Revision as of 00:44, 10 September 2014

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.

Renal

--Mark Hill (talk) 15:11, 26 August 2014 (EST) No subheadings yet and I even had to add your project title! Get moving.

--Mark Hill (talk) 16:00, 6 September 2014 (EST) OK some sub-headings and a few refs. No content yet expelling the feral component or how the references you have selected relate to the topic.

Introduction

Historic findings

Developmental Timeline

Current research models

Kidney

Structures that arise from the Ureteric bud

Structures that arise from the Metanephric mesoderm

Development of the kidneys

The kidneys first develop in the embryo by a process called nephrogenesis, in which self-renewing mesenchymal renal stem cells produce nephrons to form a simple embryonic kidney, called the pronephros. Nephrons are the main functional unit of the kidney.

An embryonic gene named gremlin (GREM1) has been found to play a key role in the formation of the kidneys and nephrogenesis in general. When fully formed, the expression of this gene is relatively low in an adult. However, it is thought that many renal diseases and their progressions are linked to an overexpression of this gremlin gene.

Nephrogenesis is stimulated by the signaling between the epithelial ureteric buds and progenitor cells, causing nephrons to develop and the ureteric buds to branch.

At birth, although the infant’s kidneys are developed enough to maintain homeostasis and are sufficient for growth and development, their functional capabilities are decreased. This is a result of the transition from depending on the placenta to maintain homeostasis of fluid and electrolyte balance while in-utero, to maturation of the neonatal glomeruli once born.

Determining nephron number is important: it can show the success/extent of nephrogenesis, and thus be used to determine if any and what genes and environmental factors may aid this process; a low nephron count has been linked to multiple cardiovascular and renal disease later in life.

Urethra

Urine Formation + Amniotic Sac

Polyhydramnios and oligohydramnios

amniotic fluid: not just urine anymore

Sebe. P., Schwentner. C., Oswald. J., Radmayr. C., Bartsch. G., Fritsch. H. Fetal development of striated and smooth muscle sphincters of the male urethra from a common primordium and modifications due to the development of the prostate: an anatomic and histologic study. Prostate (2005) [1]

Werff. V. D., Nievelstein. R.A, Brands. E., Luijsterburg. A.J., Vermeij-Keers. C. Normal development of the male anterior urethra. Teratology (2005) [2]

Sebe. P., Fritsch. H., Oswald. J., Schwentner. C., Lunacek. A., Bartsch. G., Radmayr. C. Fetal development of the female external urinary sphincter complex: an anatomical and histological study. J urol (2005) [3]

Ludwikowski B, Hayward OI, Brenner E, Fritsch H. The development of the external urethral sphincter in humans. BJU Int. 2001 Apr;87(6):565-8. [4]

Ureter

Bladder

The urinary bladder develops in the first 12 weeks of gestation from the urogenital sinus and the surrounding splanchnic mesenchyme, these development events are controlled by by complex epithelial–mesenchymal signals. The vesical part of the urogenital sinus is attached to the allantois and goes on to form the bladder.

During foetal development the bladder is supplied by an increasing number of nerves in the detrusor muscle, as the gestational period continues different peptide containing nerves are observed.

During development the bladder only produces immature reflexes rather than the voluntary bladder control that is only seen once the infant is toilet trained. It is suggested that the switch between involuntary reflexes and voluntary contractions is due to the development of the central and peripheral neural pathways that control the contraction of the bladder.

Abnormalities

The overexpression of the gremlin gene (GREM1) has been found to be a cause of renal disease.

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 ==Current research models==
+<pubmed>25143451</pubmed>
 ==Kidney==

2014 Group Project 2: Difference between revisions