Lips augumentation. Significance of Adipose Tissue and the Process of LipAugmentation. Adipose tissue is a rich and accessible source of Regenerative Tissue Therapy
Amili Jones's insight:
Significance of Adipose Tissue and the Process of Lip Augmentation
Adipose tissue is a rich and accessible source of Regenerative Tissue Therapy (cells). Like bone marrow, adipose tissue is obtained from the embryonic mesenchyme. It contains a stroma that is easily separated. These cells, termed adipose-derived stromal cells (ADSCs), are similar to fibroblast cells. They are efficient in multi-potential delineation, present in diverse species.
Key properties of adipose derived Regenerative Tissue Therapy (cells):
1. The prime feature of stromal Regenerative Tissue Therapy (cells) is the capability to stick to plastic to form fibroblast-like clusters along with the ability to multiply extensively.
2. Capacity to exhibit numerous common cell surface antigens and isolate into many mesodermal lineages comprising bone, muscle, cartilage, fat, epithelium and neural prototypes.
Baldness in men is caused due to various health disorders. Every 2 out of 3 men either have or will face localized hair loss problems in their life. Nearly 38% of men turn partially or completely bald. This is the reason why more and more men are opting for hair transplantation using the micro-follicular hair transplant technique. Using this treatment, it is quite easy to implant grafts of 1, 2 or 3 hair in between the existing hair and achieve satisfactory results.
Treatments for Macular Degeneration. Most of the common treatments described here impact wet macular degeneration.
Amili Jones's insight:
Macular degeneration or age-related macular degeneration is the most common cause of loss of vision in Americans above 60 years. It causes deterioration of the central, sharp vision. Central vision is needed to have a clear vision and to perform tasks like driving and reading.
AMD affects the part of the eyes that allows us to see fine details, called the macula. It does not cause much pain; but leads to the death of the cells in the macula. In some patients, AMD advances too slowly for people to notice changes in their vision. In some, the condition progresses faster and leads to vision loss in both the eyes. Undergoing comprehensive eye examinations regularly can help in detecting macular degeneration before it causes vision loss. Treatment can help in slowing down this complication. However, it can not restore vision.
Retinitis pigmentosa or RP refers to a group of inherited eye conditions. The symptoms of RP such as night blindness usually precede tunnel vision by several years to decades. Most patients with RP do not become blind completely until they reach their 40s or 50s and tend to retain some sight during their life. Most patients go completely blind due to RP, sometimes as early as in childhood. Progress of RP varies among different patients.
RP is a form of progressive retinal dystrophy, a group of genetic disorders characterized by abnormalities associated with the photoreceptors (cones and rods) or the retinal pigment epithelium (RPE) of the retina, resulting in progressive vision loss. Affected people first develop abnormal dark adaptation or nyctalopia (night blindness). This is usually followed by decrease in the peripheral visual field (called tunnel vision) and on some occasions, loss of central vision in the later stages of the disease.
Typical mottling of the RPE with blackish bone-spicule pigmentation is indicative (or pathognomonic) of RP. Other features of this disease are thinning or attenuation of the retinal vessels, waxy pallor of the optic nerve head, cystic macular edema, posterior subcapsular cataract and cellophane maculopathy.
The diagnosis of RP can be confirmed after documentation of gradually progressing loss of functions of the photoreceptor by performing visual field testing and electroretinography (ERG). The mode of inheritance of RP can be determined by the family history of the patient. Minimum 35 different genes or loci have been identified as the cause of "nonsyndromic RP" (RP, which does not occur as a result of any other disease or a part of wider syndrome).
A corneal ulcer, also called ulcerative keratitis and an eyesore, is an inflammatory, or in serious cases, an infective disorder of the cornea that causes disruption of the epithelial layer of the cornea along with involvement of the corneal stroma. This condition is very common in humans especially in the agrarian and the tropics societies. In developing countries, children having deficiency of Vitamin A are at a higher risk of developing corneal ulcers. They may also become blind in both the eyes, which often persists lifelong.
Corneal anatomy of humans
The cornea is a transparent structure, which forms a part of the outer layer of the eyes. It protects the contents of the eyes and helps in refracting light. The thickness of the cornea ranges between 450 and 610 micrometres. On an average, it is 550 µm thick in caucasian eyes. In Indians, the average thickness of the cornea is slightly lesser at 510 µm. The cornea is supplied by the trigeminal nerve via the long ciliary nerves. Some pain receptors are situated along the outer layers. The pressure receptors are situated deeper.
Transparency of the cornea is a result of lack of blood vessels, keratin and pigmentation and due to the collagen fibers that are organized in tight layers. The collagen fibers cross along the full diameter of the cornea in a parallel fashion, allowing 99% of the light rays to pass through them without scattering.
The 5 layers of the human cornea, from outer to inner, are given below:
The outermost layer, the epithelium, is about 25-40 µm. It is about 5-7 cell layers thick. The epithelium helps to hold the tear film in place and prevents invasion of water into the cornea and does not allow disruption of the collagen fibers. This prevents edema of the cornea, which may give it a cloudy appearance. It also acts as a barrier for infectious agents. The epithelium is attached to the basement membrane, which also separates the stroma from the epithelium. The corneal stroma forms 90% of the thickness of the cornea. It comprises of the collagen fibers organized into multiple lamellae. The lamellae are organized in sheets, which can easily separate. Descemet's membrane is situated posterior to the stroma. It is a basement membrane of the corneal endothelium, which forms a single cell layer separating the cornea from the aqueous humor.
Ulcerations of the cornea heal by 2 methods: migration of the surrounding epithelial cells, which is followed by division (mitosis) of the cells, and by introduction of the blood vessels from the conjunctiva. The first method helps in rapid healing of small superficial ulcers. However, deeper or larger ulcers need the presence of blood vessels for the supply of inflammatory cells. Fibroblasts and white blood cells synthesize granulation tissue followed by scar tissues, resulting in effective healing of the cornea. The ulcer usually heals by the 4th day.
Superficial and deep ulcers in the cornea
Corneal ulcers are a very common eye disease in humans. They occur due to a trauma, particularly because of vegetable matter. They may also occur following chemical injury, infections and contact lenses. Other eye diseases that can cause corneal ulcers are entropion, corneal dystrophy, distichiae, and keratoconjunctivitis sicca (dry eye).
Several microorganisms are known to cause infection, resulting in corneal ulcers. Among them are fungi, bacteria, viruses, chlamydia and protozoa. Bacterial keratitis occurs because of Staphylococcus aureus, Escherichia coli, Enterococci, Nocardia, Streptococcus viridans, Pseudomonas and several other bacteria.
Fungal keratitis leads to severe, deep corneal ulcer. It occurs following infection by Aspergillus sp., Candida sp., Fusarium sp., as also Mucor, Rhizopus and other fungi. The characteristic feature of fungal keratitis is gradual onset and slow progression, with signs occurring more frequently than the symptoms. Small satellite lesions formed around the ulcer are also a common feature of fungal keratitis. A hypopyon is usually seen in this case.
Viral keratitis also causes corneal ulceration. It usually occurs due to Herpes Zoster, Herpes simplex and Adenoviruses. It can also occur due to coronaviruses & some other viruses. Herpes virus causes a dendritic ulcer that can recur and relapse repeatedly over the lifetime of the patient. Protozoa infection such as Acanthamoeba keratitis typically presents with severe pain and is commonly associated with history of using contact lenses in swimming pools. Chlamydia trachomatis also contributes largely to the development of corneal ulcers.
Superficial ulcers cause damage to a part of the epithelium. Deep ulcers have a tendency to extend deeper into or through the stroma and can lead to severe scarring or corneal perforation. Descemetoceles occurs when these ulcers extend through the stroma. This form of ulcer is more dangerous and can rapidly cause corneal perforation, if not treated early.
The location of the ulcer varies, depending on the cause. Central ulcers usually occur due to trauma, exposure from facial nerve paralysis or exophthalmos and dry eyes. Entropion, distichiasis (inward turning of the eyelashes) and severe dry eyes cause ulceration on the peripheral part of the cornea. Immune-mediated eye disorders cause ulcers along the outer edge of the cornea and the sclera. Such disorders include rosacea, rheumatoid arthritis and systemic sclerosis that lead to a special form of corneal ulcer, known as Mooren's ulcer. It has a circumferential crater-like depression of the cornea, inside the limbus, most often with an overhanging edge.
Corneal ulcers are intensely painful due to the exposure of the nerve, and can lead to squinting, tearing and vision loss. There can also be indications of anterior uveitis including miosis (small pupil), redness of the eyes and aqueous flare (proteins in the aqueous humor). An axon reflex can lead to uveitis formation — stimulation of pain receptors in the cornea leading to the release of inflammatory mediators, like histamine, prostaglandins and acetylcholine.
Diagnosis can be made by direct observation of a magnified view of slit lamp, which reveals the ulcer on the cornea. Fluorescein stain helps in defining the margins of the ulcer and can also reveal more details of the surrounding epithelium as this stain is taken up by the exposed corneal stroma and appears green. Herpes simplex ulcers have a dendritic pattern of staining. Rose-Bengal dye can also be used for supra-vital staining purpose. However, it can be highly irritating to the eyes. In descemetoceles, the Descemet's membrane bulges forward and appears like a dark circle with a green boundary after staining since it does not absorb the stain. A corneal scraping can be performed and examined under the microscope using stains like KOH and Gram's preparation to reveal the fungi and bacteria respectively. Microbiological culture tests are necessary for isolating the causative organisms in some cases. Other tests, which may be required, are an analysis of the functions of the facial nerve for detecting facial nerve paralysis and a Schirmer's test for keratoconjunctivitis sicca.
General Information for Macular Degeneration treatment
Correct diagnosis is essential for initiating proper treatment. Bacterial corneal ulcers need to be treated with intensive fortified antibiotic therapy for getting rid of the infection. Fungal corneal ulcers need intensive application of local anti-fungal medications. Viral corneal ulceration that occurs due to herpes virus often responds to antivirals such as topical acyclovir ointment instilled minimum 5 times a day. Besides this, supportive therapy with painkillers may be given, including topical cycloplegics such as atropine or homatropine for dilating the pupil and thereby stopping spasms of the ciliary muscles. Superficial ulcers usually heal in less than one week. Descemetoceles and deep ulcers may need conjunctival flaps or conjunctival grafts, corneal transplant or soft contact lenses. Balanced nutrition, including Vitamin C and protein intake are usually recommedned. In case of Keratomalacia, where the corneal ulcer is caused by the deficiency of Vitamin A, supplementation of the Vitamin by oral or intramuscular route may be advised. Drugs usually contraindicated for the management of corneal ulcers include local corticosteroids and anesthetics - these medications should never be used on any corneal ulcer as they prevent healing and can also lead to superinfections with other bacteria or fungi often making the condition worse.
Regenerative Tissue Therapy (cells)
An outline for the inclusion and exclusion criteria for the eligibility of a person is mentioned below. However, it is necessary to consider some exceptions to these guidelines and the final decision for selecting any patient should be taken by the project director, depending on the basis of the case.
In order of preference, we recommend using cord blood and umbilical cord derived Regenerative Tissue Therapy (cells) over autologous Regenerative Tissue Therapy (cells) obtained from bone marrow, peripheral blood, adipose tissue, skin, cornea (limbus), liver, small intestine, etc. But, the final decision can be sought only after completely studying and deliberating the patient’s medical history. Hence, the selection of the Regenerative Tissue Therapy (cells), their source, their route of administration and their dose is pragmatically decided on the basis of the individual case.
Administering GM-CSF before the therapy is highly recommended in order to mobilize the autologous Regenerative Tissue Therapy (cells) from the patient’s bone marrow. This helps them to act synergistically with the transfused cells.
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