Tretinoin
Keratolytic Agents
Lentigo
Acne Vulgaris
Ointments
Administration, Topical
Skin Aging
Cosmetics
Chemexfoliation
Hyperpigmentation
Acitretin
Melanosis
Nicotinic Acids
Emollients
Trichloroacetic Acid
Keratosis, Actinic
Skin Care
Carcinoma, Basal Cell
Retinoids
Administration, Cutaneous
Skin
Drug Combinations
Double-Blind Method
Retinoids are produced by glia in the lateral ganglionic eminence and regulate striatal neuron differentiation. (1/5913)
In order to identify molecular mechanisms involved in striatal development, we employed a subtraction cloning strategy to enrich for genes expressed in the lateral versus the medial ganglionic eminence. Using this approach, the homeobox gene Meis2 was found highly expressed in the lateral ganglionic eminence and developing striatum. Since Meis2 has recently been shown to be upregulated by retinoic acid in P19 EC cells (Oulad-Abdelghani, M., Chazaud, C., Bouillet, P., Sapin, V., Chambon, P. and Dolle, P. (1997) Dev. Dyn. 210, 173-183), we examined a potential role for retinoids in striatal development. Our results demonstrate that the lateral ganglionic eminence, unlike its medial counterpart or the adjacent cerebral cortex, is a localized source of retinoids. Interestingly, glia (likely radial glia) in the lateral ganglionic eminence appear to be a major source of retinoids. Thus, as lateral ganglionic eminence cells migrate along radial glial fibers into the developing striatum, retinoids from these glial cells could exert an effect on striatal neuron differentiation. Indeed, the treatment of lateral ganglionic eminence cells with retinoic acid or agonists for the retinoic acid receptors or retinoid X receptors, specifically enhances their striatal neuron characteristics. These findings, therefore, strongly support the notion that local retinoid signalling within the lateral ganglionic eminence regulates striatal neuron differentiation. (+info)All-trans-retinoic acid inhibits Jun N-terminal kinase by increasing dual-specificity phosphatase activity. (2/5913)
Jun N-terminal kinases (JNKs) are serine-threonine kinases that play a critical role in the regulation of cell growth and differentiation. We previously observed that JNK activity is suppressed by all-trans-retinoic acid (t-RA), a ligand for retinoic acid nuclear receptors (RARs), in normal human bronchial epithelial cells, which are growth inhibited by t-RA. In this study, we investigated the mechanism by which t-RA inhibits JNK and the possibility that this signaling event is blocked in non-small cell lung cancer (NSCLC) cells. Virtually all NSCLC cell lines are resistant to the growth-inhibitory effects of t-RA, and a subset of them have a transcriptional defect specific to retinoid nuclear receptors. We found that in NSCLC cells expressing functional retinoid receptors, serum-induced JNK phosphorylation and activity were inhibited by t-RA in a bimodal pattern, transiently within 30 min and in a sustained fashion beginning at 12 h. Retinoid receptor transcriptional activation was required for the late, but not the early, suppression of JNK activity. t-RA inhibited serum-induced JNK activity by blocking mitogen-activated protein (MAP) kinase kinase 4-induced signaling events. This effect of t-RA was phosphatase dependent and involved an increase in the expression of the dual-specificity MAP kinase phosphatase 1 (MKP-1). t-RA did not activate MKP-1 expression or inhibit JNK activity in a NSCLC cell line with retinoid receptors that are refractory to ligand-induced transcriptional activation. These findings provide the first evidence that t-RA suppresses JNK activity by inhibiting JNK phosphorylation. Retinoid receptor transcriptional activation was necessary for the sustained inhibition of JNK activity by t-RA, and this signaling event was disrupted in NSCLC cells with retinoid receptors that are refractory to ligand-induced transcriptional activation. (+info)Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient. (3/5913)
Primary blasts of a t(11;17)(q23;q21) acute promyelocytic leukaemia (APL) patient were analysed with respect to retinoic acid (RA) and arsenic trioxide (As2O3) sensitivity as well as PLZF/RARalpha status. Although RA induced partial monocytic differentiation ex vivo, but not in vivo, As203 failed to induce apoptosis in culture, contrasting with t(15;17) APL and arguing against the clinical use of As203 in t(11;17)(q23;q21) APL. Prior to cell culture, PLZF/RARalpha was found to exactly co-localize with PML onto PML nuclear bodies. However upon cell culture, it quickly shifted towards microspeckles, its localization found in transfection experiments. Arsenic trioxide, known to induce aggregation of PML nuclear bodies, left the microspeckled PLZF/RARalpha localization completely unaffected. RA treatment led to PLZF/RARalpha degradation. However, this complete PLZF/RARalpha degradation was not accompanied by differentiation or apoptosis, which could suggest a contribution of the reciprocal RARalpha/PLZF fusion product in leukaemogenesis or the existence of irreversible changes induced by the chimera. (+info)Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells. (4/5913)
To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). RAR-, RARalpha- and RARgamma-selective agonists strongly induced mucin mRNAs in a dose-dependent manner, while the RARbeta-selective retinoid only weakly induced mucin gene expression at very high concentrations (1 microM). The pan-RXR-selective agonist by itself did not induce mucin gene expression, but acted synergistically with suboptimal concentrations of the pan-RAR agonist. A retinoid with selective anti-activator-protein-1 activity only marginally induced mucin gene expression. The RARalpha antagonist strongly inhibited mucin gene induction and mucous cell differentiation caused by RA and by the RARalpha- and RARgamma-selective retinoids. In contrast, the RARgamma antagonist only weakly inhibited RARalpha-selective-retinoid-induced mucin gene expression, but completely blocked mucin gene expression induced by the RARgamma-selective retinoid. Our studies indicate that RARalpha is the major retinoid receptor subtype mediating RA-dependent mucin gene expression and mucous cell differentiation, but that the RARgamma isotype can also induce mucin genes. Furthermore these studies suggest that RARbeta is probably not (directly) involved in RA-induced mucin gene expression. (+info)Regulation of UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosamine-1-phosphate transferase by retinoic acid in P19 cells. (5/5913)
UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosamine-1-phosphate transferase (GPT) is the first enzyme in the dolichol pathway of protein N-glycosylation, and is implicated in the developmental programmes of a variety of eukaryotes. In the present study we describe the effects of all-trans-retinoic acid (RA) on the levels of GPT protein and enzymic activity, and on the transcription rate of the GPT gene, in mouse P19 teratocarcinoma cells. RA caused a dose-dependent and protein-synthesis-dependent induction of enzyme activity. The maximum induction of GPT activity (about 3-fold) required 2 days of exposure to 1 microM RA. Induced GPT activity also resulted in an increase in the rate of incorporation of [3H]mannose into Glc3Man9GlcNAc2. Enzymic activities paralleled GPT gene expression. The GPT gene was induced (2-fold) after 7 h of RA treatment. An approx. 3-fold increase in a 48 kDa GPT protein and approx. 4-fold increases in the levels of three GPT transcripts (1.8, 2.0 and 2.2 kb) were observed after 2 days of RA treatment. The enhanced levels of GPT protein and mRNAs began to decline 3 days after the initiation of differentiation, and GPT expression was down-regulated during cellular differentiation. GPT activity decreased about 2. 8-fold to a constant level in differentiated P19 cells. The results indicate that the RA-induced enzyme activity was mainly determined by increased transcription of the GPT gene. RA-treated P19 cells were about 4-fold more resistant to tunicamycin, a fungal antibiotic which inhibits GPT, than were control cells. In addition, GPT activity in membranes from RA-treated P19 cells exhibited approx. 4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity. Furthermore, increased GPT activity had regulatory significance with regard to the rate of incorporation of [3H]mannose into Glc3Man9GlcNAc2-P-P-dolichol and into glycoproteins. Together, the data provide additional insights into the hormonal regulation of GPT and present evidence that the RA-mediated induction of GPT has a regulatory impact on the dolichol pathway. (+info)Retinoic acid stimulates the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human choriocarcinoma JEG-3 cells. (6/5913)
The syncytiotrophoblasts of the human placenta express high levels of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the enzyme responsible for the inactivation of glucocorticoids. It has been proposed that the placental 11beta-HSD2 serves as a barrier to protect the fetus from high levels of maternal cortisol. To examine the hypothesis that nutritional signals regulate the expression of 11beta-HSD2 in placental syncytiotrophoblasts, we investigated the effects of retinoic acids (RAs), the major metabolites of vitamin A, on the expression of 11beta-HSD2 using human choriocarcinoma JEG-3 cells as a model. This trophoblast-like cell line displays a number of functional similarities to the syncytiotrophoblast. Treatment for 24 h with all-trans RA (1-1000 nM) resulted in a dose-dependent increase in 11beta-HSD2 activity with a maximal effect (increase to 3-fold) at 100 nM. The effect of all-trans RA (100 nM) was also time-dependent in that the effect was detectable at 6 h and reached its maximum by 48 h. Similar increases in 11beta-HSD2 activity were observed when the cells were treated with 9-cis RA. Results from semi-quantitative reverse transcription-polymerase chain reaction demonstrated that there was a corresponding increase in 11beta-HSD2 mRNA after RA treatment. Moreover, treatment with actinomycin D (100 ng/ml) abrogated the increase in 11beta-HSD2 mRNA induced by RA, indicating an effect on transcription. In conclusion, the present study has demonstrated for the first time that RA, at physiological concentrations, induces 11beta-HSD2 gene expression and enzyme activity in JEG-3 cells. If this occurs in vivo, the present finding suggests that high expression of 11beta-HSD2 in the human placenta may be maintained, at least in part, by dietary intake of vitamin A. (+info)Constitutive degradation of PML/RARalpha through the proteasome pathway mediates retinoic acid resistance. (7/5913)
PML/RARalpha is the leukemogenetic protein of acute promyelocytic leukemia (APL). Treatment with retinoic acid (RA) induces degradation of PML/RARalpha, differentiation of leukaemic blasts, and disease remission. However, RA resistance arises during RA treatment of APL patients. To investigate the phenomenon of RA resistance in APL, we generated RA-resistant sublines from APL-derived NB4 cells. The NB4.007/6 RA-resistant subline does not express the PML/RARalpha protein, although its mRNA is detectable at levels comparable to those of the parental cell line. In vitro degradation assays showed that the half-life of PML/RARalpha is less than 30 minutes in NB4.007/6 and longer than 3 hours in NB4. Treatment of NB4.007/6 cells with the proteasome inhibitors LLnL and lactacystin partially restored PML/RARalpha protein expression and resulted in a partial release of the RA-resistant phenotype. Similarly, forced expression of PML/RARalpha, but not RARalpha, into the NB4/007.6 cells restored sensitivity to RA treatment to levels comparable to those of the NB4 cells. These results indicate that constitutive degradation of PML/RARalpha protein may lead to RA resistance and that PML/RARalpha expression is crucial to convey RA sensitivity to APL cells. (+info)Differential expression and phosphorylation of CTCF, a c-myc transcriptional regulator, during differentiation of human myeloid cells. (8/5913)
CTCF is a transcriptional repressor of the c-myc gene. Although CTCF has been characterized in some detail, there is very little information about the regulation of CTCF activity. Therefore we investigated CTCF expression and phosphorylation during induced differentiation of human myeloid leukemia cells. We found that: (i) both CTCF mRNA and protein are down-regulated during terminal differentiation in most cell lines tested; (ii) CTCF down-regulation is retarded and less pronounced than that of c-myc; (iii) CTCF protein is differentially phosphorylated and the phosphorylation profiles depend on the differentiation pathway. We concluded that CTCF expression and activity is controlled at transcriptional and post-transcriptional levels. (+info)Tretinoin is a form of vitamin A that is used in the treatment of acne vulgaris, fine wrinkles, and dark spots caused by aging or sun damage. It works by increasing the turnover of skin cells, helping to unclog pores and promote the growth of new skin cells. Tretinoin is available as a cream, gel, or liquid, and is usually applied to the affected area once a day in the evening. Common side effects include redness, dryness, and peeling of the skin. It is important to avoid sunlight and use sunscreen while using tretinoin, as it can make the skin more sensitive to the sun.
Keratolytic agents are substances that cause the softening and sloughing off of excess keratin, the protein that makes up the outermost layer of the skin (stratum corneum). These agents help to break down and remove dead skin cells, increase moisture retention, and promote the growth of new skin cells. They are commonly used in the treatment of various dermatological conditions such as psoriasis, eczema, warts, calluses, and ichthyosis. Examples of keratolytic agents include salicylic acid, urea, lactic acid, and retinoic acid.
A lentigo is a small, sharply defined, pigmented macule (flat spot) on the skin. It's usually tan, brown, or black and can appear on various parts of the body, particularly where the skin has been exposed to the sun. Lentigos are typically harmless and don't require treatment unless they're uncomfortable or for cosmetic reasons. However, some types of lentigines, such as lentigo maligna, can progress into melanoma, a type of skin cancer, so regular self-examinations and professional skin checks are important.
It is essential to differentiate between simple lentigos and lentigo maligna, which is a precancerous lesion. Lentigo maligna tends to occur in older individuals, often on the face, and can appear as a large, irregularly shaped, and darkly pigmented patch. A dermatologist should evaluate any suspicious or changing skin spots for proper diagnosis and treatment.
Acne vulgaris is a common skin condition characterized by the formation of various types of blemishes on the skin, such as blackheads, whiteheads, papules, pustules, and cysts or nodules. These lesions typically appear on areas of the body that have a high concentration of sebaceous glands, including the face, neck, chest, back, and shoulders.
Acne vulgaris occurs when hair follicles become clogged with dead skin cells and excess oil (sebum) produced by the sebaceous glands. This blockage provides an ideal environment for bacteria, particularly Propionibacterium acnes, to multiply, leading to inflammation and infection. The severity of acne vulgaris can range from mild with only a few scattered comedones (blackheads or whiteheads) to severe cystic acne, which can cause significant scarring and emotional distress.
The exact causes of acne vulgaris are not fully understood, but several factors contribute to its development, including:
1. Hormonal changes during puberty, menstruation, pregnancy, or due to conditions like polycystic ovary syndrome (PCOS)
2. Genetic predisposition
3. Use of certain medications, such as corticosteroids and lithium
4. Excessive production of sebum due to overactive sebaceous glands
5. Accumulation of dead skin cells that clog pores
6. Bacterial infection (particularly Propionibacterium acnes)
7. Inflammation caused by the body's immune response to bacterial infection and clogged pores
Treatment for acne vulgaris depends on its severity and can include over-the-counter or prescription topical treatments, oral medications, chemical peels, light therapies, or even hormonal therapies in some cases. It is essential to seek professional medical advice from a dermatologist or healthcare provider to determine the most appropriate treatment plan for individual needs.
An ointment is a semi-solid preparation, typically composed of a mixture of medicinal substance with a base, which is usually greasy or oily. The purpose of the base is to act as a vehicle for the active ingredient and allow it to be applied smoothly and evenly to the skin or mucous membranes.
Ointments are commonly used in dermatology to treat various skin conditions such as eczema, psoriasis, rashes, burns, and wounds. They can also be used to deliver medication for localized pain relief, muscle relaxation, and anti-inflammatory or antibiotic effects.
The base of an ointment may consist of various ingredients, including petrolatum, lanolin, mineral oil, beeswax, or a combination of these. The choice of the base depends on the desired properties such as consistency, spreadability, and stability, as well as the intended route of administration and the specific therapeutic goals.
Topical administration refers to a route of administering a medication or treatment directly to a specific area of the body, such as the skin, mucous membranes, or eyes. This method allows the drug to be applied directly to the site where it is needed, which can increase its effectiveness and reduce potential side effects compared to systemic administration (taking the medication by mouth or injecting it into a vein or muscle).
Topical medications come in various forms, including creams, ointments, gels, lotions, solutions, sprays, and patches. They may be used to treat localized conditions such as skin infections, rashes, inflammation, or pain, or to deliver medication to the eyes or mucous membranes for local or systemic effects.
When applying topical medications, it is important to follow the instructions carefully to ensure proper absorption and avoid irritation or other adverse reactions. This may include cleaning the area before application, covering the treated area with a dressing, or avoiding exposure to sunlight or water after application, depending on the specific medication and its intended use.
Skin aging, also known as cutaneous aging, is a complex and multifactorial process characterized by various visible changes in the skin's appearance and function. It can be divided into two main types: intrinsic (chronological or natural) aging and extrinsic (environmental) aging.
Intrinsic aging is a genetically determined and time-dependent process that results from internal factors such as cellular metabolism, hormonal changes, and genetic predisposition. The primary features of intrinsic aging include gradual thinning of the epidermis and dermis, decreased collagen and elastin production, reduced skin cell turnover, and impaired wound healing. Clinically, these changes present as fine wrinkles, dryness, loss of elasticity, and increased fragility of the skin.
Extrinsic aging, on the other hand, is caused by external factors such as ultraviolet (UV) radiation, pollution, smoking, alcohol consumption, and poor nutrition. Exposure to these environmental elements leads to oxidative stress, inflammation, and DNA damage, which accelerate the aging process. The main features of extrinsic aging are coarse wrinkles, pigmentary changes (e.g., age spots, melasma), irregular texture, skin laxity, and increased risk of developing skin cancers.
It is important to note that intrinsic and extrinsic aging processes often interact and contribute to the overall appearance of aged skin. A comprehensive approach to skincare should address both types of aging to maintain healthy and youthful-looking skin.
Cosmetics are defined in the medical field as products that are intended to be applied or introduced to the human body for cleansing, beautifying, promoting attractiveness, and altering the appearance. According to the U.S. Food and Drug Administration (FDA), cosmetics include skin creams, lotions, makeup, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, shampoos, permanent waves, hair colors, toothpastes, and deodorants, as well as any material intended for use as a component of a cosmetic product.
It's important to note that the FDA classifies cosmetics and drugs differently. Drugs are defined as products that are intended to diagnose, cure, mitigate, treat, or prevent disease, and/or affect the structure or function of the body. Some products, such as anti-dandruff shampoos or toothpastes with fluoride, can be considered both a cosmetic and a drug because they have both cleansing and therapeutic properties. These types of products are subject to regulation by both the FDA's Office of Cosmetics and Colors and its Center for Drug Evaluation and Research.
Cosmetics must not be adulterated or misbranded, meaning that they must be safe for use under labeled or customary conditions, properly packaged and labeled, and not contain any harmful ingredients. However, the FDA does not have the authority to approve cosmetic products before they go on the market, with the exception of color additives. Manufacturers are responsible for ensuring that their products are safe and properly labeled.
Chemexfoliation is a medical term that refers to the use of chemical agents to exfoliate or remove the outer layers of the skin. It is also known as chempeel, derma peeling, or chemabrasion. This procedure is commonly used in dermatology and cosmetic surgery to improve the appearance of the skin, reduce fine lines and wrinkles, treat acne, uneven pigmentation, and sun damage.
During a chemexfoliation procedure, a chemical solution is applied to the skin, which causes the outer layers to blister and eventually peel off. The type of chemical agent used depends on the individual's skin type and the desired outcome. Commonly used chemicals include alpha-hydroxy acids (AHAs), beta-hydroxy acids (BHAs), trichloroacetic acid (TCA), and phenol.
After the procedure, the skin may be red, swollen, and sensitive for several days. It is important to avoid sun exposure and use a broad-spectrum sunscreen to protect the new skin. Multiple treatments may be necessary to achieve the desired results. Chemexfoliation should only be performed by a qualified healthcare professional in a controlled medical setting.
Dermatologic agents are medications, chemicals, or other substances that are applied to the skin (dermis) for therapeutic or cosmetic purposes. They can be used to treat various skin conditions such as acne, eczema, psoriasis, fungal infections, and wounds. Dermatologic agents include topical corticosteroids, antibiotics, antifungals, retinoids, benzoyl peroxide, salicylic acid, and many others. They can come in various forms such as creams, ointments, gels, lotions, solutions, and patches. It is important to follow the instructions for use carefully to ensure safety and effectiveness.
Hyperpigmentation is a medical term that refers to the darkening of skin areas due to an increase in melanin, the pigment that provides color to our skin. This condition can affect people of all races and ethnicities, but it's more noticeable in those with lighter skin tones.
Hyperpigmentation can be caused by various factors, including excessive sun exposure, hormonal changes (such as during pregnancy), inflammation, certain medications, and underlying medical conditions like Addison's disease or hemochromatosis. It can also result from skin injuries, such as cuts, burns, or acne, which leave dark spots known as post-inflammatory hyperpigmentation.
There are several types of hyperpigmentation, including:
1. Melasma: This is a common form of hyperpigmentation that typically appears as symmetrical, blotchy patches on the face, particularly the forehead, cheeks, and upper lip. It's often triggered by hormonal changes, such as those experienced during pregnancy or while taking birth control pills.
2. Solar lentigos (age spots or liver spots): These are small, darkened areas of skin that appear due to prolonged sun exposure over time. They typically occur on the face, hands, arms, and decolletage.
3. Post-inflammatory hyperpigmentation: This type of hyperpigmentation occurs when an injury or inflammation heals, leaving behind a darkened area of skin. It's more common in people with darker skin tones.
Treatment for hyperpigmentation depends on the underlying cause and may include topical creams, chemical peels, laser therapy, or microdermabrasion. Preventing further sun damage is crucial to managing hyperpigmentation, so wearing sunscreen with a high SPF and protective clothing is recommended.
Acitretin is a synthetic form of retinoic acid, which is a type of vitamin A. It is used to treat severe psoriasis and other skin conditions. Acitretin works by slowing down the rapid growth of skin cells that cause the symptoms of psoriasis. It comes in the form of a capsule and is taken orally.
Common side effects of acitretin include dryness of the skin, lips, and mouth, itching, peeling, redness, or stickiness of the palms and soles, hair loss, and changes in nail growth. Less common but more serious side effects can include liver damage, increased levels of lipids in the blood, and birth defects if taken during pregnancy.
It is important to note that acitretin can cause birth defects, so women who are pregnant or planning to become pregnant should not take this medication. Additionally, because acitretin can remain in the body for a long time, it is recommended that women of childbearing age use effective contraception while taking this medication and for at least three years after stopping it.
Melanosis is a general term that refers to an increased deposit of melanin, the pigment responsible for coloring our skin, in the skin or other organs. It can occur in response to various factors such as sun exposure, aging, or certain medical conditions. There are several types of melanosis, including:
1. Epidermal melanosis: This type of melanosis is characterized by an increase in melanin within the epidermis, the outermost layer of the skin. It can result from sun exposure, hormonal changes, or inflammation.
2. Dermal melanosis: In this type of melanosis, there is an accumulation of melanin within the dermis, the middle layer of the skin. It can be caused by various conditions such as nevus of Ota, nevus of Ito, or melanoma metastasis.
3. Mucosal melanosis: This type of melanosis involves an increase in melanin within the mucous membranes, such as those lining the mouth, nose, and genitals. It can be a sign of systemic disorders like Addison's disease or Peutz-Jeghers syndrome.
4. Lentigo simplex: Also known as simple lentigines, these are small, benign spots that appear on sun-exposed skin. They result from an increase in melanocytes, the cells responsible for producing melanin.
5. Labial melanotic macule: This is a pigmented lesion found on the lips, typically the lower lip. It is more common in darker-skinned individuals and is usually benign but should be monitored for changes that may indicate malignancy.
6. Ocular melanosis: An increase in melanin within the eye can lead to various conditions such as ocular melanocytosis, oculodermal melanocytosis, or choroidal melanoma.
It is important to note that while some forms of melanosis are benign and harmless, others may indicate an underlying medical condition or even malignancy. Therefore, any new or changing pigmented lesions should be evaluated by a healthcare professional.
Niacin, also known as nicotinic acid, is a form of vitamin B3 (B-complex vitamin) that is used by the body to turn food into energy. It is found in various foods including meat, fish, milk, eggs, green vegetables, and cereal grains. Niacin is also available as a dietary supplement and prescription medication.
As a medication, niacin is primarily used to treat high cholesterol levels. It works by reducing the production of LDL (bad) cholesterol in the body and increasing the levels of HDL (good) cholesterol. Niacin can also help lower triglycerides, another type of fat found in the blood.
Niacin is available in immediate-release, sustained-release, and extended-release forms. The immediate-release form can cause flushing of the skin, itching, tingling, and headaches, which can be uncomfortable but are not usually serious. The sustained-release and extended-release forms may have fewer side effects, but they can also increase the risk of liver damage and other serious side effects.
It is important to note that niacin should only be taken under the supervision of a healthcare provider, as it can interact with other medications and have potentially serious side effects.
Emollients are medical substances or preparations used to soften and soothe the skin, making it more supple and flexible. They work by forming a barrier on the surface of the skin that helps to prevent water loss and protect the skin from irritants and allergens. Emollients can be in the form of creams, lotions, ointments, or gels, and are often used to treat dry, scaly, or itchy skin conditions such as eczema, psoriasis, and dermatitis. They may contain ingredients such as petroleum jelly, lanolin, mineral oil, or various plant-derived oils and butters. Emollients can also help to reduce inflammation and promote healing of the skin.
Trichloroacetic Acid (TCA) is not typically defined in the context of medical terminology, but rather it is a chemical compound used in various medical and cosmetic applications.
Medically, TCA is often used as a chemical agent for peels to treat various skin conditions such as acne, sun damage, age spots, fine lines, and wrinkles. It works by causing the top layers of the skin to dry up and peel off, revealing smoother, more even-toned skin underneath.
The medical definition of Trichloroacetic Acid is:
A colorless crystalline compound, used as a chemical peel in dermatology for various skin conditions, that works by causing the top layers of the skin to dry up and peel off. It is also used as a fixative in histological preparations and as an antiseptic and disinfectant. The chemical formula for TCA is C2HCl3O2.
Actinic keratosis, also known as solar keratosis, is a precancerous skin condition that typically develops in areas exposed to excessive sun damage over the years. It presents as rough, scaly, or crusty patches of skin, often with a pink, red, or brownish tint. These lesions usually appear on the face, ears, scalp, neck, back of the hands, and forearms.
Actinic keratosis is caused by the prolonged exposure to ultraviolet (UV) radiation from sunlight or artificial sources like tanning beds. The UV rays damage the skin's DNA, leading to abnormal skin cell growth and the formation of these precancerous lesions.
While most actinic keratoses remain benign, a small percentage can progress into squamous cell carcinoma, a type of skin cancer. Therefore, it is essential to have any suspicious or changing lesions evaluated by a healthcare professional for proper diagnosis and treatment. Prevention measures include protecting the skin from excessive sun exposure, wearing protective clothing, using broad-spectrum sunscreen with an SPF of at least 30, and avoiding tanning beds.
Skin care, in a medical context, refers to the practice of maintaining healthy skin through various hygienic, cosmetic, and therapeutic measures. This can include:
1. Cleansing: Using appropriate cleansers to remove dirt, sweat, and other impurities without stripping the skin of its natural oils.
2. Moisturizing: Applying creams or lotions to keep the skin hydrated and prevent dryness.
3. Sun Protection: Using sunscreens, hats, and protective clothing to shield the skin from harmful ultraviolet (UV) rays which can cause sunburn, premature aging, and skin cancer.
4. Skin Care Products: Using over-the-counter or prescription products to manage specific skin conditions like acne, eczema, psoriasis, or rosacea.
5. Regular Check-ups: Regularly examining the skin for any changes, growths, or abnormalities that may indicate a skin condition or disease.
6. Lifestyle Factors: Maintaining a healthy lifestyle, including a balanced diet, regular exercise, adequate sleep, and avoiding habits like smoking and excessive alcohol consumption, which can negatively impact skin health.
It's important to note that while some general skincare advice applies to most people, individual skincare needs can vary greatly depending on factors like age, skin type (oily, dry, combination, sensitive), and specific skin conditions or concerns. Therefore, it's often beneficial to seek personalized advice from a dermatologist or other healthcare provider.
Facial injuries refer to any damage or trauma caused to the face, which may include the bones of the skull that form the face, teeth, salivary glands, muscles, nerves, and skin. Facial injuries can range from minor cuts and bruises to severe fractures and disfigurement. They can be caused by a variety of factors such as accidents, falls, sports-related injuries, physical assaults, or animal attacks.
Facial injuries can affect one or more areas of the face, including the forehead, eyes, nose, cheeks, ears, mouth, and jaw. Common types of facial injuries include lacerations (cuts), contusions (bruises), abrasions (scrapes), fractures (broken bones), and burns.
Facial injuries can have significant psychological and emotional impacts on individuals, in addition to physical effects. Treatment for facial injuries may involve simple first aid, suturing of wounds, splinting or wiring of broken bones, reconstructive surgery, or other medical interventions. It is essential to seek prompt medical attention for any facial injury to ensure proper healing and minimize the risk of complications.
Carcinoma, basal cell is a type of skin cancer that arises from the basal cells, which are located in the lower part of the epidermis (the outermost layer of the skin). It is also known as basal cell carcinoma (BCC) and is the most common form of skin cancer.
BCC typically appears as a small, shiny, pearly bump or nodule on the skin, often in sun-exposed areas such as the face, ears, neck, hands, and arms. It may also appear as a scar-like area that is white, yellow, or waxy. BCCs are usually slow growing and rarely spread (metastasize) to other parts of the body. However, they can be locally invasive and destroy surrounding tissue if left untreated.
The exact cause of BCC is not known, but it is thought to be related to a combination of genetic and environmental factors, including exposure to ultraviolet (UV) radiation from the sun or tanning beds. People with fair skin, light hair, and blue or green eyes are at increased risk of developing BCC.
Treatment for BCC typically involves surgical removal of the tumor, along with a margin of healthy tissue. Other treatment options may include radiation therapy, topical chemotherapy, or photodynamic therapy. Prevention measures include protecting your skin from UV radiation by wearing protective clothing, using sunscreen, and avoiding tanning beds.
Retinoids are a class of chemical compounds that are derivatives of vitamin A. They are widely used in dermatology for the treatment of various skin conditions, including acne, psoriasis, and photoaging. Retinoids can help to reduce inflammation, improve skin texture and tone, and stimulate collagen production.
Retinoids work by binding to specific receptors in the skin cells, which triggers a series of biochemical reactions that regulate gene expression and promote cell differentiation and turnover. This can help to unclog pores, reduce the appearance of fine lines and wrinkles, and improve the overall health and appearance of the skin.
There are several different types of retinoids used in skincare products, including retinoic acid, retinaldehyde, and retinol. Retinoic acid is the most potent form of retinoid and is available by prescription only. Retinaldehyde and retinol are weaker forms of retinoid that can be found in over-the-counter skincare products.
While retinoids can be highly effective for treating various skin conditions, they can also cause side effects such as dryness, irritation, and sensitivity to the sun. It is important to use retinoids as directed by a healthcare professional and to follow proper sun protection measures when using these products.
"Cutaneous administration" is a route of administering medication or treatment through the skin. This can be done through various methods such as:
1. Topical application: This involves applying the medication directly to the skin in the form of creams, ointments, gels, lotions, patches, or solutions. The medication is absorbed into the skin and enters the systemic circulation slowly over a period of time. Topical medications are often used for local effects, such as treating eczema, psoriasis, or fungal infections.
2. Iontophoresis: This method uses a mild electrical current to help a medication penetrate deeper into the skin. A positive charge is applied to a medication with a negative charge, or vice versa, causing it to be attracted through the skin. Iontophoresis is often used for local pain management and treating conditions like hyperhidrosis (excessive sweating).
3. Transdermal delivery systems: These are specialized patches that contain medication within them. The patch is applied to the skin, and as time passes, the medication is released through the skin and into the systemic circulation. This method allows for a steady, controlled release of medication over an extended period. Common examples include nicotine patches for smoking cessation and hormone replacement therapy patches.
Cutaneous administration offers several advantages, such as avoiding first-pass metabolism (which can reduce the effectiveness of oral medications), providing localized treatment, and allowing for self-administration in some cases. However, it may not be suitable for all types of medications or conditions, and potential side effects include skin irritation, allergic reactions, and systemic absorption leading to unwanted systemic effects.
In medical terms, the skin is the largest organ of the human body. It consists of two main layers: the epidermis (outer layer) and dermis (inner layer), as well as accessory structures like hair follicles, sweat glands, and oil glands. The skin plays a crucial role in protecting us from external factors such as bacteria, viruses, and environmental hazards, while also regulating body temperature and enabling the sense of touch.
Skin pigmentation is the coloration of the skin that is primarily determined by two types of melanin pigments, eumelanin and pheomelanin. These pigments are produced by melanocytes, which are specialized cells located in the epidermis. Eumelanin is responsible for brown or black coloration, while pheomelanin produces a red or yellow hue.
The amount and distribution of melanin in the skin can vary depending on genetic factors, age, sun exposure, and various other influences. Increased production of melanin in response to UV radiation from the sun helps protect the skin from damage, leading to darkening or tanning of the skin. However, excessive sun exposure can also cause irregular pigmentation, such as sunspots or freckles.
Abnormalities in skin pigmentation can result from various medical conditions, including albinism (lack of melanin production), vitiligo (loss of melanocytes leading to white patches), and melasma (excessive pigmentation often caused by hormonal changes). These conditions may require medical treatment to manage or improve the pigmentation issues.
A drug combination refers to the use of two or more drugs in combination for the treatment of a single medical condition or disease. The rationale behind using drug combinations is to achieve a therapeutic effect that is superior to that obtained with any single agent alone, through various mechanisms such as:
* Complementary modes of action: When different drugs target different aspects of the disease process, their combined effects may be greater than either drug used alone.
* Synergistic interactions: In some cases, the combination of two or more drugs can result in a greater-than-additive effect, where the total response is greater than the sum of the individual responses to each drug.
* Antagonism of adverse effects: Sometimes, the use of one drug can mitigate the side effects of another, allowing for higher doses or longer durations of therapy.
Examples of drug combinations include:
* Highly active antiretroviral therapy (HAART) for HIV infection, which typically involves a combination of three or more antiretroviral drugs to suppress viral replication and prevent the development of drug resistance.
* Chemotherapy regimens for cancer treatment, where combinations of cytotoxic agents are used to target different stages of the cell cycle and increase the likelihood of tumor cell death.
* Fixed-dose combination products, such as those used in the treatment of hypertension or type 2 diabetes, which combine two or more active ingredients into a single formulation for ease of administration and improved adherence to therapy.
However, it's important to note that drug combinations can also increase the risk of adverse effects, drug-drug interactions, and medication errors. Therefore, careful consideration should be given to the selection of appropriate drugs, dosing regimens, and monitoring parameters when using drug combinations in clinical practice.
The double-blind method is a study design commonly used in research, including clinical trials, to minimize bias and ensure the objectivity of results. In this approach, both the participants and the researchers are unaware of which group the participants are assigned to, whether it be the experimental group or the control group. This means that neither the participants nor the researchers know who is receiving a particular treatment or placebo, thus reducing the potential for bias in the evaluation of outcomes. The assignment of participants to groups is typically done by a third party not involved in the study, and the codes are only revealed after all data have been collected and analyzed.
Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.
Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.
It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.
Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.