2014 Group Project 5

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2014 Student Projects
2014 Student Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7 | Group 8
The Group assessment for 2014 will be an online project on Fetal Development of a specific System.

This page is an undergraduate science embryology student and may contain inaccuracies in either description or acknowledgements.

Integumentary

--Mark Hill (talk) 15:16, 26 August 2014 (EST) OK you have some headings, how about some content, references, sources for each section. See Lab 3 Assessment.

--Mark Hill (talk) 11:48, 6 September 2014 (EST) This is a start. Less textbook referencing please, more research/reviews from the published literature. Textbooks should not be used as primary sources, I am happy for them to be listed as related literature.

Introduction

Development Overview

Skin

Week Description Phase Diagram
Week 4-5 Example Example
Week 5-6 Example Example
Week 8-10 Example Example
Week 12 Example Example
Week 40 (birth) Example Example
Adult Example Example

Glands

Hair

Nail

Teeth

<pubmed>19701759</pubmed>

Current Research

  • Fetal skin wound healing:[1]
  • Biology and function of fetal and pediatric skin:[2]
  • Selective D2-40 lymphatic endothelium immunoreactivity in developing human fetal skin appendages:[3]
  1. <pubmed>19803418</pubmed>|[1]
  2. <pubmed>23369584</pubmed>|[2]
  3. <pubmed>19725270</pubmed>|[3]

Historic Findings

Skin


Glands

Sebacious glands

Sweat glands

Hair

Technology

The

<pubmed>5656140</pubmed>

The development of hair was noted to be a cycling phenomenon in 1959 from Chase and Eaton's experiments on the.

In 1953 Chase, Montagna and Malone concluded that with the development of the hair follicle the surrounding skin goes under. They determined the mechanism of hair follicle development.

Downwards growth of the follicle from the level of the dermis during the quiecent phase thought he adipose layer during gowth and differntiation.

They also established that upward movement of hair inovlves the addition of ne cells from the matrix of the follicle and an enlargement of each cell.

Furthermore their research also showed that the epidermal and dermal layers were dynamic and interacting with each other.

The most significant developments in the understanding of hair follicle development came from studies investigating the differentiation pattern of cells as the follicle develops.


<pubmed>4097391</pubmed>

Nail

Teeth

Abnormalities

Skin

  • Aplasia cutis congenita
Aplasia cutis congenita (ACC) is a rare skin abnormality, characterised by the absence of all layers of the skin. It is most common to occur on the scalp (70%), specially the vertex. In severe cases, the defect can go as deep as the bone or the dura. Other sites of ACC include the skin of the limb regions. “ACC occurs in approximately 1 in 10000 live births, with a female-to-male ratio of 7:5.” The specific aetiologic agent for ACC is still unknown. It has been suggested to be genetic and/or environmental. The damage to the vertex is suggested to be the result of the biomechanical stretch at this area when the fetal brain is growing.
Presently, ACC is managed via conservative treatments or surgical treatments. Conservative treatments refer to basic wound treatments and preventing infection with the use dressings and antibiotics. Surgical treatments, specifically scalp reconstruction procedures, aim to reconstruct the damage to the skin through skin grafts, local scalp flaps, and pericardial scalp flaps. Large defects are often treated using surgical treatments.

<pubmed>22549580</pubmed> <pubmed>23147310</pubmed>

  • Neuroblastoma

Glands

  • Hypohidrotic Ectodermal Dysplasia

<pubmed>25140498</pubmed>

Hair

  • Congenital alopecia areata
Alopecia areata (AA) is an abnormality of the hair affecting anagen hair follicles, characterised by well-demarcated patches of hair loss. It is non-scarring and can occur on the scalp and/or the body. 90% of AA cases occur on the scalp. 5%-10% of patients with AA lose all hair on their scalp; this is called alopecia totalis. While others lose all of their body hair, this is called alopecia universalis. Its pathogenesis is considered to be both genetic and autoimmune. There is an abnormality with the genes related to the immune system and to the hair follicles. And histopathology shows signs of lymphatic infiltration of the hair follicles and the loss of these scalp lymphocytes allow hair follicles to recover.
There is currently no cure for AA. There are several treatments to combat AA but none of these have led to remission of the disease, the most effective being corticosteroids and topical immunotherapy. Recently, a new method of treating alopecia areata is being studied. Transepidermal drug delivery (TED) is a new treatment that functions by creating micro-channels in the epidermis. By doing so, drug delivery to the skin is improved. This treatment was highly effective and had lower rates of side effects, e.g. pain, compared to previous treatments.

<pubmed>15692503</pubmed> <pubmed>17269961</pubmed> <pubmed>16338213</pubmed> <pubmed>23947678</pubmed> <pubmed>25000998</pubmed> <pubmed>25260052</pubmed>

Nail

  • Anonychia
  • Ectopic Nail

Teeth

  • Adontia
  • Amelogenesis imperfecta