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This is the beginning of inducing an Alpha state. Alpha has been known to take away pain and is useful in healing. A Theta state is a very deep state of relaxation. This is the state used in hypnosis and dreaming. In it, the brainwaves are slowed to a frequency of four to seven cycles per second.

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In fact, sages meditate for hours and hours to reach this state, as in it they are able to access absolute calmness. Theta brainwaves can be thought of as the subconscious; they govern the part of our mind that is layered between the conscious and the unconscious. They hold memories and sensations. They also govern our attitudes, beliefs and behavior.

They are always creative, inspirational and characterized by very spiritual sensations. It is believed the Theta state allows us to act below the level of the conscious mind.

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It is the first stage of the dream state. It is the state we are in when we stand on the top of a mountain completely absorbed in our surroundings. When we access a Theta state and call upon the Creator, we connect to the Creator of All That Is to heal a person instantly. When you imagine lifting your consciousness above your head through your crown chakra and you go up and ask of God, your brainwaves shift instantly to Theta.

When I was asked what I was doing in my readings, this is what I realized. I was sitting across from the person, holding their hands and imagining myself going above my space, praying that God would grant me the reading that this person needed, and it was given to me. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue.

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. Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide. Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles. Epithelial cells climb over one another in order to migrate.

These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well. 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.

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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. Cells can only migrate over living tissue, [42] 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.

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. 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. 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.

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. Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts. At first, contraction occurs without myofibroblast involvement. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction. 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. 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.

As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun. As the phase progresses, the tensile strength of the wound increases. 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 [7] such as a venous ulcer or pathological scarring such as a keloid scar.

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

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. 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.

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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. 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.

After injury, structural tissue heals with incomplete or complete regeneration. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin. There is a subtle distinction between 'repair' and 'regeneration'. 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. 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 know 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. 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 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; [79] 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. 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 s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology.

Scarless wound healing only occurs in mammalian foetal tissues [84] and complete regeneration is limited to lower vertebrates, such as salamanders , and invertebrates. 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. This process involved cutting in a surgical slant, instead of a right angle…; it was described in various Newspapers. 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. 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 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. 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:.


Successful wound healing is dependent on various cell types, molecular mediators and structural elements. Primary intention is the healing of a clean wound without tissue loss. 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. This process is faster than healing by secondary intention.

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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, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

Following are the main growth factors involved in wound healing:. Other complications can include Infection and Marjolin's ulcer. 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. From Wikipedia, the free encyclopedia.