is the endometrium; the endometrium after the process of breakdown via the menstruation cycle heals with complete regeneration.

In some instances, after a tissue breakdown, such as in skin, a regeneration closer to complete regeneration may be induced by the use of biodegradable (collagen-glycoaminoglycan) scaffolds. These scaffolds are structurally analogous to extracellular matrix (ECM) found in normal/un-injured dermis. Fundamental conditions required for tissue regeneration often oppose conditions that favor efficient wound repair, including inhibition of (1) platelet activation, (2) inflammatory response, and (3) wound contraction. In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway. Pharmaceutical agents have been investigated which may be able to turn off myofibroblast differentiation.

A new way of thinking derived from the notion that heparan sulfates are key player in tissue homeostasis: the process that makes the tissue replace dead cells by identical cells. In wound areas, tissue homeostasis is lost as the heparan sulfates are degraded preventing the replacement of dead cells by identical cells. Heparan sulfate analogues cannot be degraded by all known heparanases and glycanases and bind to the free heparin sulfate binding spots on the ECM, therefore preserving the normal tissue homeostasis and preventing scarring.

Repair or regeneration with regards to hypoxia-inducible factor 1-alpha (HIF-1a). In normal circumstances after injury HIF-1a is degraded by prolyl hydroxylases (PHDs). Scientists found that the simple up-regulation of HIF-1a via PHD inhibitors regenerates lost or damaged tissue in mammals that have a repair response; and the continued down-regulation of Hif-1a results in healing with a scarring response in mammals with a previous regenerative response to the loss of tissue. The act of regulating HIF-1a can either turn off, or turn on the key process of mammalian regeneration.

Scarless wound healing
Scarless wound healing is a concept based on the healing or repair of the skin (or other tissue/organs) after injury with the aim of healing with subjectively and relatively less scar tissue than normally expected. Scarless healing is sometimes mixed up with the concept of scar free healing, which is wound healing which results in absolutely no scar (free of scarring). However they are different concepts.

A reverse to scarless wound healing is scarification (wound healing to scar more). Historically, certain cultures consider scarification attractive; however, this is generally not the case in the modern western society, in which many patients are turning to plastic surgery clinics with unrealistic expectations. Depending on scar type, treatment may be invasive (intralesional steroid injections, surgery) and/or conservative (compression therapy, topical silicone gel, brachytherapy, photodynamic therapy). Clinical judgment is necessary to successfully balance the potential benefits of the various treatments available against the likelihood of a poor response and possible complications resulting from these treatments. Many of these treatments may only have a placebo effect, and the evidence base for the use of many current treatments is poor.

Since the 1960s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology. Currently, the principal goals in wound management are to achieve rapid wound closure with a functional tissue that has minimal aesthetic scarring. However, the ultimate goal of wound healing biology is to induce a more perfect reconstruction of the wound area. Scarless wound healing only occurs in mammalian foetal tissues and complete regeneration is limited to lower vertebrates, such as salamanders, and invertebrates. In adult humans, injured tissue are repaired by collagen deposition, collagen remodelling and eventual scar formation, where fetal wound healing is believed to be more of a regenerative process with minimal or no scar formation. Therefore, foetal wound healing can be used to provide an accessible mammalian model of an optimal healing response in adult human tissues. Clues as to how this might be achieved come from studies of wound healing in embryos, where repair is fast and efficient and results in essentially perfect regeneration of any lost tissue.

The etymology of the term scarless wound healing has a long history. In print the antiquated concept of scarless healing was brought up in the early 20th century and appeared in a paper published in the London Lancet. This process involved cutting at a surgical slant to the skin surface, rather than at a right angle it; the process was described in various Newspapers.

Cancer
After inflammation, restoration of normal tissue integrity and function is preserved by feedback interactions between diverse cell types mediated by adhesion molecules and secreted cytokines. Disruption of normal feedback mechanisms in cancer threatens tissue integrity and enables a malignant tumor to escape the immune system. An example of the importance of the wound healing response within tumors is illustrated in work by Howard Chang and colleagues at Stanford University studying breast cancers.

Oral collagen supplements
Preliminary results are promising for the short and long-term use of oral collagen supplements for wound healing and skin aging. Oral collagen supplements also increase skin elasticity, hydration, and dermal collagen density. Collagen supplementation is generally safe with no reported adverse events. Further studies are needed to elucidate medical use in skin barrier diseases such as atopic dermatitis and to determine optimal dosing regimens.

Wound dressings
Modern wound dressing to aid in wound repair has undergone considerable research and development in recent years. Scientists aim to develop wound dressings which have the following characteristics:
 * Provide wound protection
 * Remove excess exudate
 * Possess antimicrobial properties
 * Maintain a humid environment
 * Have high permeability to oxygen
 * Are easily removed from a wound site
 * Possess non-anaphylactic characteristics

Cotton gauze dressings have been the standard of care, despite their dry properties that can adhere to wound surfaces and cause discomfort upon removal. Recent research has set out to improve cotton gauze dressings to bring them closer in line to achieve modern wound dressing properties, by coating cotton gauze wound dressing with a chitosan/Ag/ZnO nanocomposite. These updated dressing provide increase water absorbency and improved antibacterial efficacy.

Wound cleansing
Dirt or dust on the surface of the wound, bacteria, tissue that has died, and fluid from the wound may be cleaned. The evidence supporting the most effective technique is not clear and there is insufficient evidence to conclude whether cleaning wounds is beneficial for promoting healing or whether wound cleaning solutions (polyhexamethylene biguanide, aqueous hydrogen peroxide, etc.) are better than sterile water or saline solutions to help venous leg ulcers heal. It is uncertain whether the choice of cleaning solution or method of application makes any difference to venous leg ulcer healing.

Simulating wound healing from a growth perspective
Considerable effort has been devoted to understanding the physical relationships governing wound healing and subsequent scarring, with mathematical models and simulations developed to elucidate these relationships. The growth of tissue around the wound site is a result of the migration of cells and collagen deposition by these cells. The alignment of collagen describes the degree of scarring; basket-weave orientation of collagen is characteristic of normal skin, whereas aligned collagen fibers lead to significant scarring. It has been shown that the growth of tissue and extent of scar formation can be controlled by modulating the stress at a wound site.

The growth of tissue can be simulated using the aforementioned relationships from a biochemical and biomechanical point of view. The biologically active chemicals that play an important role in wound healing are modeled with Fickian diffusion to generate concentration profiles. The balance equation for open systems when modeling wound healing incorporates mass growth due to cell migration and proliferation. Here the following equation is used:

Dtρ0 = Div (R) + R0,

where ρ represents mass density, R represents a mass flux (from cell migration), and R0 represents a mass source (from cell proliferation, division, or enlargement). Relationships like these can be incorporated into an agent-based models, where the sensitivity to single parameters such as initial collagen alignment, cytokine properties, and cell proliferation rates can be tested.

Wound closure intentions
Successful wound healing is dependent on various cell types, molecular mediators and structural elements.

Primary intention
Primary intention is the healing of a clean wound without tissue loss. In this process, wound edges are brought together, so that they are adjacent to each other (re-approximated). Wound closure is performed with sutures (stitches), staples, or adhesive tape or glue.

Primary intention can only be implemented when the wound is precise and there is minimal disruption to the local tissue and the epithelial basement membrane, e.g. surgical incisions.

This process is faster than healing by secondary intention. There is also less scarring associated with primary intention, as there are no large tissue losses to be filled with granulation tissue, though some granulation tissue will form.
 * Examples of primary intention include: well-repaired lacerations, well reduced bone fractures, healing after flap surgery.
 * Early removal of dressings from clean or clean-contaminated wounds does affect primary healing of wounds.

Secondary intention

 * Secondary intention is implemented when primary intention is not possible because of significant tissue damage or loss, usually due to the wound having been created by major trauma.
 * The wound is allowed to granulate.
 * Surgeon may pack the wound with a gauze or use a drainage system.
 * Granulation results in a broader scar.
 * Healing process can be slow due to presence of drainage from infection.
 * Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation.
 * Using antibiotics or antiseptics for the surgical wound healing by secondary intention is controversial.
 * Examples: gingivectomy, gingivoplasty, tooth extraction sockets, poorly reduced fractures, burns, severe lacerations, pressure ulcers.
 * There is insufficient evidence that the choice of dressings or topical agents affects the secondary healing of wounds.
 * There is lack of evidence for the effectiveness of negative pressure wound therapy in wound healing by secondary intention.

Tertiary intention
(Delayed primary closure):
 * The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.
 * The wound is purposely left open.
 * Examples: healing of wounds by use of tissue grafts.

If the wound edges are not reapproximated immediately, delayed primary wound healing transpires. This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization, collagen deposition, and maturation are occurring. Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas. Usually the wound is closed surgically at this juncture, or the scab is eaten, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

Overview of involved growth factors
Following are the main growth factors involved in wound healing:

Complications of wound healing
The major complications are many:

 * 1) Deficient scar formation: Results in wound dehiscence or rupture of the wound due to inadequate formation of granulation tissue.
 * 2) Excessive scar formation: Hypertrophic scar, keloid, desmoid.
 * 3) Exuberant granulation (proud flesh).
 * 4) Deficient contraction (in skin grafts) or excessive contraction (in burns).
 * 5) Others: Dystrophic calcification, pigmentary changes, painful scars, incisional hernia

Other complications can include infection and Marjolin's ulcer.

Biologics, skin substitutes, biomembranes and scaffolds
Advancements in the clinical understanding of wounds and their pathophysiology have commanded significant biomedical innovations in the treatment of acute, chronic, and other types of wounds. Many biologics, skin substitutes, biomembranes and scaffolds have been developed to facilitate wound healing through various mechanisms. This includes a number of products under the trade names such as Epicel, Laserskin, Transcyte, Dermagraft, AlloDerm/Strattice, Biobrane, Integra, Apligraf, OrCel, GraftJacket and PermaDerm.

title: Wound healing


text:
User talk:TZanc

Welcome
Hello, welcome to Wikipedia.

You might find these links helpful in creating new pages or helping with the above tasks: How to edit a page, How to write a great article, Naming conventions, Manual of Style. You should read our policies at some point too.

If you have any questions, see the help pages, add a question to the village pump or ask me on my talk page. I hope you enjoy editing here and being a Wikipedian!

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Again, welcome! - Flockmeal 03:18, Mar 9, 2004 (UTC)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: User talk:TZanc


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Tranmere

Tranmere may refer to:

Australia

 * Tranmere, Tasmania, a suburb of Hobart
 * Tranmere, South Australia, a suburb of Adelaide

England

 * Tranmere, Merseyside
 * Tranmere Rovers F.C., a football club
 * Tranmere Oil Terminal, a docking facility on the River Mersey
 * Tranmere railway station (1846–1857)

title: Tranmere


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Tayeb Salih

Tayeb Salih (الطيب صالح; 12 July 1929 – 18 February 2009) was a Sudanese writer, cultural journalist for the BBC Arabic programme as well as for Arabic journals, and a staff member of UNESCO. He is best known for his novel Season of Migration to the North, considered to be one of the most important novels in Arabic literature. His novels and short stories have been translated into English and more than a dozen other languages.

Biography
Born in Karmakol, a village on the Nile near Al Dabbah, Sudan, in the Northern Province of Sudan, he graduated from University of Khartoum with a Bachelor of Science, before leaving for the University of London in the United Kingdom. Coming from a background of small farmers and religious teachers, his original intention was to work in agriculture. However, excluding a brief spell as a schoolmaster before moving to England, he worked in journalism and the promotion of international cultural exchange.

For more than ten years, Salih wrote a weekly column for the London-based Arabic language newspaper al Majalla, in which he explored various literary themes. He worked for the BBC's Arabic Service and later became director general of the Ministry of Information in Doha, Qatar. The last ten years of his working career, he spent at UNESCO headquarters in Paris, where he held various posts and was UNESCO's representative for the Arab states of the Persian Gulf.

Literary career
Salih's writing draws important inspiration from his youth in a Sudanese village; life that is centered on rural people and their complex relationships. "At various levels and with varying degrees of psychoanalytic emphasis, he deals with themes of reality and illusion, the cultural dissonance between the West and the exotic Orient, the harmony and conflict of brotherhood, and the individual's responsibility to find a fusion between his or her contradictions." Furthermore, the motifs of his books are derived from his religious experience as a Muslim in 20th-century Sudan, both pre- and post-colonial. Another, more general subject of Salih's writing is the confrontation of the Arab Muslim and the Western European world.

In 1966, Salih published his novel Mawsim al-Hijrah ilâ al-Shimâl (Season of Migration to the North), for which he is best known. It was first published in the Beirut journal Hiwâr. The main concern of the novel is with the impact of British colonialism and European modernity on rural African societies in general, and on Sudanese culture and identity in particular. His novel reflects the conflicts of modern Sudan and depicts the brutal history of European colonialism as shaping the reality of contemporary Sudanese society. Season of Migration to the North is a story told to an unspecified audience by the unnamed narrator, a “traveled man” and an African who has returned after having spent years abroad. He returns to his Sudanese village of Wad Hamid on the Nile in the 1950s after having written a PhD thesis on ‘the life of an obscure English poet’. Mustafa Sa'eed, the main protagonist of the novel, is a child of British colonialism, and a fruit of colonial education.

In his essay "The New Novel in Sudan", published in Banipal magazine's issue of spring 1966 on Sudanese Literature today, Sudanese writer Emad Blake remarked that Salih "confronted the crucial issues of his time, such as the clash of Eastern and Western civilizations, as well as boldly employing sex and a style of writing we might term the 'impossible easy'."

The Damascus-based Arab Literary Academy named it one of the best novels in Arabic of the twentieth century. Upon its publication, it was banned in Salih's native Sudan for several years, because of its partly sexual content and despite the fact that it won him prominence and international fame.

Urs' al-Zayn (published in English as The Wedding of Zein) is a novella, published in 1966, centering on the unlikely nuptials of the town eccentric Zein. Tall and odd-looking, with just two teeth in his mouth, Zein has made a reputation for himself as the man who falls in love over and over with girls who promptly marry other men, – to the point where mothers seek him out in hopes that he will draw the eye of available suitors to their eligible daughters. "The Wedding of Zein" was made into a drama in Libya and won Kuwaiti filmmaker Khalid Siddiq an award at the Cannes Film Festival in the late 1970s.

In his reflections on Salih's literary style, his translator Denys Johnson-Davies wrote that Salih "exploited to the full the richness of the literary language in his narrative and uses the vivid local dialect for his dialog. [...] Tayeb Salih’s work shows his wide reading in the byways of Arabic literature, including poetry, which has helped to fashion a style which is direct and fluent, a style which an Arab critic has described as being closer to dramatic writing than that of the novel."

Awards in honour of Tayeb Salih
In 1998, a group of Salih's friends formed a committee to honour him, and collected $20,000 for his personal use. He chose to use the money to establish the Tayeb Salih Creative Writing Award.

Awarded since 2002, the al-Tayeb Salih Prize for Literary Creativity is a literary prize for Sudanese novels, presented by the Abdel Karim Mirghani Cultural Center in Omdurman, and is dedicated to first novels by emerging Sudanese writers.

Since 2010, another award, called the al-Tayeb Salih Award for Creative Writing, has been granted to outstanding modern Arab writers in the fields of novel, short story, and critical studies. The award has been sponsored by telecommunications company Zain Sudan and has been critically seen by some Sudanese intellectuals, calling it “an attempt to control the Sudanese cultural scene” by the Ministry of Culture.

Death
Salih died on 18 February 2009 in London. His body was buried on 20 February in Sudan, where the funeral ceremony was attended by a large number of prominent personalities and Arab writers, as well as the then Sudanese President Omar Al-Bashir, writer and former Prime Minister Sadiq Al Mahdi, and Muhammad Othman Al-Mirghani.

Tribute
On July 12, 2017, Google Doodle commemorated Tayeb Salih's 88th birthday.

title: Tayeb Salih


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King of Egypt

King of Egypt (ملك مصر) was the title used by the ruler of Egypt between 1922 and 1951. When the United Kingdom issued the Unilateral Declaration of Egyptian Independence on 28 February 1922, thereby ending its protectorate over Egypt, Egypt's Sultan Fouad I issued a decree on 15 March 1922 whereby he adopted the title of King of Egypt. It has been reported that the title change was due not only to Egypt's newly independent status, but also to Fouad I's desire to be accorded the same title as the newly installed rulers of the newly created kingdoms of Hejaz, Syria and Iraq. The second monarch to be styled King of Egypt was Fouad I's son Farouk I, whose title was changed to King of Egypt and the Sudan in October 1951 following the Wafdist government's unilateral abrogation of the Anglo-Egyptian Treaty of 1936. The monarchy was abolished on 18 June 1953 following the Egyptian Revolution of 1952 and the establishment of a republic. The third king, the infant Fuad II of Egypt (Farouk having abdicated following the revolution), went into exile in Italy. The position was replaced by the President of Egypt on June 18 1953.

The rulers of ancient Egypt may be described using the title King (a translation of the Egyptian word nsw) or pharaoh (derived from pr ˤ3). The story of Moses in the Quran includes his interaction with the ruler of Egypt, named Pharaoh (فرعون). The earlier story of Joseph in Islam refers to the Egyptian ruler as a king (ملك).

title: King of Egypt


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Spiderhunter

The spiderhunters are birds of the genus Arachnothera, part of the sunbird family Nectariniidae. The genus contains thirteen species found in the forests of south and southeastern Asia. They are large representatives of the sunbird family, with drab plumage and long strongly curved bills. They feed on both nectar and a range of small arthropods.

Distribution and habitat
Unlike the rest of the family, which is more widespread, the spiderhunters are confined to the Oriental zoogeographic region, occurring from India east to the Philippines and from the Himalayas south to Java; they reach their greatest species diversity in the Thai-Malay peninsula, Sumatra and Borneo. The spiderhunters are mostly forest birds, occupying a wide range of forest types including true rainforest, dipterocarp forest, swamp forest, bamboo forest, secondary forest, forest edge and other highly degraded forest. In addition several species occur in human-created habitat such as gardens or plantations. Most species are lowland species, but the Whitehead's spiderhunter is more of a montane species.

Description
The spiderhunters are amongst the largest of their family, measuring between 13 and 22 cm in length. The spectacled spiderhunter is the heaviest of the sunbirds, weighing as much as 49 g. The bills of the spiderhunters are long, at least twice the length of the head, and are decurved and stout. The tongue forms a complete tube for most of its length. The plumage is much drabber than the other brightly coloured sunbirds, is the same for both sexes, and contains no iridescence. The uppersides of most species are olive-green and the undersides dull white or yellow - in half the species the undersides are streaked. The most atypical spiderhunter plumage is that of the Whitehead's spiderhunter, which is dark brown with white streaking on the undersides and back and a yellow rump.

The calls of the spiderhunters are very simple, typically a metallic chip which is repeated multiple times to form the song. The song of the little spiderhunter is described as an "incessant squeaky whistle".

Diet and feeding
The spiderhunters are omnivorous. As their name suggests they will eat spiders, and are capable of extracting spiders from the centre of their webs, a tricky task. They also consume a wide range of other small arthropod prey including crickets, caterpillars, butterflies, ants and other insects. In addition to animal prey they also consume nectar from flowers. Their tubular tongue is pushed against the top of the upper mandible of the bill, then pulled in and out, creating a pressure difference which allows the nectar to be sucked into the mouth. Spiderhunters may be important pollinators of some species of plants, and species pollinated by spiderhunters have long tubular flowers. They may also participate in nectar robbing, which consists of inserting the bill into the side of the flower to extract nectar without being dabbed with pollen. Little is known about their territorial behaviour, but there have been reports of some species defending territories. The spiderhunters are less gregarious than other sunbirds, and are usually seen alone or as part of a pair.

Breeding
The spiderhunters are thought to be monogamous like most of the rest of the family. They vary from the other sunbirds in the nature of their nest, which is suspended underneath a large leaf, usually a banana leaf but sometimes a palm frond or even a branch. The style of nest can be quite variable, a simple cup in the case of the streaked spiderhunter, an elongated tube for the yellow-eared spiderhunter and a bottle shape for the long-billed spiderhunter. The nests are suspended from the leaf by using spider web or by pushing plant fibres through the leaf. The nests are made of grasses and leaves and lined with soft materials. Nest construction, as is typical of the family, is carried out by the female alone. Unlike the other sunbirds, however, both the male and female incubate the eggs. The spiderhunters lay two or three eggs. Their nests are sometimes parasitised by cuckoos.

Species
The genus contains 13 species:

title: Spiderhunter


text:
File:Arms-beckenham.jpg

Arms of Beckenham Borough Council. From civicheraldry.co.uk, with permission.

About the civic heraldry images...

title: File:Arms-beckenham.jpg


text:
Norbiton railway station

Norbiton Railway Station is a railway station located in Norbiton, a suburb in the Royal Borough of Kingston upon Thames, in southwest London. It is on the Kingston Loop Line, 11 mi down the line from London Waterloo. The station and all trains serving it are operated by South Western Railway. It is in Travelcard Zone 5 and is a short walk from Kingston Hospital. It is also the most convenient station for the Kingsmeadow football ground.

History
Coaching interests in Kingston were opposed to having a railway in the town and consequently, the London and South Western Railway built its line to Southampton further south through Surbiton. This opposition continued even during the laying of the line from Twickenham although this line did reach a terminus in Kingston in 1863. In 1869 the line was extended through Norbiton to connect to the central line southwest of the present New Malden station.

When Queen Victoria visited distinguished residents in the Coombe Hill area, the royal train stopped at Norbiton, the only station in the area where the platform is at ground level. New Malden and Kingston have many steps. It is the only remaining Victorian railway architecture in the Royal Borough of Kingston upon Thames.

Station facilities
In February and March 2012 a secure, swipe-card accessible cycle park for 50 cycles was built on Platform 1 replacing the previous set of shelters and bike racks

In August 2009 the platforms were fenced with high steel railings before the installation of ticket barriers. In 2011 the single-width 'off-peak' gated exit from platform 2 was doubled in width to cope with the large numbers of passengers leaving the station when the barriers are not operational. In 2014 the gated exit was widened again.

During the autumn of 2014, platforms 1 and 2 were raised and the edges reconstructed to reduce the step and gap for passengers getting on and off the trains. Earlier in 2014, the platforms were extended in preparation for longer trains.

There is a 38-space car park and space for 5 vehicles reserved for South Western Railway staff.

Platforms
Norbiton station has two platforms.

 * Platform 1 – Trains to London Waterloo via Wimbledon.
 * Platform 2 – Trains to London Waterloo via Kingston & Richmond and trains to Shepperton.

Services
All services at Norbiton are operated by South Western Railway.

The typical off-peak service in trains per hour is:
 * 4 tph to London Waterloo via Wimbledon
 * 2 tph to Shepperton
 * 2 tph to Teddington, returning to London Waterloo via Richmond

On Sundays, the services to and from London Waterloo via Wimbledon are reduced to 2 tph and the services to and from Shepperton and Teddington are reduced to hourly.

Popular culture references
In the British sitcom The Fall and Rise of Reginald Perrin, the station was used as the filming location from which the title character caught his train each morning (with decreasing punctuality). Although Reggie's home town in the series was called Climthorpe, a panning shot of the front of the station in the first episode shows him walking into Norbiton station. (The area remains largely unchanged, with the Frederick W. Paine funeral parlour and the zebra crossing across Coombe Road still in place, although a small number of buildings in front of the main station entrance have since been demolished.) David Nobbs may have thought of Climthorpe as near Norbiton, since various other stations between New Malden and London are named in Reggie's multiple excuses to explain his poor punctuality.

The station also appeared briefly in a 1971 episode of the Rodney Bewes sitcom Dear Mother...Love Albert.

Connections
London Buses routes 57, K2, K3, K4 and K5 serve the station.

title: Norbiton railway station


text:
Add Insult to Injury

Add Insult to Injury is the fourth studio album by British electronic musicians Add N to (X). It was released on 16 October 2000 by Mute Records. The album is essentially two mini-albums fused together, as half was written and performed by Ann Shenton and Steve Claydon, while the other half was written and performed by Barry 7, with occasional help from Dean Honer from The All Seeing I.

Early prints of the album came with 'scratch and sniff' panels (it smelt of grass), and stickers.

Track listing

 * 1) "Adding N to X" (Claydon/Shenton) – 2:39
 * 2) "Brothel Charge" (Allum/Claydon/Shenton) – 3:02
 * 3) "You Must Create" (Allum/Claydon/Shenton) – 4:05
 * 4) "Kingdom of Shades" (Allum/Claydon/Shenton) – 3:47
 * 5) "Monster Bobby" (Barry/Honer/Smith) – 4:03
 * 6) "Poke 'er 'ole" (Allum/Claydon/Shenton) – 4:25
 * 7) "Plug Me In" (Barry/Honer/Smith) – 5:31
 * 8) "Hit for Cheese" (Allum/Claydon/Shenton) – 3:05
 * 9) "MDMH (Miami Dust Mite Harvest)" (Allum/Claydon/Shenton) – 4:24
 * 10) "B.P. Perino" (Allum/Claydon/Honer/Shenton) – 6:51
 * 11) "Incinerator No. 1" (Barry/Smith) – 5:33
 * 12) "The Regent Is Dead" (Barry/Honer/Smith) – 15:56
 * 13) "Violent Breath" (hidden track)

Adding N to X

Steve Claydon – Synthesizer, Bass, Cello, Keyboards, Vocals, Mellotron, Vocoder, Omnichord, Pedals

Ann Shenton – Synthesizer, Flute, Cello, Keyboards, Theremin, Vocals, Mellotron, Harmonica

Brothel Charge/You Must Create/Kingdom of Shades/Poke/Hit for Cheese/MDMH

Rob Allum – Synthesizer, Bass, Percussion, Drums, Pedals

Steve Claydon – Synthesizer, Bass, Cello, Keyboards, Vocals, Mellotron, Vocoder, Omnichord, Pedals

Ann Shenton – Synthesizer, Flute, Cello, Keyboards, Theremin, Vocals, Mellotron, Harmonica

Monster Bobby/Plug Me In/The Regent Is Dead

Barry Seven – Synthesizer, Celeste, Keyboards, Organ, Clavinet, Mellotron

Dean Honer – arranger

B.P. Perino

Rob Allum – Synthesizer, Bass, Percussion, Drums, Pedals

Steve Claydon – Synthesizer, Bass, Cello, Keyboards, Vocals, Mellotron, Vocoder, Omnichord, Pedals

Dean Honer – arranger

Ann Shenton – Synthesizer, Flute, Cello, Keyboards, Theremin, Vocals, Mellotron, Harmonica

Incinerator No. 1

Barry Seven – Synthesizer, Celeste, Keyboards, Organ, Clavinet, Mellotron

Violent Breath

Dean Honer – arranger

Rob Allum – Synthesizer, Bass, Percussion, Drums, Pedal

Barry Seven – Synthesizer, Celeste, Keyboards, Organ, Clavinet, Mellotron

Ann Shenton – Synthesizer, Flute, Cello, Keyboards, Theremin, Vocals, Mellotron, Harmonica

Steve Claydon – Synthesizer, Bass, Cello, Keyboards, Vocals, Mellotron, Vocoder, Omnichord, Pedals

Personnel

 * Dave Williamson – bass
 * Joe Dilworth – drums, Photography
 * Rob Allum – Synthesizer, Bass, Percussion, Drums, Bass Pedals, Machines
 * David Titlow – Photography
 * Add N to (X) – Artwork
 * Ann Shenton – Synthesizer, Flute, Arranger, Cello, Keyboards, Theremin, Vocals, Choir, Chorus, Moog Synthesizer, Producer, Mellotron, Korg Synthesizer, Mixing, Accompaniment, Arp 2600, Harmonica (Electric)
 * Barry Seven – Synthesizer, Arranger, Celeste, Keyboards, Organ (Hammond), Stick, Clavinet, Moog Synthesizer, Producer, Engineer, Mellotron, Korg Synthesizer, Guitar Synth, Roland Synthesizer, Chords
 * Steve Claydon – Synthesizer, Bass, Arranger, Cello, Keyboards, Stick, Vocals, Moog Synthesizer, Producer, Mellotron, Korg Synthesizer, Vocoder, Omnichord, Bass Pedals, Mixing, Throat, Accompaniment, Micro Moog
 * Richard Hermitage – Management
 * Ben Rymer – vocals
 * Dean Honer – arranger
 * Ross Orton – drums

title: Add Insult to Injury


text:
File:Arms-bexley-bc.jpg

Arms of Bexley Borough Council. From civicheraldry.co.uk, with permission.

About the civic heraldry images...

title: File:Arms-bexley-bc.jpg


text:
Sebastinae

Sebastinae is a subfamily of marine fish belonging to the family Scorpaenidae in the order Scorpaeniformes. Their common names include rockfishes, rock perches, ocean perches, sea perches, thornyheads, scorpionfishes, sea ruffes and rockcods. Despite the latter name, they are not closely related to the cods in the genus Gadus, nor the rock cod, Lotella rhacina.

Taxonomy
Sebastinae, or Sebastidae, was first formally recognised as a grouping in 1873 by the German naturalist Johann Jakob Kaup. Some authorities recognise this family as distinct from Scorpaenidae. FishBase, a finfish database generated by a consortium of academic institutions, does, but the United States Federal government's Integrated Taxonomic Information System and the 5th Edition of Fishes of the World do not, FotW classify it as a subfamily of the Scorpaenidae.

Tribes and genera
Sebastinae is divided into two tribes and seven genera:

 * Tribe Sebastini Kaup, 1873
 * Helicolenus Goode & Bean, 1896
 * Hozukius Matsubara, 1934
 * Sebastes Cuvier, 1829
 * Sebastiscus Jordan & Starks, 1904
 * Tribe Sebastolobini Matsubara, 1943
 * Adelosebastes Eschmeyer, T. Abe & Nakano, 1979
 * Sebastolobus Gill, 1881
 * Trachyscorpia Ginsburg, 1953

Characteristics
Sebastinae species have a compressed body with the head typically having ridges and spines. The gill membranes are not attached to the isthmus. There is a venom gland in the spines of the dorsal, anal and pelvic fins. The largest species is the shortraker rockfish ( Sebastes borealis) which attains a maximum total length of 108 cm while the smallest species is Sebastes koreanus which reaches a maximum total length of 13.7 cm.

Distribution and habitat
Sebastinae rockfishes are found in the Pacific, Indian and Atlantic Oceans with most species in the largest genus, the ovoviviparous Sebastes with over 100 species, in the North Pacific. They can be found in marine and brackish waters.

title: Sebastinae


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Spinnaker

A spinnaker is a sail designed specifically for sailing off the wind on courses between a reach (wind at 90° to the course) to downwind (course in the same direction as the wind). Spinnakers are constructed of lightweight fabric, usually nylon, and are often brightly colored. They may be designed to perform best as either a reaching or a running spinnaker, by the shaping of the panels and seams. They are attached at only three points and said to be flown.

Etymology
Some dictionaries suggest that the origin of the word could be traced to the first boat to commonly fly a spinnaker, a yacht called Sphinx, mispronounced as Spinx. Sphinx first set her spinnaker in the Solent in 1865, and the first recorded use of the word was in 1866 in the August edition of Yachting Calendar and Review (p. 84). In addition, the term may have been influenced by the spanker, originally a gaff rigged fore-and-aft sail.

Another suggestion is that the idea for the sail was conceived in 1865 by William Gordon, owner of the racing yacht Niobe. He wanted to name the sail after his yacht but a crewman's comment, "Now there's a sail to make her spin" became "spin maker" which developed into the commonly accepted term spinnaker. Gordon was widely known in the yachting world of the time as "Spinnaker Gordon".

It has been pointed out, however, that the skippers of Thames sailing barges also used the term spinnaker for their jib staysails. Unlike the other, tanned sails of these boats, the spinnakers were usually white. It has thus been suggested that the term could be "connected with the obsolete word spoon, meaning to run before the wind (cf. spindrift)." Early usage of the verb to spoon can be traced back to the 16th century; the change from spoon to spin in the term spindrift is attributed to a local Scottish pronunciation. According to Merriam Webster's dictionary, however, spindrift derives from a local Scottish pronunciation of speen (not spoon), meaning "to drive before a strong wind."

According to Merriam-Webster's etymology, the origin of the word spinnaker is simply unknown.

Types
There are two main categories of spinnakers, symmetric and asymmetric depending on whether a plane of symmetry exists for that particular sail. Asymmetric spinnakers operate more like a jib, generating lift from the side, rather than the top like a symmetric spinnaker. This makes asymmetrics a better choice on reaching courses than symmetric spinnakers, which excel when running. While a fully equipped racing boat might have a number of spinnakers, both symmetric and asymmetric, to cover all courses and wind conditions, cruising boats almost always use an asymmetric, due to the broader application and easier handling afforded by the asymmetric.

Symmetric

The symmetric one is the most classic type, running symmetrically alongside the boat controlled by lines known as a sheet and a guy running from the lower two corners of the sail. The windward line, or guy, is attached to the corner called the tack of the sail, and is stabilized by a spinnaker pole. The leeward (downwind) line is called the sheet. It attaches to the clew of the spinnaker and is used to control the shape of the sail. The spinnaker pole must be moved in each gybe, and is quite difficult for beginners to use. However, it can be sailed in all downwind wind directions.

Symmetric spinnakers when sailing across the wind (reaching) develop most of their lift on the forward quarter, where the airflow remains attached. When correctly set for reaching, the leading edges of a symmetric spinnaker should be nearly parallel to the wind, so the flow of air over the leading edge remains attached. When reaching, the sail camber allows only some attached flow over the leeward side of the spinnaker. On running the spinnaker is angled for maximum drag, with the spinnaker pole at right angles to the apparent wind. The symmetric spinnaker also requires care when packing, since the three corners must be available on the top of the packing.

Parasailor
A Parasailor is a symmetrical spinnaker with a paraglider wing inserted into a gap in the sail approximately mid-way up. This feature makes the sail easier to keep inflated, but detracts from its performance. The sail may be flown on a spinnaker pole or with the tack attached to the bow of the boat.

Asymmetric
Asymmetrical spinnakers resembling large jibs and flown from spinnaker poles are not a new idea and date back to at least the 19th century. However, in the 1980s a new concept appeared, starting with the Sydney Harbour 18ft Skiff fleet.

Since the 1960s, many faster sailing craft, starting with catamaran classes, have discovered that it is faster to sail downwind on a series of broad reaches with efficient airflow across the sail rather than directly downwind with the sails stalled. This technique had developed to the extent that in bar conversation at the end of one season Andrew Buckland observed that the 18s had sailed all season without pulling the spinnaker pole back from the forestay and that all the systems could be simplified by eliminating the pole and setting the spinnaker from a fixed (but often retractable) bowsprit. The concept quickly evolved to a sail with a loose luff much more like a conventional spinnaker than the old jib-style asymmetric sails. Julian Bethwaite was the first to rig and sail a boat with one the next season, followed shortly by Andrew Buckland. The first modern offshore sailboats to incorporate a retractable bow sprit and an asymmetric spinnaker was the J/Boats J/105.

The concept has spread rapidly through the sailing world. The tack of the sail may be attached at the bow like a genoa but is frequently mounted on a bowsprit, often a retracting one. If the spinnaker is mounted to a special bowsprit, it is often possible to fly the spinnaker and the jib at the same time; if not, then the spinnaker will be shadowed by the jib, and the jib should be furled when the spinnaker is in use.

The asymmetric has two sheets, very much like a jib, but is not attached to the forestay along the length of the luff, but only at the corners. Unlike a symmetric spinnaker, the asymmetric does not require a spinnaker pole, since it is fixed to the bow or bowsprit. The asymmetric is very easy to gybe since it only requires releasing one sheet and pulling in the other one, passing the sail in front of the forestay. Asymmetrics are less suited to sailing directly downwind than spinnakers, and so instead the boat will often sail a zig-zag course downwind, gybing at the corners. An asymmetric spinnaker is particularly effective on fast planing dinghies as their speed generates an apparent wind on the bow allowing them to sail more directly downwind. It is also particularly useful in cruising yachts in the form of a cruising spinnaker or cruising chute, where the ease of handling is important.

Cruising
A cruising chute is a form of asymmetric spinnaker used by cruising yachts and designed for easy use when short-handed. Two sheets are used, with the tack line eased by a foot or so before gybing. Alternatively, only one sheet is used, with the sail snuffed before a gybe.

Code Zero
A Code Zero is a light-weight sail that approaches the dimensions of a genoa jib, for light airs and points of sail up to a close reach. It may be launched furled on its own stay.

Ratings
The following codes are used for both symmetric and asymmetric sails.

 * Code 1 is a light air reaching sail, where the apparent wind angles at low speeds has a significant effect to create angles of less than 90 degrees.
 * Code 2 is a medium air running sail, used for apparent wind angles over 90 degrees.
 * Code 3 is a medium air reaching sail, used for apparent wind angles near 90 degrees.
 * Code 4 is a heavy air running sail, used in the heaviest winds normally expected.
 * Code 5 is a heavy air reaching sail, used in the heaviest winds normally expected.
 * Code 6 is a storm sail, for running in storm conditions.

Setting the sail

Since they will only be used on certain points of sail, raising and lowering the spinnaker is a task that is often performed while under sail. Due to the size of spinnakers (the spinnaker is often double or more the size of the mainsail) this can be a difficult operation, since the sail will immediately catch the wind.

Symmetric
Typically the symmetric spinnaker is packed in its own bag, called a turtle, with the three corners on top for ready access. The clews (lower corners) are controlled by lines called sheets. The sheets are run in front (outside) of the forestay and lead to the back of the boat. The head (top corner) is attached to the spinnaker halyard, which is used to raise the sail up the mast.

Symmetric spinnakers have the windward clew secured to a spinnaker pole. The pole is attached to the mast and holds the windward edge of the sail in position. Lines that control the spinnaker pole are called guys or braces. The spinnaker pole may be allowed to raise and lower with the force of the wind, or it may have lines attached to it to raise (the topping lift) and lower (the foreguy or downhaul) the angle of the pole. If these lines are used, they are generally set up before setting sail and left in place even when the spinnaker is stowed.

Since spinnakers are downwind sails, they are never tacked, they are only jibed. When jibing a symmetric, the pole is removed from one corner and attached to the opposite corner. This corner now becomes the windward corner. There are two ways this is done. Generally on smaller boats, an end-for-end jibe is accomplished by disconnecting the pole at the mast-end and connecting the mast end to the opposite side of the sail. The old sail end is disconnected and then attached to the mast. This prevents the pole from getting loose during the procedure and allows the use of only two control lines that alternate as sheet and guy (more on this below). End-for-end jibing requires a pole with identical fittings at either end. Larger boats do a dip-pole gybe (jibe) in which the pole remains attached to the mast and the outer end is lowered until it can clear the head-stay and is then raised back up on the other side of the boat to the proper height with the topping lift. The guys are adjusted as before to set the sail angle on the new course. Dip-pole jibing can use a pole with one mast end and one sail end.

Smaller boats tend to use only one line on each clew (a combination guy and sheet). The windward line that runs through the jaw of the spinnaker pole is referred to as the guy (as opposed to foreguy) and the one on the free-flying corner is referred to as the sheet. During a jibe, these roles and thus the names are reversed. Larger boats may choose to use both a sheet and guy on each corner, with the guy being a heavier line. Having 2 sets of lines will makes the jibe easier as the kite is flown by the two sheets while the crew at the bow and at the mast are removing one guy from the pole and attaching it to the other with no tension on them.

Retrieving the spinnaker is a multi-step process, and the take-down depends on wind position. First, the windward corner is detached from the spinnaker pole and the guy is released. This step is referred to as blowing the guy. This allows the spinnaker to collapse into the shadow of the mainsail, where the foot is gathered by a crew member. The halyard is then lowered, and a crew member gathers the sail and stuffs it carefully into the turtle, corners out, and ready for the next deployment. There are, however many other ways to retrieve the spinnaker depending on the conditions and intent. It may or may not go into a turtle. It may be pulled back into the cockpit & then down below to be repacked for the next hoist or be pulled in a foredeck hatch and left free for the next hoist.

Asymmetric
Like the symmetric, the asymmetrical spinnaker is often stored in a turtle, with the corners on top for easy access. While a symmetric spinnaker is flown with a "guy" and a "sheet", an asymmetric spinnaker is flown with a tackline and a "sheet." The tack attaches to the bow or (often retractable) bowsprit, and the two sheets attach to the clew. The head of the sail is attached to the spinnaker halyard, which is used to raise the sail. The sheets are passed to either side of the forestay, attached to the clew; they may be passed forward of the luff of the asymmetric, or aft of the luff of the asymmetric, between the tack line and the forestay. The sheet on the downwind (lee) side of the hull is used to trim the sail, and the opposite sheet is left slack. Often a tack line is used at leading edge to provide adjustable tension on the luff of the spinnaker. To keep the tack near the centerline of the boat, it may be attached to the forestay with a sliding collar (often riding over the furled jib on parrel beads, tacker or similar device) adjustable with a down haul, or tack line. This allows the tack to slide up and down the forestay to adjust the luff tension. On racing boats, the tack of the asymmetric is often rigged to a retractable bowsprit, which increases the foretriangle area and prevents interference with the jib. As this trend becomes more popular in racing boats, it may result in similar adaptations to cruising boats as well.

Jibing with the asymmetric is much less complex than the symmetric, due to the lack of the spinnaker pole. Much like a jib, all that is required is to change sheets; however, since the asymmetric still flies in front of the forestay, the operation is reversed. The loaded sheet is slackened, and the opposite (lazy) sheet is pulled in, which allows the sail to pass around in front of the forestay, and then be sheeted in on the new lee side of the boat.

Retrieving the asymmetric is similar to the process for the symmetric. The sheets are released, allowing the sail to collapse to the front of the boat. The foot of the sail is then gathered, the halyard released and the head of the sail lowered, where it is packed into the turtle.

Dousing socks
The dousing sock, "spinnaker sleeve", snuffer, or just sock, is a device used to make deploying and retrieving the spinnaker a much easier task. The sock is a long fabric tube with a ring in one end to hold it open. Since the spinnaker is stored in the sock, the first step is to set up the sock. Two lines are attached to the sock; one is attached to a bridle on the ring, for pulling the sock down, and one is up the inside, from the ring, through the top, and back down, for raising the sock; these lines may be two ends of the same line, to form a loop. The head of the spinnaker is attached to the top of the sock and the ring runs down to the tack. The resulting bundle is stuffed into the spinnaker bag. The top of the sock will have provisions for attaching to the spinnaker halyard.

The spinnaker is raised as normal, but with the sock in place, the spinnaker is unable to catch the wind. Once the spinnaker is raised and the guys are ready to set, the sock is raised, releasing the spinnaker. The sock remains bundled up at the head of the sail while the spinnaker is deployed. To retrieve the spinnaker, the sheet or the tack is released and the sock is pulled down, gathering the sail. The halyard is then dropped and the sail may be packed away.

Spinnaker launching and dousing systems
As of 2006, there were a variety of means to aid the launching (hoisting) and dousing (taking down) of a spinnaker—a sail which, in lacking luff support, is "more unstable and more difficult" to handle in these and related situations. One system focuses on the launching of the spinnaker, only, and it makes use of special sail-packing and a funnel system that places breakable elastic bands as the sail is launched, bands that break as sheet and guy of the filled spinnaker are trimmed.

Other systems use means that assist with both launching and dousing, and such systems include:

 * sail modification to include a center patch and cringle to attach a retriever line (also termed a "takedown line") to use in sail launching and dousing, and use of a funnel-terminating, hull-affixed tubular launcher for storage and launching (through which the retriever passes); and
 * used of a tubular, ring-ended sleeve or "sock" which also stores the sail, which after launching (sock hoisting) is rigged such that the sock's top ring is toward the halyard and bottom ring toward the deck, where release of the spinnaker is accomplished by rigging that draws the bottom ring toward the halyard, allowing the bottom of the sail to fill, a design that leaves the collapsed sock aloft "at the head of the spinnaker while it is flying".

Spinnaker chutes
A spinnaker chute is a means of launching and dousing (recovery) of the spinnaker consisting of a tube or aperture in the deck close to the forestay, most commonly on modern dinghy designs and updated older classes. To allow recovery of the spinnaker into the chute during dousing, the spinnaker is fitted with one or more recovery patches to which or through which the tail of the spinnaker halyard is attached or passed; the spinnaker and its halyard thus form a continuous loop, passing through the chute.

If the spinnaker chute penetrates the hull and is required to be watertight, it takes the form of a hard tube sealed to the hull at both ends. If a watertight arrangement is not required, a cloth tube may be used to contain the lowered spinnaker.

Other uses
A masthead, symmetrical spinnaker is occasionally used for entertainment at anchor to loft a person hanging beneath it above the water. To work, the vessel must be anchored stern to the wind to allow the sail to extend out over the bow.

title: Spinnaker


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Arms of Bromley Borough Council. From civicheraldry.co.uk, with permission.

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