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Hi my name's Paul, I'm studying A levels in a school in Kent and am aspiring to go to The University of Nottingham to study Plant Bioscience. Enjoy my blogs, they will mainly be about Biology. Contact me at rubiscoactivase@gmail.com

Tuesday, 31 July 2012

Outline of GM Ethics

Genetic modification has the potential to do amazing things for the standard of living of millions of people across the world, however many people are still against the notion of altering an organisms genetic code. Here are some ethical issues associated with genetic modification.

- The possibility of species extinction. If an organism escapes the controlled environment of a lab and is able to breed with other organisms we could see specific gene codes eradicated, hence possibly seeing the genetic extinction of a species.

- Health risks. Although no health risks have been identified as a result of the consumption of genetically modified food, the possibility can not be entirely ruled out. We digest millions of nitrogenous bases from different species every day, changing the code is just changing their order, so there shouldn't be any health risks associated with that.

- Environmental impact. As mentioned in the first point, there is the possibility of species extinction due to the release of genetically modified organisms. There is also the risk of a GM organism out competing rival species, and hence driving the to extinction.

- Harm caused to the subject. When working with animals and species with advanced nervous systems, there is the possibility that stress or discomfort is caused when modifying their genetic code. The new protein synthesised as a result of the modification to the organism's genetic code could cause adverse effects in the organism, leading to stress or even pain.

These are some of the main points of argument for people opposed to genetic modification. What are your opinions on this matter, do the positives outweigh the risks outlined above? Are there any other arguments against genetic modification that I failed to address?  

Thursday, 12 July 2012

New Book!

Right, so basically I hardly ever post here any more, and I want to change that. I recently got a new biology book, one that I am going to be using for my university course and I was thinking that I could maybe share some of the knowledge within it. It will help me learn it and if you're interested in Biology then you might find it interesting. The book is called "Biology" and is edited by Solomon, Berg and Martin 9th edition. A quick warning too, most of the information will not be in context and will be in note form, so this might add to the confusion, so sorry about that. 

Basic classification of plants 

Annuals - herbaceous plants that grow, reproduce and die in one year or less eg. corn 
Biennials -  herbaceous plants that take two years to complete their life cycles. During the first year they produce extra carbohydrates which they store and are then used in the second year eg. foxgloves 
Perennials - herbaceous and woody plants that have the potential to live for more than two years. In temperate climates aerial steams of herbaceous perennials die and their underground parts become dormant. Through dormancy the plant lowers its metabolism to a minimum in order to survive unfavourable conditions. All woody plants are perennials, many are also deciduous, meaning they shed their leaves before winter and produce new ones in spring. Some, however are evergreen, and shed their leaves over a long period, meaning there is always leaves present.  

Saturday, 23 June 2012

Exams are over!

Yesterday was my last exam so it's back to normal in terms of posting wise. I will try and post two or three times a week.

As for the content I will be posting, I may include some topics and interesting things from my list of summer reading that I got from sent by the university, this way it will help me learn and hopefully be interesting for you guys.

Sunday, 27 May 2012

The Importance of Oxygen in Aerobic Respiration

Oxygen is used in Oxidative Phosphorylation to form water.
Reduced NAD and reduced FAD (made in glycolysis, link reaction and krebs cycle) are used in the electron transport chain to supply an electron, and also give a proton, which will be pumped into the inter membrane space of the mitochondria.
Basically the electron transport chain pumps the H+ into the inter membrane space in order to create a electrochemical gradient. This is used to generate ATP using ATPsynthase. The oxygen is used in order to take the H+ away from the cell so there is still an electrochemical gradient, in the reaction shown below.
4H+   + 4e-   + O2 -----> 2H2O
The electrons are supplied by the electron transport chain.
The electrochemical gradient is key in maintaining the production of ATP.

Sunday, 13 May 2012

Coordination of the heart beat

Cardiac output = Stroke Volume x Heart rate

(ECG) show voltage against time. A normal ECG will show five distinct peaks

P Wave – excitation of the atria
QRS complex – excitation of the ventricles
T waverepolarisation of the ventricles 

Cardiac muscles are myogenic  (self exciting) and have an intrinsic rhythm
-          The sinoatrial node is responsible for the coordination of the heart beat and is found in the wall of the right atrium
-          The sinoatrial node sends out a wave of depolarisation that spreads over the left and right atria. This stimulates the myocardium (heart muscle) of both atria to contract.
-          The wave of excitation then reaches the atrioventricular node (found in the right atrium) which then sends a wave of depolarisation to the bundle of His and purkyne fibres (located in the septum)
-          The wave of excitation continues along the purkyne fibres to the apex of the heart and then up through each ventricle. This causes the ventricle to contract, forcing blood out of the heart.
-          Note there is a slight delay after the atria contract to ensure the ventricles are full of blood and to insure that the atrioventricular valves are closed.

Using ECGs to Diagnose Heart Disease  
-          If the heart behaves abnormally, the normal electrical activity of the heart is disrupted, causing the rhythm to change. Different rhythms are known as arrhythmias and can be detected using ECGs.
-          If the heart is starved of oxygen (ishaemic) then it cannot empty or fill
-          Atrial fibrillation : atria beat too fast, increasing chance of a clot
-          Tachycardia: heart beats too quickly, can be caused by stress
-          Ventrical fibrillation: ventricles contract weakly and erratically, hence little blood is pumped out of the heart. It is often a rapid drop in blood pressure, so the brain, body and heart are rapidly starved of oxygen and glucose. This can lead to a heart attack.

In some cases, an abnormal heart rate can be corrected by giving the heart a large electrical shock with a defibrillator.

Friday, 11 May 2012

Action Potential

Resting Neurons - Do not have an action potential and the membranes are polarised

Polarised Neuron - The outer surface of the membrane is positively charged and the inner surface of the membrane is negatively charged. The difference between the membranes is -70mV and is known as Resting Potential. An impulse can only travel when the resting potential is achieved.

The resting potential is generated by sodium potassium pumps in the cell membrane. They move 3 sodium ions and 2 potassium ions by active transport (requires ATP). Potassium gets moved into the neuron and sodium gets moved out of the neuron. The Potassium within the cell then gets taken out of the cell via potassium channels (facilitated diffusion). This allows more sodium to be pumped out by the sodium potassium pump. At -70mV there is no net movement of potassium.  
This causes the inner membrane to become more negatively charged than the outer membrane because more positively charged ions move out. There are also lots of negatively charged proteins within the cell

Depolarisation of the Membrane 

- when a neuron is stimulated, sodium channels open and sodium diffuses into the cell
- the increase in positive charge in the cell causes the potential difference to change from -70mV to +40mV
- +40mV is known as threshold, and it's at this point that adjacent sodium channels open
- an action potential is generated
- depolarisation can only occur at the nodes of ranvier, a process known as saltatory conduction

Repolarisation (recovery of the resting potential)

1- Sodium channels close and potassium channels open
2- Potassium diffuses out by facilitated diffusion
3- Outside of cell is more positive, making the the potential difference more negative
4- Potential difference drops below resting potential (-70mV), which is known as hyperpolarisation 
At this point there is lots of potassium outside the cell and lots of sodium inside the cell. This is reversed by the sodium potassium pump. This occurs until resting potential is reached, only then can another action potential travel along the neuron. The refractory period is when the membrane is returning to it's resting potential.

Thursday, 10 May 2012

Brain Inbalances

Many drugs that are aimed at effecting the nervous system interfere with the normal functioning on the synapse.
Below are 5 ways in which a drug can effect the synapse
-1- Effect the synthesis or storage of the neurotransmitter
-2- Effect the release of the neurotransmitter from the presynaptic membrane
-3- Effect the interaction of the neurotransmitter with the receptors on the post synaptic membrane
-4- Prevent the re-uptake of the neurotransmitter into the presynaptic membrane
-5- Inhibit the enzymes responsible for breaking down the neurotransmitter in the synaptic cleft, resulting in a high concentration of the neurotransmitter in the synapse. This results in repetition of the action potential in the postsynaptic membrane

Case study drugs

Serotonin selective reuptake inhibitor (SSRI) (Depression)
Effects serotonin levels in the brain. Serotonin is a neurotransmitter linked to feelings of reward and pleasure.
A lack of serotonin causes severe clinical depression.
SSRI help increase the levels of serotonin in the synapses by blocking the process which would normally remove serotonin.

Levodopa Drugs (L-dopa) (Parkinson's Disease)
These drugs effect the level of dopamine in the brain. Dopamine is a neurotransmitter that is active in neurons in the frontal cortex, brain stem and spinal cord. It is responsible for the control of movement and emotional responses.
A lack of dopamine is linked with Parkinson's Disease.
L-dopa drugs aim to increase the concentration of dopamine in the brain. Because Dopamine can not pass the blood brain barrier, L-dopa is used because it can and once in the brain in is used to make more Dopamine

Monoamine Oxidase B Inhibitor (MOAB) (Parkinson's Disease)
MOAB inhibitors have a similar effect to L-dopa except their mode of action works in a different way. MOAB inhibitor drugs inhibit the action of the enzyme MOAB in order to increase levels of Dopamine.
MOAB inhibitors are less frequently used then L-dopa because they have a lot of side effects.    

Ecstasy (MDMA)
MDMA drugs are illegal because they severely damage the brain function. It acts as a stimulant, increasing the heart rate and effects the serotonin levels in the brain.
MDMA blocks the serotonin reuptake transport system, meaning the synapses are completely flooded with serotonin, which cannot return to the presynaptic knob.
Long term use of MDMA results in over stimulation of neurons which causes damage to the presynaptic knob. This dramatically reduces the functionality of these neuron pathways, leading to depression.