How Hair And Maintenance Depend On The Different Signaling Interaction Between The Epithelium And Underlying Mesenchyme

In our study, the epidermal expression of LXRα was more pronounced in the basal cell layer. This is in agreement with the finding of Russell et al. who supposed an explanation that it may correlate with the site of hair follicle melanocytes or may be due to presence of LXRα in primary immortalized epidermal keratinocytes which locate basally [13]. The presence of LXRα and LXRβ mRNA within human primary immortalized epidermal keratinocytes was also documented by Hanley et al. [20].

Many people limit alopecia to one thing, human hair loss. However, it has a tremendous impact on many species in our society Et. Al’s Frey, Rebecca J., PhD, and Taryn Terry (2016). When thinking about alopecia, many people only think about the hair on top of their head. Alopecia can be found anywhere on the human body also on some animals. There is a wide spectrum that results in having alopecia ranging from inflammation, harsh chemicals, mental disorders too hereditary Kapes, Beth A., et al. "Alopecia." (2015). For centuries men, woman, and animals has suffered from this disease. Research is still ongoing till this day, but many treatments has been found to help Et. Al’s Frey, Rebecca J., PhD, and Taryn Terry (2016).

Purpose: The purpose of this study was to determine whether or not degenerated hair cells within the cochlea could be regenerated using the introduction of ATOH1. ATOH1 is a transcription factor that is known to be essential to hair cell growth and development. Typically, damaged hair cells within the cochlea result in permanent sensorineural hearing loss and this study aimed to see if these results could be reversed using guinea pigs as the study participants.

In basic terms, alopecia is a term used in medical circles to refer to baldness. With that in mind, it can be noted that alopecia areata is just one of the many conditions associated with hair loss. In most cases, the condition is occasioned by some round patches of bald spots in the affected individual's head. In some cases, affected individuals can experience total hair loss. In this text, I will discuss the condition and amongst other things highlight its causes, symptoms and treatment.

Losing hair is very frustrating that affects most of the people around the world. Today, about 50% of women and 60% of men suffer from hair loss. The most common type of hair loss is androgenic alopecia that affects both the sexes, it is also known as “male pattern baldness” and female pattern baldness”. People shed 100 hairs per day based on their scalp that contain hair follicles (100,000 hair follicles is average). But what causes hair loss? There are many reasons behind hair loss such as anemia, some disease, low vitamin and protein level, stress, aging, menopause, pregnancy, puberty, crash diet and others.

The mitochondrial pathway, also called intrinsic pathway, because it is initiated from inside the cell. Various stimuli such as growth factors withdrawal, DNA-damage, hypoxia, and oxidative stress can induce apoptosis through this cascade. These insults cause increasing permeability of the outer mitochondrial membrane and opening of the mitochondrial permeability transition (MPT) pore which is controlled by members of the Bcl-2 family proteins. This large family of proteins is defined by the presence of conserved Bcl-2 homology domains (BH1 to BH4). Up to 30 Bcl-2 family genes have been identified in mammals, which have either pro-apoptotic or anti-apoptotic functions. Some of the anti-apoptotic members include Bcl-2 itself, Bcl-XL, Bcl-w, BAG and Mcl-1 which possess all domains of BH1 to BH4. The pro-apoptotic family proteins can be divided into two subgroups: consists of Bak, Bax, and Bok with possess BH1 to BH3 domains, and Bad, Bid, Bik, BNIP3, Bim, Bmf, Blk, Hrk, Noxa, Puma, and Spike) that only possesses BH3 domain [Cory, 2002; Mund, 2003]. It is believe that BH3-only proteins interfere with the fine-tuned balance of homo- or hetero-oligomerization between pro-apoptotic multidomains (eg., Bax/Bak) and anti-apoptotic members (eg., Bcl-2/Bcl-XL) (Figure 3). In general, oligomers of Bak, Bax, and Bok induce PMT, either by forming channels by themselves or by interacting with components of the PMT [Antonsson, 2000]. Bad can also heterodimerize

Also known as Cicatrical Alopecia, Scarring Alopecia is usually caused by complications of other conditions like scleroderma or discoid lupus. Here, the hair follicle (the little opening in your skin where your single hair grows out of) is totally crushed, resulting to the hair not having the capacity to grow back. Unlike Alopecia Areata, the bald patches in the scalp look more “ragged.” This is due to the destruction of the hair follicle that occurs below the skin surface so there may not be much to actually see on the scalp skin surface other than patchy hair loss. Up until today, less is known about the causes of Scarring Alopecia. What is known is that the affected areas may be smooth and clean, or may have redness,

According to Rachel Krause, a strand of hair can support a weight of one-hundred grams. When a strand is multiplied by one hundred thousand to one hundred fifty thousand strands, the approximated number of hairs on a human head, the hair on one’s head can support the weight of two elephants (Krause). Mammals can grow hair on nearly every part of their bodies; therefore, something so small and common must be simple and not complicated-- false. Hair actually has rather complex components including the necessary factors and structure.

LASSO enriched landmark genes with 421, 333, 123 features in the CM profiles of {\textit{NOMILIN}}, {\textit{ZARDAVERINE}}, and {\textit{HYDROCOTARNINE}}, respectively (Supplementary Table 2). We did not find a significant similarity between cell morphological gene sets associated with morphological features in response to the compound treatments, and different gene sets enriched with an indicated morphological change (Supplementary Figure~25). These findings suggest that landmark genes do not acting immediately proximal to a variety of regulatory molecules involved in cell morphology and organization of components of the cytoskeleton.

Our hair is made up of two parts. The shaft is the colored part that we see, and the root is the part that attaches the hair to the scalp. The roots of our hair is surrounded by follicles, which are tubes of tissue located under the skin. The follicles have pigment cells in them that produce a chemical called melanin. Melanin is what gives our hair its color, and also gives humans their skin tone. As we age, pigment cells in our hair begin to die which causes less melanin to be created. The fewer melanin in your hair, the more gray your hair will become. Getting gray hair is genetic, and because of this individuals get gray hair around the same time that their parents or grandparents did. Getting gray hair is also associated with aging.

The composition of hair is made up of different complex fibers. The composition of hair has chemical elements. The essential elements are amino acids, keratin, protein and melanin. There are many components of hair which means the system is unified. A unified system of hair is different chemical elements come together to maintain a system of unified hair. For example, the unified system, if properly maintained, can develop water, proteins, lipids and hair pigments.

Although the exact mechanisms underlying the biological effects of Polyp still remain to be elucidated, it could be concluded that Polyp has an important role in cell proliferation and apoptosis. (19, 24). Based on the studies mentioned above, Polyp regulates the apoptosis and cell proliferation via different mechanisms including; activation of caspase-3, externalization of phosphatidylserine, arresting the cell cycle and altering the interaction between histone and DNA(14,19). This observation would imply that Polyp could modulate apoptosis inside the cell, but evidences is insufficient. It was also found that Polyp plays an important role in regulating the cell

There are approximately one hundred thousand hairs on a healthy human scalp (Roe 2011). The three stages of the hair growth cycle are: The first stage is the anagen phase or growing stage; the catagen phase is when the production of hair follicle stops and; the telogen phase or the resting stage is when the hair begins falling (Philip Kingsley,

To accomplish this, researchers knocked down Malat1 expression using short hairpin RNA (shRNA) molecules, which resulted in elevated levels of myogenic RNA and protein markers2. Therefore, the reduction in Malat1 expression following shRNA knockdown allowed for increased myogenic protein synthesis. Consequently, Malat1 expression suppressed C2C12 differentiation and promoted cellular proliferation2. Additionally, an RNA immunoprecipitation assay (RIP) was used to study the mechanism of interaction between Malat1 ncRNA and the repressive cofactor Suv39h12. Researchers utilized antibodies with an affinity for Suv39h1 to precipitate the cofactor out of the C2C12 myoblasts2. Once the Suv39h1 complexes were precipitated, the cellular material was purified and analyzed using reverse transcription polymerase chain reaction (RT-PCR)2. Following RT-PCR analysis, researchers found significant quantities of Malat1 associated with the precipitated antibody/cofactor complex, indicating that Malat1 interacted with Suv39h1to repress the MyoD gene loci in the differentiating

Inhibition of this pathway was seen to decrease the neuroblastoma tumour mass as well as the oncogene MYCN protein expression, and in neuroblastoma cells lines the use of AKT specific inhibitors induced apoptotic cell death. Another pathway relevant to MYCN is the glycogen synthase kinase 3 (GSK3) pathway which is known to be involved in a large number of signalling pathways [e.g., Wnt, PI3K/Akt, mitogen–activated protein kinase (MAPK), and p53], many of which are associated with the neural crest. Wnt signalling is known to be crucial in the induction, delamination and differentiation of the neural crest and GSK3 is seen to be a negative mediator of this pathway. Mammalian GSK3 is generated from two genes GSK3α and GSK3β, GSK3β phosphorylates and stabilizes the MYCN protein, this in turn can enable the dephosphorylation of a different site that can lead to MYCN degradation.