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Lab attendance

--Nathan Weller 10:42, 10 March 2011 (EST)

--Nathan Weller 09:11, 17 March 2011 (EST)

--Nathan Weller 09:54, 24 March 2011 (EST)

--Nathan Weller 09:23, 31 March 2011 (EST)

--Nathan Weller 09:09, 7 April 2011 (EST)

--Nathan Weller 10:45, 14 April 2011 (EST)

--Nathan Weller 09:22, 21 April 2011 (EST)

Lab 1 questions

1) What are the key cell biology journals? 
  • Journal of cell biology
  • Nature of cell biology
  • Trends in cell biology
  • Cell
  • Public library of science
2) Which journals allow you to reuse their published content
  • PLOS
  • Journal of cell biology
  • BMC cell biology

Work area

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Intro lab

Cell bio

Lab 2 questions

--Mark Hill 08:00, 24 March 2011 (EST) Hi. WHere are your lab 2 answers?

  1. Which chromosomes contribute to the nucleolus?

Chromosomes 13 14 15 21 22 contribute to the nucleolus which is the site for ribosomal RNA transcription.

  1. Identify and add a link to your page of a recent cell biology article using confocal microscopy from the Pubmed database.
  • "Confocal imaging from deep brain tissue" [1] |

Work area

Lab 3 questions

1) "Safety data sheet for chloroform"

Has been noted as cancer causing in laboratory animals and is also a carcinogen in humans. Exposure through inhaling or ingestion is toxic and can be fatal. Dermatitis can be caused by exposure to the skin.

2) Pic 2.jpg

Lab 4 Questions

1. Identify a commercial supplier of an antibody that relates to your group project topic.

Abcam is a supplier of antibodies relating to synaptic junctions. They produce Piccolo antibody-A synaptic marker. [2]

2. In mitochondria, where is the gene located that encode Cytochrome C and what keeps this protein trapped within the mitochondria?

The gene that encode Cytochrome C is located in the nucleus of the cell. This protein is a part of the electron transport chain location in the inner membrane of the mitochondria. This protein is soluble in water and is contained by the outer membrane of the mitochondria.

Lab 6 questions

[Cell bio graph.jpeg]

1 a) What are the changes in phenotypes that you observe between group A and B?


Group A contains Tm4 and Group B is the control.

-Phenotype A shows no Tm4. -Phenotype B and C are similar in ratio with less Tm4 compared to the control. -Phenotype D and F shows a significant increase in Tm4 compared to the control. -Phenotype E shows a slightly higher amount of Tm4 than the control.


Group A there is a generally pink appearance with yellow edges and blue nuclei. Prolonged phenotype and cells are likely to be close together.

Group B they are red with purple nuclei and fanned phenotype. The cells are bound together.

b) How does Tm 4 mediate these changes Tm4 is an actin-binding protein and is a stabilizer in the cytoskeleton of non muscle cells. It has mediated the differences in the two groups as it has caused a prolonged phenotype in the cells in A whereas there is a more fan like appearance in B. This is because the Tm4 has stabilized the actin filaments in the cells in Group A hence the prolonged phenotype.

Random work

Parkinson’s disease

Parkinson's disease is one of the most common movement disorders, mostly effecting people over 60. Historically a person suffering from Parkinson's generally has a hunched posture due to 'tremors' that slowly worsen and cause mobility degeneration. James Parkinson studied the disease over the late 1800's, noticing the debilitating effects over time. This particular disease effects the production of the neurotransmitter Dopamine in the substantia nigra for reasons still unclear. Skilled movement in distal muscles is hindered as the synapse function is disstorted by an imbalance of Dopomine and Acetylcholine. pic

Epidemiology: Is the most common movement related dissorder in the world (effects 1% of adults over 60).

Global burden of Parkinson's disease, measured in disability adjusted life years per 100,000 inhabitants in 2004 pic

 no data
 < 5
 > 80

Etiology: Dopomine is produced in the Substantia nigra in the brain (rostral midbrain, Superior Colliculus) by specialised cells. These cells are destroyed in a Parkinson’s patient by reasons which are still unclear, theories of the cause of Parkinson’s include:

o Genetic disorder

o Free radicals

o External toxins

o Ageing

• Pathogenisis: Without the appropriate amounts of Dopomine being produced, the synaptic junctions begin to deterioate in function. In addition MAO-B is a chemical in the synapse that breaks down dopamine to maintain a balance with acetylcholine. Due to this imbalance the synapse cannot function properly, especially in fine or smooth movement of muscles. [1]

Morphology : Macroscopically there is distinct atrophy of the substantia nigra. Microscopically the neuropil shows a loss of pigmentation and lewy bodies are present. As seen in the histological section below, the brown lewy body is present In the substantia nigra[2] Lewy body.JPG

Clinical [3]: There are three major sighns of Parkinson’s:

o Resting tremor: Common to occur in hands and worsens over time.

o Rigidity : During movement there is increased resistance on the joint.

o Bradykinesia: Inability to perform fine movement tasks like writing or tieing shoe laces.

o Other signs include a loss of balance and increasingly poor posture. A retropulsion test can be be carried out to test balance by pulling the patient backwards and noting if they correct themselves properly.

Treatment: This varies with every patient and also to what extent the disease has destroyed the dopamine producing cells in the substantia nigra.

1) In its early stages, exercise and physical therapy is recommended to maintain mobility and deal with tremors that result from Parkinson’s.

2) When this fails, medication can be sought. Non-dopomine drugs are used first including Amantidine which increases mobility and ability to exercise.

3) Ropinirole is a dopomine agnostic that helps stop tremors and stiffness and is used if the condition worsens.

4) The most effective treatment is the drug Levodopa which is a dopomine replacement and dramatically increases motor function. However this may have long-term effects from its use including drug-induce dyskinesia causing erratic involuntary movements. Motor movement complications were found in 1/3 of patients after only a 2 year use of the drug making this a last resort. [4]

As of yet there is no cure for Parkinson’s disease.

• Prognosis[5] : This disease takes its course over a long period of time and isn’t the direct cause of death in its patient. Symptoms intensify over approximately a ten year period before a sufferer is iether completely bed ridden, needed to be placed in perminant care or occurances of comlications that can lead to death.

Treatments mentioned erlier have become more effective over time and make life dealing with Parkinson’s a lot easier. Over time ther is no stopping the continual deteriation, immunity and other systems are effected. The synaptic junctions where Psrkinson’s clinically manifests, eventually becaome unbalanced all over the body which cause complications which can cause death.

Myasthenia Gravis

Myasthenia Gravis is another disease which causes dysfunction within a synapse. It has a major effect on the neuromuscular junction, causing muscle weakness. Parkinson’s disease showed how the effects of a disruption in the neurotransmitters can affect a synaptic junction, this time the receptors on the post-synaptic membrane are the cause.

• Epidemiology:[6] It is common disorder of the neuromuscular junction, effecting over 60 000 people in the USA alone, expected to rise with an aging population. Studies have shown two groups that have a high correlation with Myasthenia gravis: 1. Age 10-40 in women. 2. Age 50-75 in males

• Etiology: This is still unclear.

• Pathogenesis : Myasthenia Gravis is highly mediated by production of Antibodies to the Acetylcholine receptor (AChR) by the thymus (75% of patients have abnormalities in the thymus). These antibodies are responsible for dysfunction of the synaptic junctions within skeletal muscle fibers in three ways that lead to muscle weakness:

a. These antibodies are directed at the AChR’s located on the sodium/potassium ion channels in the post-synaptic membranes of the neuromuscular junctions. This disrupts depolarization of the muscle if the number of antibodies is sufficient to block the opening of this channel. This is the main cause of muscle weakness in cases of Myasthenia Gravis.

b. Antibodies increase internalization, which causes an increased rate of degradation in AChR’s. The replacement of receptors cannot keep up with the increased internalization leading to a low number of AChR’s in the postsynaptic membrane.

c. The bodies own immune response to antibodies binding to AChR’s causes a complement cascade of inflammatory molecules. In the process of inflammation, the problem won’t be resolved and attempts to repair it only leads to the destruction of the receptors over time. [7]

• Morphology: Histological sections show very little change in skeletal muscle anatomy. All that is shown is slight myofiber II atrophy from weakness and disuse of the muscle. Within the connective tissue, lymphocytes are prominent. Within the synaptic junction affected, the number of AChR’s can decrease by 2/3 in chronic cases. This number falls over the period of the disease.

• Clinical manifestations: As mentioned the major symptom is muscle weakness, which worsens with increased amounts of contractions, for example caused by exercise. Main affected area is the cranium (mastication and head rigidity) mainly the muscles of the eyelid causing ptosis (drooping). [8]

• Diagnosis: Done through blood tests looking for elevated levels of AChR antibodies seen in Myasthenia Gravis patients. The Edrophonium test to see improvements in response to drugs that block the antibodies (Tensilon). Electromyography can be used to examine an effected synaptic junction in skeletal muscle to measure action potentials with electrical shocks. With diagnosis of Myasthenia Gravis, it is rarely carried out quickly due to the symptoms being related to many other neurological disorders. A severity criteria is also available depending on the level of neurological deteriation:

Osserman’s scale [9]

(Myasthenia Gravis=MG) 0. No MG symptoms. 1. MG with purely ocular muscle weakness. 2. MG patients with mild generalized weakness, usually with ocular muscle weakness but without bulbar involvement. Respiratory muscles are not involved. 3. MG with mild generalized weakness including bulbar involvement with dysarthria, dysphagia, and poor mastication. 4. MG patients with moderate generalized weakness, usually with moderate bulbar and respiratory muscle weakness. 5. MG with severe generalized, bulbar, and respiratory muscle weakness, or death due to MG-related complications.


• Treatment: To treat the symptoms of Myasthenia gravis, immunosuppressive corticosteroids are administered to relive the large proportion of antibodies. In worse cases plasmapheresis is carried out with good results. [11]. Thymectomy is the removal of the thymus which is responsible for the over-production of AChR antibodies and can relieve the symptoms or show total remission.

• Prognosis: With treatment the outlook is very good for patients with <5% mortality rate. If death occurs it may be caused by complications due to muscle weakness in the respiratory system leading to cardiac failure. however with treatment patients have a high chance of living a normal life.

  1. Ondo W, Jankovic J, Shwartz K, Almaguer M, Simpson RK. Unilateral thalamic deep brain stimulation for refractory essential tremor and Parkinson's disease tremor. Neurology 1998; 51: 1063-1069.
  2. Kumar, Cotran, Robbins. Basic Pathology 7th edition. 2003; 844.
  3. <pubmed>15172778</pubmed>
  4. Levodopa in the treatment of Parkinson’s disease: an old drug still going strong Werner Poewe1 Angelo Antonini2 Jan CM Zijlmans3 Pierre R Burkhard4 François vingerhoets5, Department of Neurology, Medical University of Innsbruck, Austria;
  5. <pubmed>0001762</pubmed>
  6. The Epidemiology of Myasthenia Gravis, Lawrence H. Phillips II, M.D.
  7. Fundamentals of neurologic disease By Larry Ernest Davis, Molly K. King, Jessica L. Schultz
  8. Kumar, Cotran, Robbins. Basic Pathology 7th edition. 2003; 780.
  9. Osserman and Genkins, 1971; Det- terbeck et al., 1996
  10. Seronegative myasthenia gravis: disease severity and prognosis F. Romi, J. A. Aarli and N. E. Gilhus
  11. Current and emerging therapies for the treatment of myasthenia gravis, Renato Mantegazza, Silvia Bonanno, Giorgia Camera, et al

File:Parkinson's prevalence.jpg.JPG