Hair
Hair Follicle
Hair Cells, Auditory
Hair Cells, Auditory, Inner
Hair Cells, Vestibular
Hair Cells, Auditory, Outer
Hair Preparations
Saccule and Utricle
Cochlea
Organ of Corti
Differential behaviors toward ultraviolet A and B radiation of fibroblasts and keratinocytes from normal and DNA-repair-deficient patients. (1/194)
Xeroderma pigmentosum (XP) and trichothiodystrophy (TTD) are rare genodermatoses transmitted as recessive and autosomal traits that result in reduced capacity to repair UV-induced DNA lesions. Although XP, but not TTD, patients are prone to basal and squamous cell carcinomas, to date no comparative studies of the XP and TTD phenotypes have included epidermal keratinocytes. We compared the DNA repair capacity (by unscheduled DNA synthesis) and cell survival (by clonal analysis) of epidermal keratinocytes and dermal fibroblasts grown from normal individuals and patients with xeroderma pigmentosum and trichothiodystrophy following UVA and UVB irradiation. The same dose of UVB (1000 J/m2) induced twice as many DNA lesions in normal fibroblasts as in normal keratinocytes. UV survival rates were always higher in keratinocytes than in fibroblasts. Normal and TTD keratinocytes survived better following UVA and UVB irradiation than XP-C and XP-D keratinocytes. XP-C keratinocytes exhibited exacerbated sensitivity toward UVA radiation. Unscheduled DNA synthesis at UV doses leading to 50% cell survival indicated that the ratio of DNA repair capacity to cell survival is higher in keratinocytes than in fibroblasts. In addition, UVA and UVB irradiation induced a transition from proliferative to abortive keratinocyte colonies. This transition varied between donors and was in part correlated with their cancer susceptibility. Altogether these data provide the first evidence of the differential behaviors of normal, XP, and TTD keratinocytes toward UV radiation. (+info)The relative expression of mutated XPB genes results in xeroderma pigmentosum/Cockayne's syndrome or trichothiodystrophy cellular phenotypes. (2/194)
The human XPB DNA helicase is a subunit of the DNA repair/basal transcription factor TFIIH, involved in early steps of the nucleotide excision repair pathway. Two distinct clinical phenotypes, xeroderma pigmentosum associated with Cockayne's syndrome (XP/CS) and trichothiodystrophy (TTD), can be due to mutations in the XPB gene. In the present work, we studied cellular DNA repair properties of skin fibro-blasts from two patients mutated in the XPB gene: an XP/CS patient cell (XPCS2BA) with a T296C (F99S) transition and a TTD patient cell (TTD6VI) exhibiting an A355C (T119P) transversion. Both cells are clearly associated with different levels of alterations in their response to UV light. To establish the relationship between the relative expression level of these two alleles and DNA repair properties, we transfected SV40-transformed XPCS2BA (XPCS2BASV) cells with a plasmid (pTTD6VI) carrying the XPB-A355C cDNA and examined DNA repair properties after UV irradiation (cell survival, unscheduled DNA synthesis and kinetics of photoproduct removal) in stable transfectants. We isolated three clones, which express the XPB-A355C gene (Cl-5) or the XPB-T296C gene (Cl-14) or both genes (Cl-19). This con-stitutes a model system allowing us to correlate the relative expression levels of the XPB-A355C (TTD) and XPB-T296C (XP/CS) genes with various DNA repair properties. Overexpression of the XPB-A355C (TTD) gene in an XP/CS cell gives rise to a cellular phenotype of increased repair similar to that of TTD6VI cells, while equal expression of the two mutated genes leads to an intermediate cellular phenotype between XP/CS and TTD. (+info)Squamous cell carcinomas and increased apoptosis in skin with inhibited Rel/nuclear factor-kappaB signaling. (3/194)
The Rel/nuclear factor-kappaB (Rel/NF-kappaB) transcription factors have been implicated previously in control of apoptosis, cell proliferation, and oncogenesis. Here we show that selective inhibition of Rel/NF-kappaB signaling in murine skin, by targeted overexpression of a super-repressor form of IkappaB-alpha, results in an increased basal frequency of apoptotic cells and the spontaneous development of squamous cell carcinomas. Presence of hyperplasia and hair follicle degeneration demonstrate an important role for Rel/NF-kappaB signaling in normal epidermal development and homeostasis. Transgenic skin, in addition, showed an enhanced sensitivity to UV-induced apoptosis. These data suggest an involvement of the Rel/NF-kappaB signaling pathway in apoptosis and cancer development of the skin. (+info)Mouse model for the DNA repair/basal transcription disorder trichothiodystrophy reveals cancer predisposition. (4/194)
Patients with the nucleotide excision repair (NER) disorder xeroderma pigmentosum (XP) are highly predisposed to develop sunlight-induced skin cancer, in remarkable contrast to photosensitive NER-deficient trichothiodystrophy (TTD) patients carrying mutations in the same XPD gene. XPD encodes a helicase subunit of the dually functional DNA repair/basal transcription complex TFIIH. The pleiotropic disease phenotype is hypothesized to be, in part, derived from a repair defect causing UV sensitivity and, in part, from a subtle, viable basal transcription deficiency accounting for the cutaneous, developmental, and the typical brittle hair features of TTD. To understand the relationship between deficient NER and tumor susceptibility, we used a mouse model for TTD that mimics an XPD point mutation of a TTD patient in the mouse germline. Like the fibroblasts from the patient, mouse cells exhibit a partial NER defect, evident from the reduced UV-induced DNA repair synthesis (residual repair capacity approximately 25%), limited recovery of RNA synthesis after UV exposure, and a relatively mild hypersensitivity to cell killing by UV or 7,12-dimethylbenz[a]anthracene. In accordance with the cellular studies, TTD mice exhibit a modestly increased sensitivity to UV-induced inflammation and hyperplasia of the skin. In striking contrast to the human syndrome, TTD mice manifest a dear susceptibility to UV- and 7,12-dimethylbenz[a]anthracene-induced skin carcinogenesis, albeit not as pronounced as the totally NER-deficient XPA mice. These findings open up the possibility that TTD is associated with a so far unnoticed cancer predisposition and support the notion that a NER deficiency enhances cancer susceptibility. These findings have important implications for the etiology of the human disorder and for the impact of NER on carcinogenesis. (+info)Monilethrix: a novel mutation (Glu402Lys) in the helix termination motif and the first causative mutation (Asn114Asp) in the helix initiation motif of the type II hair keratin hHb6. (5/194)
Monilethrix, a rare human hair disorder with autosomal dominant transmission, can be caused by mutations in hair keratins. Up to now, causative mutations have only been found in two type II cortex keratins, hHb6 and hHb1. In these hair keratins, the helix termination motif, HTM, was the only site in which mutations were located. The most frequent mutation, which has been found in 22 cases, was a Glu413Lys substitution in hHb6, whereas other mutations, i.e., hHb6 Glu413Asp, hHb1 Glu413Lys, and hHb1 Glu402Lys, have been reported in a distinctly lower number of cases. In this study, we describe the equivalent of the hHb1 Glu402Lys mutation in the HTM of cortex keratin hHb6. The mutation occurred in an American family in which it could only be detected in one clinically affected individual. Thus the underlying G-->A transition represents a spontaneous germ-line mutation in the hHb6 gene. This new mutation indicates that both the hHb6/hHb1 Glu413Lys substitution and the hHb6/hHb1 Glu402Lys substitution, represent mutational hotspots in the HTM of type II cortex keratins. However, we also describe a monilethrix-causing mutation in the helix initiation motif, HIM, of the cortex keratin hHb6. The critical Asn114Asp substitution was only found in affected members of a large Swedish three-generation family. Considering that since childhood, half of the affected individuals suffer from complete baldness and follicular keratosis, the new HIM mutation seems to be associated with a rather severe disease phenotype. In conclusion, our data strongly suggest that monilethrix is a disease of the hair cortex, whose etiology is interesting in that causative mutations seem to be restricted to type II hair keratins. (+info)Identification of novel mutations in basic hair keratins hHb1 and hHb6 in monilethrix: implications for protein structure and clinical phenotype. (6/194)
Monilethrix is an hereditary hair dystrophy recently shown to be due to mutations in the helix termination motif of two type II (basic) human hair keratin genes, hHb1 and hHb6. It has been suggested that mutation in hHb1 produces a less severe phenotype. We have studied hair keratin genes and clinical features in 18 unrelated pedigrees of monilethrix from Germany, Scotland, Northern Ireland, and Portugal, in 13 of which mutations have not previously been identified. By examining the rod domains of hHb1, hHb3 and hHb6, we have identified mutations in nine of the new pedigrees. We again found the glutamine-lysine substitution (E413K) in the helix termination motif of hHb6 in two families, and in another, the corresponding E413K substitution in the hHb1 gene. In four families a similar substitution E402K was present in a nearby residue. In addition two novel mutations within the helix initiation motif of hHb6 were found in Scottish and Portuguese cases, in whom the same highly conserved asparagine residue N114 was mutated to histidine (N114H) or aspartic acid (N114D) residues, respectively. In four other monilethrix pedigrees mutations in these domains of hHb1, hHb3, and hHb6 were not found. The mutations identified predict a variety of possible structural consequences for the keratin molecule. A comparison of clinical features and severity between cases with hHb1 and hHb6 mutations does not suggest distinct effects on phenotype, with the possible exception of nail dystrophy, commoner with hHb1 defects. Other factors are required to explain the marked variation in clinical severity within and between cases. (+info)The cancer-free phenotype in trichothiodystrophy is unrelated to its repair defect. (7/194)
The DNA repair-deficient genetic disorders xeroderma pigmentosum (XP) and trichothiodystrophy (TTD) can both result from mutations in the XPD gene, the sites of the mutations differing between the two disorders. The hallmarks of XP are multiple pigmentation changes in the skin and a greatly elevated frequency of skin cancers, characteristics that are not seen in TTD. XP-D and most TTD patients have reduced levels of DNA repair, but some recent reports have suggested that the repair deficiencies in TTD cells are milder than in XP-D cells. We reported recently that inhibition of intracellular adhesion molecule-1 (ICAM-1) expression by UVB irradiation was similar in normal and TTD cells but increased in XP-D cells, suggesting a correlation between ICAM-1 inhibition and cancer proneness. In the first part of the current work, we have extended these studies and found several other examples, including XP-G and Cockayne syndrome cells, in which increased ICAM-1 inhibition correlated with cancer proneness. However, we also discovered that a subset of TTD cells, in which arg112 in the NH2-terminal region of the XPD protein is mutated to histidine, had an ICAM-1 response similar to that of XP-D cells. In the second part of the work, we have shown that TTD cells with this specific NH2-terminal mutation are more sensitive to UV irradiation than other TTDs, most of which are mutated in the COOH-terminal region, and are indistinguishable from XP-D cells in cell killing, incision breaks, and repair of cyclobutane pyrimidine dimers. Because the clinical phenotypes of these patients do not obviously differ from those of TTDs with mutations at other sites, we conclude that the lack of skin abnormalities in TTD is independent of the defective cellular responses to UV. It is likely to result from a transcriptional defect, which prevents the skin abnormalities from being expressed. (+info)Activation of the Notch pathway in the hair cortex leads to aberrant differentiation of the adjacent hair-shaft layers. (8/194)
Little is known about the mechanisms underlying the generation of various cell types in the hair follicle. To investigate the role of the Notch pathway in this process, transgenic mice were generated in which an active form of Notch1 (Notch(DeltaE)) was overexpressed under the control of the mouse hair keratin A1 (MHKA1) promoter. MHKA-Notch(DeltaE) is expressed only in one precursor cell type of the hair follicle, the cortex. Transgenic mice could be easily identified by the phenotypes of curly whiskers and wavy, sheen pelage hair. No effects of activated Notch on proliferation were detected in hair follicles of the transgenic mice. We find that activating Notch signaling in the cortex caused abnormal differentiation of the medulla and the cuticle, two neighboring cell types that did not express activated Notch. We demonstrate that these non-autonomous effects are likely caused by cell-cell interactions between keratinocytes within the hair follicle and that Notch may function in such interactions either by directing the differentiation of follicular cells or assisting cells in interpreting a gradient emanating from the dermal papilla. (+info)Eye manifestations refer to any changes or abnormalities in the eye that can be observed or detected. These manifestations can be related to various medical conditions, diseases, or disorders affecting the eye or other parts of the body. They can include structural changes, such as swelling or bulging of the eye, as well as functional changes, such as impaired vision or sensitivity to light. Examples of eye manifestations include cataracts, glaucoma, diabetic retinopathy, macular degeneration, and uveitis.
Hair diseases is a broad term that refers to various medical conditions affecting the hair shaft, follicle, or scalp. These conditions can be categorized into several types, including:
1. Hair shaft abnormalities: These are conditions that affect the structure and growth of the hair shaft. Examples include trichorrhexis nodosa, where the hair becomes weak and breaks easily, and pili torti, where the hair shaft is twisted and appears sparse and fragile.
2. Hair follicle disorders: These are conditions that affect the hair follicles, leading to hair loss or abnormal growth patterns. Examples include alopecia areata, an autoimmune disorder that causes patchy hair loss, and androgenetic alopecia, a genetic condition that leads to pattern baldness in both men and women.
3. Scalp disorders: These are conditions that affect the scalp, leading to symptoms such as itching, redness, scaling, or pain. Examples include seborrheic dermatitis, psoriasis, and tinea capitis (ringworm of the scalp).
4. Hair cycle abnormalities: These are conditions that affect the normal growth cycle of the hair, leading to excessive shedding or thinning. Examples include telogen effluvium, where a large number of hairs enter the resting phase and fall out, and anagen effluvium, which is typically caused by chemotherapy or radiation therapy.
5. Infectious diseases: Hair follicles can become infected with various bacteria, viruses, or fungi, leading to conditions such as folliculitis, furunculosis, and kerion.
6. Genetic disorders: Some genetic disorders can affect the hair, such as Menkes syndrome, which is a rare inherited disorder that affects copper metabolism and leads to kinky, sparse, and brittle hair.
Proper diagnosis and treatment of hair diseases require consultation with a healthcare professional, often a dermatologist or a trichologist who specializes in hair and scalp disorders.
Medically, hair is defined as a threadlike structure that grows from the follicles found in the skin of mammals. It is primarily made up of a protein called keratin and consists of three parts: the medulla (the innermost part or core), the cortex (middle layer containing keratin filaments) and the cuticle (outer layer of overlapping scales).
Hair growth occurs in cycles, with each cycle consisting of a growth phase (anagen), a transitional phase (catagen), and a resting phase (telogen). The length of hair is determined by the duration of the anagen phase.
While hair plays a crucial role in protecting the skin from external factors like UV radiation, temperature changes, and physical damage, it also serves as an essential aspect of human aesthetics and identity.
A hair follicle is a part of the human skin from which hair grows. It is a complex organ that consists of several layers, including an outer root sheath, inner root sheath, and matrix. The hair follicle is located in the dermis, the second layer of the skin, and is surrounded by sebaceous glands and erector pili muscles.
The hair growth cycle includes three phases: anagen (growth phase), catagen (transitional phase), and telogen (resting phase). During the anagen phase, cells in the matrix divide rapidly to produce new hair fibers that grow out of the follicle. The hair fiber is made up of a protein called keratin, which also makes up the outer layers of the skin and nails.
Hair follicles are important for various biological functions, including thermoregulation, sensory perception, and social communication. They also play a role in wound healing and can serve as a source of stem cells that can differentiate into other cell types.
Auditory hair cells are specialized sensory receptor cells located in the inner ear, more specifically in the organ of Corti within the cochlea. They play a crucial role in hearing by converting sound vibrations into electrical signals that can be interpreted by the brain.
These hair cells have hair-like projections called stereocilia on their apical surface, which are embedded in a gelatinous matrix. When sound waves reach the inner ear, they cause the fluid within the cochlea to move, which in turn causes the stereocilia to bend. This bending motion opens ion channels at the tips of the stereocilia, allowing positively charged ions (such as potassium) to flow into the hair cells and trigger a receptor potential.
The receptor potential then leads to the release of neurotransmitters at the base of the hair cells, which activate afferent nerve fibers that synapse with these cells. The electrical signals generated by this process are transmitted to the brain via the auditory nerve, where they are interpreted as sound.
There are two types of auditory hair cells: inner hair cells and outer hair cells. Inner hair cells are the primary sensory receptors responsible for transmitting information about sound to the brain. They make direct contact with afferent nerve fibers and are more sensitive to mechanical stimulation than outer hair cells.
Outer hair cells, on the other hand, are involved in amplifying and fine-tuning the mechanical response of the inner ear to sound. They have a unique ability to contract and relax in response to electrical signals, which allows them to adjust the stiffness of their stereocilia and enhance the sensitivity of the cochlea to different frequencies.
Damage or loss of auditory hair cells can lead to hearing impairment or deafness, as these cells cannot regenerate spontaneously in mammals. Therefore, understanding the structure and function of hair cells is essential for developing therapies aimed at treating hearing disorders.
I'm sorry for any confusion, but "hair color" is not a term that has a medical definition in the same way that a term like "myocardial infarction" (heart attack) does. Hair color can be described in various ways, such as being a natural hair color (like blonde, brunette, red, or black) or describing a change in hair color due to factors like aging (gray or white hairs) or hair dye usage.
However, it's worth noting that changes in hair color can sometimes be associated with certain medical conditions. For example, premature graying of the hair before the age of 30 can be a feature of certain genetic disorders or vitamin B12 deficiency. Similarly, some skin conditions like alopecia areata or vitiligo can cause patchy changes in hair color. But these associations don't provide a medical definition for 'hair color'.
Auditory inner hair cells are specialized sensory receptor cells located in the inner ear, more specifically in the organ of Corti within the cochlea. They play a crucial role in hearing by converting mechanical sound energy into electrical signals that can be processed and interpreted by the brain.
Human ears have about 3,500 inner hair cells arranged in one row along the length of the basilar membrane in each cochlea. These hair cells are characterized by their stereocilia, which are hair-like projections on the apical surface that are embedded in a gelatinous matrix called the tectorial membrane.
When sound waves cause the basilar membrane to vibrate, the stereocilia of inner hair cells bend and deflect. This deflection triggers a cascade of biochemical events leading to the release of neurotransmitters at the base of the hair cell. These neurotransmitters then stimulate the afferent auditory nerve fibers (type I fibers) that synapse with the inner hair cells, transmitting the electrical signals to the brain for further processing and interpretation as sound.
Damage or loss of these inner hair cells can lead to significant hearing impairment or deafness, as they are essential for normal auditory function. Currently, there is no effective way to regenerate damaged inner hair cells in humans, making hearing loss due to their damage permanent.
Hair removal is the deliberate elimination or reduction of body hair. This can be achieved through various methods, both temporary and permanent. Some common temporary methods include shaving, waxing, tweezing, and depilatory creams. Permanent methods may involve laser hair removal or electrolysis, which target the hair follicle to prevent future growth. It's important to note that some methods can have side effects or risks, so it's recommended to consult with a healthcare professional or dermatologist before starting any new hair removal regimen.
Hair dyes are chemical substances that are used to change the color of hair. They contain various types of dyes, including natural dyes derived from plants and minerals, synthetic dyes, and combinations of both. Hair dyes work by penetrating the outer layer of the hair shaft (the cuticle) and bonding with the hair's pigment (melanin) or depositing new color particles within the hair shaft.
There are three main types of hair dyes: temporary, semi-permanent, and permanent. Temporary hair dyes coat the outside of the hair shaft and wash out after a few shampoos. Semi-perermanent hair dyes penetrate slightly into the hair shaft and fade gradually over several washes. Permanent hair dyes contain chemicals that open the cuticle and allow the dye to penetrate deep into the hair shaft, where it reacts with the hair's natural pigment to create a new color that is resistant to fading and washing out.
It is important to note that some hair dyes may contain potentially harmful chemicals, such as coal tar dyes, para-phenylenediamine (PPD), and resorcinol, which have been linked to allergic reactions, skin irritation, and other health problems. It is recommended to perform a patch test before using any new hair dye product and to follow the manufacturer's instructions carefully to minimize the risk of adverse effects.
Vestibular hair cells are specialized sensory receptor cells located in the vestibular system of the inner ear. They play a crucial role in detecting and mediating our sense of balance and spatial orientation by converting mechanical stimuli, such as head movements and gravity, into electrical signals that are sent to the brain.
The hair cells are shaped like a tuft of hair, with stereocilia projecting from their tops. These stereocilia are arranged in rows of graded height, and they are embedded in a gel-like structure within the vestibular organ. When the head moves or changes position, the movement causes deflection of the stereocilia, which opens ion channels at their tips and triggers nerve impulses that are sent to the brain via the vestibular nerve.
There are two types of vestibular hair cells: type I and type II. Type I hair cells have a large, spherical shape and are more sensitive to changes in head position, while type II hair cells are more cylindrical in shape and respond to both linear and angular acceleration. Together, these hair cells help us maintain our balance, coordinate our movements, and keep our eyes focused during head movements.
Auditory outer hair cells are specialized sensory receptor cells located in the cochlea of the inner ear. They are part of the organ of Corti and play a crucial role in hearing by converting sound energy into electrical signals that can be interpreted by the brain.
Unlike the more numerous and simpler auditory inner hair cells, outer hair cells are equipped with unique actin-based molecular motors called "motile" or "piezoelectric" properties. These motors enable the outer hair cells to change their shape and length in response to electrical signals, which in turn amplifies the mechanical vibrations of the basilar membrane where they are located. This amplification increases the sensitivity and frequency selectivity of hearing, allowing us to detect and discriminate sounds over a wide range of intensities and frequencies.
Damage or loss of outer hair cells is a common cause of sensorineural hearing loss, which can result from exposure to loud noises, aging, genetics, ototoxic drugs, and other factors. Currently, there are no effective treatments to regenerate or replace damaged outer hair cells, making hearing loss an irreversible condition in most cases.
Hair preparations refer to cosmetic or grooming products that are specifically formulated to be applied to the hair or scalp for various purposes such as cleansing, conditioning, styling, coloring, or promoting hair growth. These preparations can come in different forms, including shampoos, conditioners, hair masks, serums, gels, mousses, sprays, and dyes. They may contain a wide range of ingredients, such as detergents, moisturizers, proteins, vitamins, minerals, and other nutrients that can help improve the health, appearance, and manageability of the hair. Some hair preparations may also contain medications or natural extracts that have therapeutic properties for treating specific hair or scalp conditions, such as dandruff, dryness, oiliness, thinning, or hair loss.
Alopecia is a medical term that refers to the loss of hair or baldness. It can occur in various parts of the body, but it's most commonly used to describe hair loss from the scalp. Alopecia can have several causes, including genetics, hormonal changes, medical conditions, and aging.
There are different types of alopecia, such as:
* Alopecia Areata: It is a condition that causes round patches of hair loss on the scalp or other parts of the body. The immune system attacks the hair follicles, causing the hair to fall out.
* Androgenetic Alopecia: Also known as male pattern baldness or female pattern baldness, it's a genetic condition that causes gradual hair thinning and eventual hair loss, typically following a specific pattern.
* Telogen Effluvium: It is a temporary hair loss condition caused by stress, medication, pregnancy, or other factors that can cause the hair follicles to enter a resting phase, leading to shedding and thinning of the hair.
The treatment for alopecia depends on the underlying cause. In some cases, such as with telogen effluvium, hair growth may resume without any treatment. However, other forms of alopecia may require medical intervention, including topical treatments, oral medications, or even hair transplant surgery in severe cases.
The saccule and utricle are components of the vestibular system, which is responsible for maintaining balance and spatial orientation within the inner ear. Here are the medical definitions:
1. Saccule: A small sac-like structure located in the vestibular labyrinth of the inner ear. It is one of the two otolith organs (the other being the utricle) that detect linear acceleration and gravity. The saccule contains hair cells with stereocilia, which are embedded in a gelatinous matrix containing calcium carbonate crystals called otoconia. When the head changes position or moves linearly, the movement of these otoconia stimulates the hair cells, sending signals to the brain about the direction and speed of the motion.
2. Utricle: Another sac-like structure in the vestibular labyrinth, similar to the saccule but slightly larger. The utricle is also an otolith organ that detects linear acceleration and head tilts. It contains hair cells with stereocilia embedded in a gelatinous matrix filled with otoconia. When the head tilts or moves linearly, the movement of the otoconia stimulates the hair cells, providing information about the position and motion of the head to the brain.
In summary, both the saccule and utricle are essential for maintaining balance and spatial orientation by detecting linear acceleration and gravity through the movement of otoconia on their hair cell receptors.
The cochlea is a part of the inner ear that is responsible for hearing. It is a spiral-shaped structure that looks like a snail shell and is filled with fluid. The cochlea contains hair cells, which are specialized sensory cells that convert sound vibrations into electrical signals that are sent to the brain.
The cochlea has three main parts: the vestibular canal, the tympanic canal, and the cochlear duct. Sound waves enter the inner ear and cause the fluid in the cochlea to move, which in turn causes the hair cells to bend. This bending motion stimulates the hair cells to generate electrical signals that are sent to the brain via the auditory nerve.
The brain then interprets these signals as sound, allowing us to hear and understand speech, music, and other sounds in our environment. Damage to the hair cells or other structures in the cochlea can lead to hearing loss or deafness.
The Organ of Corti is the sensory organ of hearing within the cochlea of the inner ear. It is a structure in the inner spiral sulcus of the cochlear duct and is responsible for converting sound vibrations into electrical signals that are sent to the brain via the auditory nerve.
The Organ of Corti consists of hair cells, which are sensory receptors with hair-like projections called stereocilia on their apical surfaces. These stereocilia are embedded in a gelatinous matrix and are arranged in rows of different heights. When sound vibrations cause the fluid in the cochlea to move, the stereocilia bend, which opens ion channels and triggers nerve impulses that are sent to the brain.
Damage or loss of hair cells in the Organ of Corti can result in hearing loss, making it a critical structure for maintaining normal auditory function.
The scalp is the anatomical region located at the upper part of the human head, covering the skull except for the face and the ears. It is made up of several layers: the skin, the connective tissue, the galea aponeurotica (a strong, flat, tendinous sheet), loose areolar tissue, and the periosteum (the highly vascularized innermost layer that attaches directly to the skull bones). The scalp has a rich blood supply and is home to numerous sensory receptors, including those for touch, pain, and temperature. It also contains hair follicles, sebaceous glands, and sweat glands.
Hair disease
HSE - Skin at work: Work-related skin diseases - Hair Dressing
Report Alopecia - A hair loss disease | symptoms
Genetic Hair Loss Linked to Other Diseases?
Genetics of Menkes Kinky Hair Disease: Background, Pathophysiology, Epidemiology
Dumaguing: Grey hair linked with increased heart disease risk in men - SUNSTAR
Graft-versus-Host Disease: Skin, Hair and Nails | BMT Infonet
A Case Report of Cushing's Disease Presenting as Hair Loss | Case Reports in Dermatology | Karger Publishers
Lyme disease has an often overlooked symptom: hair loss
PRIME PubMed | Restoration of hair growth in mice with an alopecia areata-like disease using topical anthralin
7-YEAR-OLD SPRING VALLEY GIRL WITH BLOOD DISEASE GIVES BACK, CUTS HER TWO FEET OF HAIR | East County Magazine
Stress Hormones In Hair of Pigs Offer Potential to Help Identify Genetic Lines Resilient to Disease | Farms.com
Trichoscopy Advances Hair and Scalp Disease Diagnoses
Hair Product May Increase Risk for Uterine Disease
Excessive or unwanted hair in women: MedlinePlus Medical Encyclopedia
fine hair | Hereditary Ocular Diseases
Hair loss and Lou Gehrig's Disease: Are They Related? - Miami Hair Institute
Autoimmune Diseases And Hair Loss - ST. TROPICA
Hair Loss and Crohn's Disease?
Ayurvedic Treatment for Hair / Trichology Disease
Skin and hair diseases Hormone therapies - Dr HERTOGHE MEDICAL SCHOOL
Common Diseases Of Skin And Hair
Hair loss, erectile dysfunction: Treatment of common diseases in men
Autoimmune Disease And Hair Loss | Guci Image
Heart Disease Archives | Hair Loss Cure 2020
