From Embryology

Individual Assessments

Lab 1 Assessment

1. Identify the origin of In Vitro Fertilization and the 2010 nobel prize winner associated with this technique and add a correctly formatted link to the Nobel page.

The History of In Vitro Fertilisation

In vitro fertilisation (IVF) refers to the process of artificial fertilisation conducted ex vivo. The IVF technique was first described for non-human use. The earliest known research conducted was by Walter Heape from Cambridge University in the 1890s who reported the first known case of embryo transplantation in rabbits. In 1959, Dr. Min Chueh Chang published his work in Nature describing the first successful mammalian live birth (rabbits) after IVF therapy.

Eventually, the use of IVF for humans became a possibility and then a reality: in 1978, the first successful birth from IVF occurred in England. The success of this IVF birth is credited to Patrick Steptoe and Robert Edwards. In 2010, Edwards was awarded the Nobel Prize in Medicine for the development of human IVF therapy. Because of IVF, many couples have been given a chance to conceive. However, the history of IVF is still in the making with constant improvements in the technology being developed and applied.

2. Identify and add a PubMed reference link to a recent paper on fertilisation and describe its key findings (1-2 paragraphs).

Research in Fertilisation

In order for fusion between mammalian gametes to occur, a spermatozoon must first pass through the external layers surrounding the oocyte: the cumulus oophorus and the zona pellucida (ZP). It is believe that the acromosome reaction (AR) of the spermatozoa starts upon contact with the zona pellucida. Consequently, the cumulus cell layer is typically removed in studies of mouse sperm-oocyte interactions in order to facilitate fertilisation. The recent experiments of Jin et al. [1] sought to answer the question: "Where does the fertilising mouse spermatozoon begin the AR - in the cumulus [of the oocyte] or the zona pellucida?" Jin et al. [1] utilised fluorescence microscopy and transgenic mouse spermatozoa to conduct their investigation. Additionally, Jin et al. [1] used cumulus-free oocytes and cumulus-enclosed oocytes to study the role of the cumulus cells in fertilisation.

From the experiment, Jin et al. [1] found that most fertilising spermatozoa begin the AR before their first contact with the ZP. The significance of this finding was that the spermatozoa with intact acromosomes at the ZP seldom had the ability to penetrate through [1]. In contrast, spermatozoa which had already began the AR could easily penetrate the ZP. In regards to the role of the cumulus cells, it was found that cumulus-enclosed oocytes had a higher incidence of fertilisation compared to cumulus-free oocytes [1]. Moreover, cumulus-free oocytes had an increased incidence of in vitro fertilisation when incubated with other cumulus-enclosed cells; this finding suggests that cumulus cells harbour an important role in fertilisation [1]. However, it is notable that when cumulus-free oocytes were incubated in a cumulus-conditioned medium, no increase in fertilisation rate was noted[1]. Overall, two conclusions were made: firstly, that the AR is required by the spermatozoa prior to meeting the ZP for effective fertilisation[1]. Secondly, the cumulus oophorus confers benefit in increasing the chance of fertilisation[1].


  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 <pubmed>21383182</pubmed>

--Mark Hill 16:58, 11 September 2012 (EST) Question 1 is answered well and linked to appropriate resources. Question 2 is also quite a complete answer to what I requested. The formatting of your description could have been better organised, while it is correct to cite the paper when referring to the findings, this is a little overboard with 9 times within 2 paragraphs. If you had organised the information differently this could have been reduced to 1-2 citations within the text. Alternatively the findings could have been provided as a bullet or numbered list. 10/10

Lab 2 Assessment

1. Upload an image from a journal source relating to fertilization or the first 2 weeks of development as demonstrated in the practical class. Including in the image “Summary” window: An image name as a section heading, Any further description of what the image shows, A subsection labeled “Reference” and under this the original image source, appropriate reference and all copyright information and finally a template indicating that this is a student image.

Patterns of ZPC Deposition in Porcine Oocyte-Cumulus Complexes

Patterns of ZPC Deposition in Porcine Oocytes.jpg

Immunofluorescence Detection for ZPC and Ubiquitin in a Porcine Oocyte [1]


  1. <pubmed>21383844</pubmed>

2. Identify a protein associated with the implantation process, including a brief description of the protein's role (1-2 paragraphs).

Trophinin and Implantation

Trophinin is a membrane protein expressed in chorionic villi trophoblasts and in the maternal endometrium. In the early stages of pregnancy, trophinin is strongly expressed along with tastin and bystin, which form a complex; this complex mediates apical cell adhesion between the trophoblasts and the endometrial epithelial cells[1]. The time frame in which trophinin is expressed on the apical aspect of the endometrial cells coincides with the "implantation window"[1]; the period in which successful implantation is possible. Trophonin-trophonin adhesion during implantation occurs via signal transduction with bystin and tastin[2]. As a consequence of trophinin-trophinin adhesion, trophectoderm cells become activated for implantation[2]. Moreover, there have been reports that endometrial epithelial cells undergo apoptosis upon blastocyst adhesion; human trophoectoderm cells express the Fas ligand which interacts with Fas expressed on the endometrium[2]. However, other studies have shown that trophinin-mediated cell adhesion can induce endometrial cell apoptosis through mechanisms other than the Fas/FasL cascade[2].

In regards to ectopic pregnancies located within the fallopian tube, research has shown that trophinin is strongly expressed by both the embryonic trophoblasts and maternal fallopian tube epithelium, induced by human chorionic gonadotrophin (hCG)[1]. These findings highlight the function of trophonin in facilitating implantation in conjunction with its role in the pathogenesis of ectopic pregnancies.


  1. 1.0 1.1 1.2 <pubmed>14633596</pubmed>
  2. 2.0 2.1 2.2 2.3 <pubmed>22201876</pubmed>

--Mark Hill 17:04, 11 September 2012 (EST) Question 1 image has been correctly uploaded and contains all the requested information in the summary box. Question 2 is a good description of this recent paper on trophinin and Implantation. 10/10

Lab 3 Assessment

1. Identify the difference between "gestational age" and "post-fertilisation age" and explain why clinically "gestational age" is used in describing human development.

Gestational Age versus Post-Fertilisation Age

Gestation is the period of time between conception and birth (Kaneshiro, 2011; Vishton, 2011). Gestational age is the developmental age of the conceptus based on the presumed first day of the last normal menstrual period to the current date, measured in weeks (Kaneshiro, 2011; Vishton, 2011). In contrast, post-fertilisation age refers to the age of the conceptus expressed in elapsed time since fertilisation (Vishton, 2011). Gestational age is approximately two weeks greater than post-fertilization age (Kaneshiro, 2011; Vishton, 2011). Gestational age is used in human development because its start date can be determined by asking the mother when was the presumed first day of the last normal menstrual period (Kaneshiro, 2011; Vishton, 2011). In contrast, the moment of fertilization must be inferred (Vishton, 2011).


Kaneshiro, N. K. (2011). Gestational age. Retrieved from

Vishton, P. M. (2011). Embryo Foetus Development Stages. Retrieved from

2.Identify using histological descriptions at least 3 different types of tissues formed from somites.

Tissues Derived From Somites

1. Bone (Sclerotome)

Bone tissue consists of cells separated by an extracellular matrix with organic and inorganic components (Marieb, Wilhem & Mallatt, 2010). The organic components of bone consists of cells, collagen fibres and ground substance. The cells include osteoprogenitor cells which give rise to osteoblasts: the producers of new bone matrix (osteoid). Mature osteoblasts, called osteocytes, are trapped in lacunae where they maintain the mature bone; osteocytes may revert to osteoblasts in the incidence of a fracture. Osteoclasts are multinucleated cells with ruffled plasma membrane borders and are involved in bone resorption. Bone resorption is important for bone remodelling to improve tensile strength as well as remodel the newly deposited woven bone into mature bone after a fracture. There are two types of mature (lamellar) bone: compact bone and spongy bone (Marieb et al., 2010). The compact bone occurs towards the periphery and is arranged in Haversian systems: lamellae concentrically arranged around a central Haversian canal containing blood vessels, nerves and osteocytes (Marieb et al., 2010). The different Haversian systems communicate with each other, the periosteum and endosteum through the Volkmann's canals. In contrast, spongy bone in the mature adult appears towards the centre of the diaphysis and metaphysis and is arranged in bony shelves (trabeculae) (Marieb et al., 2010). The gross porous arrangement of spongy bone is important for housing the bone marrow (Marieb et al., 2010)

2. The Skin (Dermotome)

a. Dermis: The dermis is made up of two main regions: (1) the superficial papillary layer and (2) the deeper reticular layer (Marieb et al., 2010). The superficial papillary layer makes up 20% of the dermis and is areolar connective tissue consisting of collagen and elastic fibres; it includes the dermal papillae which extend into the overlying epidermis to strengthen the dermal-epidermal junction and increase surface area for nutrient, gas and waste exchange with the avascular epidermis (Marieb et al., 2010). The reticular layer is composed of dense irregular connective tissue with thick bundles of collagen and elastic fibres arranged in different planes (Marieb et al., 2010). Other cells interspersed among the connective tissue of the dermis include fibroblasts, macrophages, mast cells and other white blood cells including lymphocytes(Marieb et al., 2010). The dermis is highly vascular and supplied with nerve fibres (Marieb et al., 2010). There are two vascular plexuses; the deep dermal plexus and the subpapillary plexus (Marieb et al., 2010). These vessels serve not only for nutrient supply to the dermis and epidermis, but for temperature regulation as well (Marieb et al., 2010).

b. Hypodermis: The subcutaneous layer, or fatty hypodermis, consists of areolar and adipose connective tissue(Marieb et al., 2010). The cellular components include adipocytes as well as white blood cells (Marieb et al., 2010). The hypodermis serves to store fat and anchor the skin to underlying structure in a manner that the skin can slide over structures(Marieb et al., 2010). Additionally, the adipose in the hypodermis serves an insulator.

3. Skeletal Muscle (Myotome) Skeletal muscle fibres come together to form a larger skeletal muscle surrounded by different levels of connective tissue "coats": the epimysium surrounds the whole skeletal muscle, the perimysium covers each fascicle and the loose CT endomysium separates each skeletal muscle fibre (Marieb et al., 2010). The skeletal muscle fibres are long cylindrical cells with a diameter between 10-100um (Marieb et al., 2010) . These muscle fbres are formed by the fusion of embryonic cells and hence contain many nuclei which are located at the periphery of each fibre beneath the sarcolemma, the skeletal muscle cell membrane (Marieb et al., 2010). These muscle fibres appear striated because of the internal organelles of the muscle fibres: myofibrils, the contractile organelles of muscle tissue (Marieb et al., 2010).


Marieb, E. N., Wilhelm, P. B., Mallatt, J. (2010). Human Anatomy (6th ed.). San Francisco, CA: Pearson Education, Inc.

--Mark Hill 17:10, 11 September 2012 (EST) Question 1 Clearly identified and cited the difference between "gestational age" and "post-fertilisation age". Question 2 you have also identified histological descriptions at least 3 different types of tissues formed from somites. For both questions you could have formatted the references and the reference list by using the <ref></ref> tags and simply inserted any text that you wanted in your list between the tags. 10/10

Lab 4 Assessment

Prenatal Diagnostic Techniques

1. Identify the 2 invasive prenatal diagnostic techniques related to the placenta and 2 abnormalities that can be identified with these techniques.

  • Amniocentesis [1]: Amniocentesis refers to sampling of the amniotic fluid by inserting a needle through the mother's anterior abdominal and uterine walls into the amniotic cavity by piercing the chorion and amnion. This technique is performed at 15 and 18 weeks gestation. Amniocentesis is often used to detect genetic disorders as it allows for chromosome analysis. One abnormality which can be detected is trisomy 21 (Down's Syndrome)[1]. Additionally, amniocentesis can be utilised for alpha-fetoprotein assays to detect neural tube defects like spina bifida [1].
  • Chorionic Villus Sampling [1]: Biopsies of trophoblastic tissue are obtained by inserting a needle through the mother's abdominal wall and uterine walls to the uterine cavity. Sampling can also be performed through the cervix with a polyethylene catheter, guided by real-time ultrasonography. CVS can be performed sooner than amniocentesis at 10 and 12 weeks of gestation. However, the rate of miscarriage from CVS is higher than amniocentesis. Like amniocentesis, CVS can be used to detect chromosomal abnormalities like trisomy 21 as well as trisomy 18. Additionally, Tay-Sachs disease can be detected with CVS [1].

The Therapeutic Use of Cord Stem Cells

2. Identify a paper that uses cord stem cells therapeutically and write a brief (2-3 paragraph) description of the paper's findings.

Fu et al. (2006) sought to isolate human umbilical cord mesenchymal stem cells (HUCMSCs) and transform them into dopaminergic neurons in vitro [2]. The experiment was carried out in the interest of finding a potential cure for Parkinson's disease from HUCMSCs [2]. The procedure involved isolating human mesenchymal stem cells from Wharton's jelly of the umbilical cord and culturing the HUCMSCs in a neuronal conditioned medium (NCM) [2]. The differentiation of the HUCMSCs into dopaminergic neurons was induced through stepwise culturing with the NCM, sonic hedgehog and FGF-8 [2]. The successfully transformed HUCMSCs into dopaminergic neurons were selected by positive immunohistochemistry staining for tyrosine hydroxylase (TH), the rate-limiting catecholaminergic synthesizing enzyme, and dopamine secretion [2]. These neurons were then transplanted into the striatum of rats with induced Parkinson's disease by unilateral striatal lesioning with neurotoxin (6-hydroxydopamine hydrogen chloride)[2]. The effects of stem cell transplantation were examined in the Parkinsonian animals by quantification of rotations in the mice in response to amphetamine at 0, 1, 2, 3 and 4 months [2].

Despite a success rate of 12.7% of transformed HUCMSCs, the study found that the original number of HUCMSCs doubled after 3 days of culture [2]. Additionally, the transformed HUCMSCs were still viable in the rats 4 months post-transplantation without the need for immunosuppression [2]. These findings highlight HUCMSCs as a potentially safe source of organs due to their viability post-surgery and the lack of a negative host response to the newly transplanted tissues. Additionally, positive TH staining showed migration of the transformed HUCMSCs rostrally and caudally from the location of implantation [2]. Hence, the transformed HUMSCs were able to integrate properly into the patient (Parkinsonian mouse), putting forth their suitability as a tissue source for transplantation.

The clinical effects of the HUCMSCs on the Parkinsonian mice were assessed by comparing test subjects to two control groups. The first control group consisted of normal, non-Parkinsonian mice with a low score of rotation in response to amphetamine. The second control group contained Parkinsonian mice which received no treatment and had a high rotation score [2]. It was found that the second control group showed no improvement in rotation score and deteriorated further over time. Similarly, mice treated with non-transformed HUCMSCs did not have observable improvements and had a similar deteriorating rotation score to the untreated Parkinsonian animals [2]. This finding highlights that untransformed HUCMSCs confer no clinical benefit in the setting of simulated Parkinson's disease [2]. The Parkinsonian mice treated with transformed HUCMSCs at first had no observable improvement but over time showed significantly improved rotational scores relative to the Parkinsonian control group [2]. However, the transformed HUCMSCs group did not show improvement to the extent of returning to a normal level (non-Parkinsonian rat). These findings suggest that HUCMSCs could be a potential stem cell source for transplantation, however, the procedures for HUMSCs transformation and transplantation must first be reviewed [2]. Fu et al. (2006) suggested that, the number of dopaminergic neurons of implanted cells may have been relatively inadequate to alleviate the Parkinsonism symptoms in the affected rats. Additionally, the transplanted cells may take time to integrate into the host brain: only two rats in the transformed HUCMSCs group survived for at least 8 months, with amphetamine-induced rotation behavior remaining similar to that 4 months after transplantation. Hence, in order to properly assess HUCMSCs to treat Parkinson's disease, the long-term effects of transplantation must be studied [2].


  1. Moore, K. L., Persaud, T. V. N. & Torchia, M. G. (2013). The Developing Human (9th ed.). Philadelphia, PA: Elsevier Saunders.
  2. <pubmed>16099997</pubmed>

--Mark Hill 17:18, 11 September 2012 (EST) Question 1 well answered in terms of technique and specific abnormalities. Question 2 human umbilical cord mesenchymal stem cells in Wharton's jelly have been used in several studies as potential sources of therapeutic cells. Perhaps a more recent paper next time. 10/10

Lab 7 Assessment

Muscle Satellite Cells

1. (a) Provide a one sentence definition of a muscle satellite cell

Satellite cells are quiescent cells located beneath the basal lamina of each myofibre and function as myogenic precursors (stem cells) for postnatal muscle growth and repair [1].

(b) In one paragraph, briefly discuss two examples of when satellite cells are activated ?

Muscle satellite cells are at rest (G0) when skeletal muscle is not active[2]. Activation can occur in the settings of physical activity and mechanical trauma [3]. When satellite cells are activated, they proliferate and are converted to myoblasts which further differentiate and fuse with existing muscle fibres or form new fibres [3]. The myonuclei accumulated in the tissue are of key importance for myogenesis: they aid in increasing protein synthesis and enable muscle growth (hypertrophy and hyperplasia) and regeneration[1]. Without satellite cells, mature muscle fibres are unable to undergo regeneration [1]. There is much speculation as to the exact mechanisms and factors which activate muscle satellite cells. It is proposed that strenuous exercise, mechanical muscle injury or myodegenerative disease result in the inflammatory response which recruits neutrophils and macrophages to the area of damage; the inflammatory mediators released in conjunction with growth factors secreted by the myofibres promote myosatellite activation [3]. One proposed "triggering agent" is the production of sphingosine-1-phosphate from the inner part of the plasma membrane leading to satellite cell entry into the cell cycle [4]. Additionally, mechanical stretch to the muscle fibre has been shown to trigger intracellular signals, such as nitric oxide synthesis which results in hepatocyte growth factor (HGF) release [4]. Nitric oxide also induces follistatin, a fusigenic secreted molecule, which is an antagonist to myostatin. Myostatin is expressed by quiescent satellite cells and exerts a negative effect on satellite cell activation [4]. IGF-IEa and MGF have also been implicated in satellite cell activation: Hill et al. (2003) demonstrated that these mediators are produced by active muscle in rodents and appear to be positive regulators of muscle hypertrophy[3]. However, whilst MGF is acutely induced and is said to precede satellite cell activation, IGF-IEa has a delayed effect involved in the later phase of regeneration[3]. Interestingly, in dystrophic muscles MGF is not produced, suggesting the importance of effective muscle repair to avoid the pathogenesis of muscular dystrophy syndromes [3].

Once activated, the satellite cells migrate out of the basal lamina and enter the cell cycle with coexpression of Pax7 and MyoD [4]. This process occurs in conjunction with the Notch signaling pathway[5]. The skeletal myoblasts that are produced divide, express myogenin and downregulate Pax7 then fuse to form myofibres[4].

The Effects of Motor Nerve Damage on Skeletal Muscle

2. In one brief paragraph, describe what happens to skeletal muscle fibre type and size when the innervating motor nerve sustains long term damage such as in spinal cord injury?

Chronic spinal cord injury (SCI) affects muscles below the level of the lesion. In terms of fibre type, one review [6]describes the progressive change in fibre type toward faster phenotypes. The fibre phenotype is classified according to its myosin heavy chain (MHC) molecule which is an actin-based motor protein associated with muscle fibre contraction[6]. These three MHC isoforms are MHC I, MHC IIa, and MHC IIx [6]. In SCI there is a reduction of type I fibres (slow) and upregulation of type IIA and IIX fibres (fast)[6]. The metabolism of the fast fibres is characterised by a predominantly anaerobic metabolism with fewer mitochondria, unlike type I fibres which undergo aerobic metabolism [6]. This is in part due to a reduction in absolute activities of the muscle metabolic enzymes in SCI, favouring the fast glycolytic/oxidative type which fatigue more easily [6].

In terms of fibre size, a study by Castro et al. (1998) [7] found that all fibre types underwent significant atrophy and decreased in size from the 6th to 24th week after injury[7]. Moreover, average fibre cross-sectional area decreased by 22% by the 6th week post-injury [7]. The changes were accompanied by either complete paralysis or loss of force with increased susceptibility to fatigue depending on the extent of injury [7]. Note that whilst type II fibre atrophy is seen during the first months after complete SCI, type I fibres undergo atrophy in the later stages [6].

Interestingly, the level of the motor neuron lesion can affect the outcome of the muscle atrophy: a study by Stilwill and Sagha [8]found that lower motor neuron lesions led to muscle fibre grouped atrophy and fibre-type grouping, whereas upper motor neuron lesions led to preferential atrophy of type II fibers with fibre-type grouping.


  1. 1.0 1.1 1.2 <pubmed>16051152</pubmed>
  2. <pubmed>22649641</pubmed>
  3. 3.0 3.1 3.2 3.3 3.4 3.5 <pubmed>12892408</pubmed>
  4. 4.0 4.1 4.2 4.3 4.4 <pubmed>17996437</pubmed>
  5. <pubmed>22493066</pubmed>
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 <pubmed>19705475</pubmed>
  7. 7.0 7.1 7.2 7.3 <pubmed>9887150</pubmed>
  8. <pubmed>66912</pubmed>

Mark Hill - Excellent referenced answers. 10/10

Lab 8 Assessment

1. Each student should now look at each of the other Group projects in the class.

2. Next prepare a critical assessment (should include both positive and negative issues) of each project using the project assessment criteria.

3. This assessment should be pasted without signature on the top of the specific project's discussion page. (minimum length 3-5 paragraphs/project)

4. This critical assessment should also be pasted on your own student page. Each student should therefore have 5 separate reports pasted on their own page for this assessment item. Length, quality and accuracy of your reports will be part of the overall mark for this assessment (there will be a greater loading on this than simple question assessments).


In regards to the information presented (outcomes 1 and 9), as the project is still in progress it is understandable that some areas are incomplete. There is so far good, concise information on the structure of the development of the eye and the structures involved in vision. It would be useful to include information on the genetic factors involved in vision development as well as have a section explaining the processes involved with vision. Also, for the Current Research section (outcome 5), it would be better to explain the aims and findings of the research papers cited rather than just referencing the papers and images without describing their significance to research progress. In terms of peer teaching (outcome 4), the page contains a good balance between technical terms and simple language for understanding on the development of structures for vision; additionally, the inclusion Glossary helps to clarify any technical terms.

The most striking part of the layout (outcome 2) is the use of images to demonstrate the development of structures involved in vision. This is great because it makes the page interesting and provides a visual understanding on the development of the eye. However, at times the images could be better placed: for example, in the introduction the pictures appear stacked on top of one another. Additionally, the images in the introduction show similar structures, so perhaps select only one to better aid the flow and appearance of the page. Throughout the page, the images utilised could be provided with more description and linked to the text in order to improve flow and enhance written explanation. Perhaps some information, such as the timeline, could be sorted into a table to improve the layout.

In regards to outcome 3, some of the information provided (e.g. in the section on Development) is not referenced. Additionally, some of the references in the Reference list need to be formatted correctly with author, date, title of the page, publisher (if required) and any other necessary information. It would be useful to follow the style of the automatic default referencing. Hope the feedback helps and all the best with your project!


The introduction is good in that there is a description of the role of somatosensory functions as well as an overview of its development. To improve further, perhaps avoid trailing off in the final sentence and perhaps put something that concludes your introduction.

In regards to the information presented and layout (outcomes 1, 2, 4 and 9), the history of discoveries is very brief and requires more research. Additionally, it would be useful to set up a timeline to add interest. The section on the central somatosensory differentiation appeared very well researched with a very interesting picture to accompany the text – good work. The section on Touch would better be placed in a table and have accompanying images to avoid getting too ‘wordy’. Also, this section does not have any consistent referencing in the bulk of the content – please cite where you find your information. The section on pain is well researched and has a strong content, however, to enhance this section I would suggest using dot points to describe the different fibres and add a relevant image. Similarly, the hot/cold and pressure sections were great in terms of content but could use with some dot points and visual explanation to make the page more interesting. Just a note on pressure – avoid getting repetitive; the page had already defined the Ruffini’s endings/corpuscles etc in the section of Touch. Additionally, the 2 urls at the bottom of this section are distracting, make sure to incorporate these in your reference list of add them to an ‘External Links’ section. Your Current Research section requires some proof reading and additional articles to make it more comprehensive. However, you have referenced the image well and referred to it in the accompanying text.

In terms of referencing, I noticed some areas where the in-text references were not correctly formatted and were in the (Author, date) style. Perhaps have a look at the referencing tutorial on the Embryology ‘Students’ page to get an understanding of the codes required for citations. For peer teaching (outcome 4), make sure that you define all technical terms – your Glossary only has 2 definitions provided. Other than this, the content overall is interesting to read just make sure you are striking a balance between images and text. Hope it helps and all the best!


In regards to the information presented (outcomes 1 and 9), the timeline for the development is good and written with clarity. However, I noticed the section on structure only referred to the adult state rather than focusing on the embryonic origin of each structure (ectoderm, endoderm and mesoderm). I would suggest that you elaborate on the developmental stages introduced in the timeline in order to build on the information you have already provided. This is important in regards to outcome 6 so that you can relate your research to embryology – the development of taste should be your focus. The history timeline was great to read as it was very concise and clear.

The page shows a good level of peer teaching with clear language and a good balance between images and text (outcome 4) with technical terms explained in the glossary. An improvement could be to make a link between any technical language and the glossary to avoid scrolling up and down to the page. Your Current Research section (outcome 5) was very interesting to read and showed you went beyond the scope of basic research on taste – good work!

In terms of layout (outcome 2), whilst the images are interesting and relevant to the text, some are not appropriately referenced nor described; make sure to reference appropriately and at least write one or two sentences to make the images relevant to the reader. Additionally, the introduction should not be under another subheading (Gustatory system) as it creates some confusion; I would suggest making the introduction its own heading in order to make the page flow. Similarly, the history timeline would best be placed towards the beginning of the page, under the introduction.

I noticed some areas (such as the section on Structure) were not appropriately or consistently referenced. Make sure to include a citation anytime you introduce a researched idea or information to avoid being accused of plagiarism. I noticed the history timeline had good consistent referencing; however the numbers just need to be formatted so they come under the reference list. If you click on the Tutorial: References page linked from the student page, it tells you how to do this. Hope the feedback helps and all the best for your project!

Abnormal Vision

"The introduction is good in the manner that it provides some brief background information regarding the normal development of the eye and abnormalities. Additionally, I liked how the introduction described the aims of the page because it sets up a structure for the reader to follow. Just make sure to proof read this section: “The development of the eye is very sensitive and REQUIRES accurate...”

In regards to the information presented and layout (outcomes 1, 2, 4 and 9):

1. Normal Eye Development: This section appears very well researched. I like how you referred to the stages throughout development. However, this section could be enhanced by adding an image of the normal eye structure and development – this acts as a reference point for your page viewers, allowing for a clear visual comparison between the abnormalities and normal structure.

2. Abnormal Development: I like the overview provided at the beginning as it sets the scene for what points you will be covering in this section. Great job. All sections are quite good, just perhaps include more images to further enhance your page.

a. Abnormal lens development: I liked how you first described the function of the gene in development and then stated any abnormalities that arise when the gene is not expressed or mutated. I liked how you included an image for the crystalline genes; just make sure to refer to the image in text (e.g. see fig. 1. or see accompanying image).

b. Abnormal corneal development: Similar to the abnormal lens section, there is a good explanation provided for each gene involved. Just some improvements: make sure to reference all information; e.g. No reference provided for “The ion transporter SLC4A11 promote sodium-dependent transport of borate as well as flux of sodium and hydroxyl ions. It has been shown that SLC4A11 is expressed in the endothelial cells of the cornea, and mutation of....”. The accompanying image has been referenced correctly and described, good work!

c. Abnormal retinal development: Once again, a great scope of research and information and suitable image. I liked how you described the impact of each mutation explicitly such as in Albinism “ganglion cells of retina decreased by 25%”. This really helps the reader to understand the extent of the abnormalities from certain gene mutations.

3. Ocular manifestations: the opening sentence is slightly vague. Could you please state which two separate sections that you are referring to? The section that follows could be better organised. It seems to jump from genetic issues to a research timeline then to future research on that disease to another example of a genetic mutation which produces abnormalities. I would suggest putting the research timeline shortly after the introduction and integrating research history not just on LCA but other abnormalities as well. However, the content for all these sections is well referenced and interesting to read. The balance between text and images between LCA and anopthalmia/micropthalmia sections is good and are both really interesting to read! I liked how you provided some epidemiological data and clinical manifestations in depth accompanied by suitable images. However, the environmental abnormalities section could use with more dot-point styles and images to enhance the presentation and aid in your descriptions.

In regards to peer teaching (outcome 5), this page was an absolute joy to read and all technical language was explained in the glossary. Just make sure to pay attention to those minor improvements. Good job!"


The humorous image at the beginning accompanied by the “CAN YOU HEAR ME” in the introduction was a very clever way of drawing the reader in and making your message loud and clear, with all pun intended. Great work! I like how you also clearly introduced what your page will discuss.

No issues with the history timeline – it is well set out and very clear and concise. The section of the Adult Anatomy is quite clear also, however you refer to histology in the title – perhaps include an image that shows the histology of a certain structure. In regards to the section on Development, it is very clear that a lot of work has gone into this. However, be aware that you must reference all your information to avoid being penalised or accused of plagiarism. Additionally, images would help your explanations – it is slightly word dense at the moment so perhaps arrange some of the content into dot points in order to engage your reader. The sections on the Otic Placode and Otocyst are great examples of webpage layout, with the dot points and a clear image which links to the content. I especially liked how a summary of the inner ear was included – this demonstrates an awareness of peer teaching and reiterates your key points. Excellent!

The section on abnormal hearing was a joy to read and was cleverly set out in tables – the information will be even more enhanced by the images I can see you have indicated you will add. I also liked how you divided the different congenital abnormalities into environmental and genetic. In order to enhance these sections, incorporate some dot points or a diagram showing how viruses/drugs can cross the placenta.

The “Technologies to Detect” would best be organised under subheadings – at present it is a little daunting to read in the paragraph-paragraph format which is a shame because the information is very interesting! Also, be aware of correct referencing formats which you can find on the tutorial page – your in text references should be numbers and the references should go at the end of the webpage. I liked the “Technologies to overcome the problems” – may I suggest including images or diagrams of these technologies?

It would be great to see more examples of Current Research. However, what you have presented thus far is great – you have clearly described the aims and findings of research.

Overall, good work – just make sure you are consistent with referencing and strike a balance between images and text.

Mark Hill - Excellent peer assessment and feedback. 10/10

Lab 9 Assessment

Embryonic Blood Flow and Oxygen and the Developing Pancreas

1. Identify and write a brief description of the findings of a recent research paper on development of one of the endocrine organs covered in today's practical.

A study by Shah et al.[1] sought to investigate whether enhanced blood flow and oxygen in a developing mouse pancreas correlates with changes in differentiation during embryonic pancreatic development. This investigation was prompted because "there is a fundamental lack of understanding of how organs in early mammalian embryos are able to form despite receiving little or no blood flow" according to Shah et al.

The methods involved injecting fluorescein-conjugated tomato lectin (a vascular tracer) into the hearts of developing mouse embryos in utero at different stages of development, guided by ultrasound backscatter microscopy. The vascular tracer was left to circulate for 10 minutes and then the mice embryos were harvested for analysis of blood flow and oxygenation. One key finding discovered through immunohistochemistry was that the developing pancreas had dense vascularity, though numerous vessels early in gestation were non-perfused. Vessels that were not perfused with blood did not induce differentiation of adjacent pancreatic epithelium. In contrast, vessels perfused with blood were surrounded by glucagon-positive and insulin-positive cells; these are indications of pancreatic cell differentiation. However, in vitro it was found that the hypoxic embryonic pancreas shows proliferation but not differentiation. Interestingly, the endocrine areas tended to be areas with flow and higher oxygenation compared to the exocrine areas of the pancreas. Moreover, later embryonic stages when global pancreatic perfusion occurred correlated with a rapid increase in exocrine differentiation. Overall, Shah et al. concluded that vascular flow with oxygenated blood, as opposed to just vascular endothelium alone, may provide specific signals for pancreatic differentiation in the early embryo.

Developing Teeth

2. Identify the embryonic layers and tissues that contribute to the developing teeth.

Through the interaction between the neural crest and the ectoderm, 10 teeth buds form in the the embryo on in the early embryo[2]. Each tooth bud has an outer area of ectodermal orgign (the enamel organ) with an inner area of dental pulp made up of solidified mesenchyme of neuroectodermal origin. The neuroectodermal mesenchyme also forms the dental follicle from which the periodontium and cement of the tooth root arise.

  • Ectoderm of the oral cavity produces:
    • Ameloblasts which produce the teeth enamel in the direction of the tooth pulp.
  • Surrounding mesoderm (mesenchyme) in conjunction with neural crest produces:
    • Odontoblasts excrete predentin below the ameloblast layer; dentin then arises through calcium salt deposition in the predentin.
    • Cementoblasts in the root of the tooth produce cement.


  1. <pubmed>21050843</pubmed>
  2. Universities of Fribourg, Lausanne and Bern. (2012). Development of the Teeth. Retrieved from

Mark Hill - 10/10

Lab 11 Assessment

Identify a recent research article (using the pubmed tags to cite) on iPS cells and summarise in a few paragraphs the main findings of the paper.

The CCCTC-binding factor, CTCF, has been shown in the past to be involved in transcriptional control and chromatin interactions within the cell’s nucleus[1]. A recent study by Hiroseu et al. [2] sought to analyse the role of CTCF in induced pluripotent stem cells (iPS) by examining three cell lines: iPS cells induced from fibroblasts (201B7), human diploid fibroblasts (IMR90) and IMR90 cells undergoing oncongene-induced senescence (OIS) after Ras activation.

Hiroseu et al. noticed that CTCF mRNA was up-regulated in the iPS cells and down-regulated in the OIS cells in comparison to the IMR90 cells[2]. Similarly, high levels of CTCF protein were expressed in the iPS cells whilst the OIS cells showed little CTCF protein expression [2]. In order to clarify these results, Hiroseu et al. studied the interaction between CTCF and the and the INK4/ARF locus which encodes p15INK4b, p16INK4a and ARF: reprogramming regulators in the cell cycle which induce senescence[3]. Using genome wide assay as well as CTCF binding profiles from data from past experiments, Hiroseu et al. where able to identify three CTCF enriched sites in the INK4/ARF locus: IC1, IC2 and IC3[2]. These findings are significant as they suggest a relationship between CTCF function and INK4/ARF transcription.

Chromatin precipitation showed that CTCF could bind to IC1, IC2 and IC3 in all three cell lines[2]. The affinity of CTCF binding was found to be significantly high in the iPS cells compared to IMR90 cells[2]. Additionally, chromosome conformation capture assay showed that in both the iPS cells and IMR90 cells, p15INK4b, p16INK4a and ARF were silenced[2]. In contrast, the OIS cells showed weak CTCF binding with increased expression of p15INK4b and p16INK4a[2]. Data analysis uncovered that the inverse relationships of expression are a result of the interaction between the CTCF enriched sites and the , p15INK4b, p16INK4a and ARF promoters[2]. IC1 and IC2 strongly interacted with the p15INK4b and ARF promoters respectively[2]. Moreovereover, the IC1/ p15INK4band IC2/ARF “binding site-promoter complexes”, the p16INK4a promoter and IC3 were found to be colocalised in the nucleus; Hiroseu et al. suggested that these gene interactions involve the formation of chromosome loops in the INK4/ARG locus[2]. This hypothesis was supported by CTCF knockdown which was found to decrease the colocalisation of the genes, leading to a looser chromatin formation; this was coupled with increased expression of p15INK4b, p16INK4a [2]. From these findings, Hiroeu et al. drew the conclusion that the CTCF complex is important for compact chromatin formation at the INK4/ARF locus[2].

In OIS cells, chromatin was found to undergo active decompaction which was related to its senescence as it allowed the expression of p15INK4b and p16INK4a[2]. In contast, repressive compaction and intermediate compaction was demonstrated in the IMR90 and iPS cells respectively, explaining the silencing of the genes in the INK4/ARF locus[2]. The implications of these findings for iPS research are two fold. Firstly, that CTCF is crucial for higher-order chromatin organization in the INK4/ARF locus in a reprogrammed cell[2]. Additionally, the chromatin decompation in the INK4/ARF locus shown in the OIS cells coupled with induction of the INK4 genes and senescence-associated nuclear changes may be a barrier for reprogramming to iPS cells[2][3].


  1. <pubmed>20020479</pubmed>
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 <pubmed>22340434</pubmed>
  3. 3.0 3.1 <pubmed>19668188</pubmed>

Mark Hill - 10/10

Lab Attendance

Lab 1 --Z3333038 11:49, 25 July 2012 (EST)

Lab 2 --Z3333038 10:05, 1 August 2012 (EST)

Lab 3 --Z3333038 10:01, 8 August 2012 (EST)

Lab 4 --Z3333038 10:00, 15 August 2012 (EST)

Lab 5 --Z3333038 09:59, 22 August 2012 (EST)

Lab 6 --Z3333038 10:10, 29 August 2012 (EST)

Lab 7 --Z3333038 10:09, 12 September 2012 (EST)

Lab 8 --Z3333038 10:00, 19 September 2012 (EST)

Lab 9 --Z3333038 10:03, 26 September 2012 (EST)

Lab 10 --Z3333038 10:04, 3 October 2012 (EST)

Lab 11 --Z3333038 10:18, 10 October 2012 (EST)

Lab 12 --Z3333038 09:39, 17 October 2012 (EST)

Full lab attendance logged --Mark Hill 07:25, 18 October 2012 (EST)