Someone Rear-Ended Me Yesterday

So yesterday I was driving, minding my own business.  It had just rained so the ground was wet.  I went over a hill and the light at the bottom of the hill was yellow.  So I slowed down and stopped.  A few seconds later I hear a screech and feel my car jolt forward into the intersection.  Some girl wasn't paying attention and didn't see me stop.  So I get out of the car and look at the damage.  My car, a 1997 Ford Taurus, didn't have hardly a scratch.  She went under my bumper.  She was driving a 2006 Chevy Cobalt.  And her car was in bad shape.  The radiator was busted, and her hood was quite crinkled.  So we pulled off the road and called the cops.  They came, filled out a police report, and we went on our way.  I have Geico insurance, but not collision, so I will have to get my bumper repaired through her insurance.  Oh well, wasn't my fault.  Sucks for her though, but she had insurance, so she should be fine.  Just a testament to Ford over Chevy.

Got a "B" on an Exam Today

So I graduated from Purdue University not too long ago with an engineering degree.  I did very well, and have done well at work since then.  I recently decided to get my Master's degree in my spare time, so that is what I do when I'm not designing new product lines and testing them out, or performing research.  The thing I hate about getting my Master's is that I have to redo the things that I have already done years ago.  One course I am taking is a math course, focusing on upper level differential equations.  I took this same course at Purdue like four years ago, and got an A with no problems.  But this course is different.  It seems as if the professor likes math to be done his way, and not the traditional way.  So we had our first exam and I got a "B".  Not a big deal, but I usually do better.  Solving proofs is not, as I see it, the duty of an engineer.  Especially solving them without any reference material.  I hate closed book exams.  The way I see it, my job as an engineer is to apply these math concepts, and if I need to solve some equations, that is what I write Matlab and Excel programs for, or I can look them up in differential tables.  Oh well, the school is paying me to get my Master's, so I don't really care too much.  It is just something to do and gives me extra spending money on top of my work salary and patent income.  So I got a B... I have the rest of the semester to turn it into an A.  Or am I just being too picky?

Numerical Symmetry on 10/10/10

So I thought this was worth sharing:  Today I was driving my car and looked down at the odometer and it read 201102 miles.  I then looked at the trip odometer and it read 555.5 miles.  Pretty cool.  If I wasn't on the highway I would have stopped to get my camera to take a pic, but by then it would have been too late.  I later realized that today is 10/10/10.  This kind of numerical symmetry rarely happens unplanned, but when it does it does it makes you glad you realized that it did.

Spectrophotometry to Calculate Enzyme kinetics, based on Concentration, pH and Inhibitors

Here is another school paper that I wrote in 2006.  I hope it is useful to someone out there, or at least furthers someone's knowledge on some basic chemistry regarding enzymes.

Abstract:

The goal of this study was to use spectrophotometry to assess the kinetics of the enzyme glucose oxidase, to analyze the effects of an inhibitor, and also to determine the optimal pH at which glucose oxidase acts. This was done by combining glucose oxidase with a glucose substrate under varying conditions, allowing the reaction to proceed while being read in a spectrophotometer, and using the data read over a time interval to draw conclusions about the varying conditions affecting the rate of reactions to product. Michaelis-Menten and Lineweaver-Burk plots were constructed based on the absorbance values determined from the spectrophotometer readings. The findings of this experiment show that the rate of reaction to products had a maximum velocity of -1.609*10-6M/sec, with a Km value of 0.1796. Other findings show that D-glucal is a competitive inhibitor, and that the optimal pH for glucose oxidase to perform is 6.

Introduction:

The purpose of this research endeavor was to determine the use of enzymes in biological systems, to use a spectrophotometer to assess the kinetics of the enzyme glucose oxidase, as well as to analyze the effects of an inhibitor, and also to determine the optimal pH at which glucose oxidase acts. Enzymes act to increase the speed of a chemical reaction without being changed or used up in the reaction that they catalyze (#1). This is done by lowering the activation energy of the reaction (#1). The Michaelis-Menten equation shows how initial reaction rate and substrate concentration are related. A Lineweaver-Burk plot can also be used to determine kinetics of a reaction, and is generally the reciprical of both sides of the Michaelis-Menten equation. Inhibition can be determined as well from Lineweaver-Burk plots. Competitive inhibition is when an inhibitor of a similar structure to the substrate binds to the active site and vies with the substrate for binding (#2). Non-competitive inhibition is when the inhibitor binds to a site other than the active site and changes the conformation of the active site to inactivate the enzyme (#2). By utilizing the enzyme glucose oxidase to catalyze a reaction, and analyzing that reaction over time through a spectrophotometer, substrate concentration and reaction rate may be determined. By plotting results of spectrophotometric readings, Km and Vmax values may be found. By performing another reaction with D-glucal used as an inhibitor, a supporting graph is used to find out if D-glucal is competitive or non-competitive. Varying the pH of the reaction can also show the optimal pH value that glucose oxidase performs.

Materials and Methods:

pH 7 buffer, glucose oxidase stock, and ABTS/HRP stock is added to wells of a 96-well plate, and water is added as a blank. A concentration gradient of glucose solution is added to the same wells and the samples are read in a spectrophotometer at a wavelength of 725nm every 10 seconds over the course of 3 minutes, and the results are recorded.

pH 7 buffer, glucose oxidase stock, and ABTS/HRP stock is added to wells of a 96-well plate, and water is added as a blank. A concentration gradient of glucose solution is mixed with D-glucal stock solution, and this solution is added to the wells. The samples are read in a spectrophotometer every 10 seconds over the course of 3 minutes and the results are recorded.

pH 4, 5, 6, and 7 buffer are added to wells of a 96-well plate, glucose oxidase stock and ABTS/HRP stock solution is added to these wells, and water is put in the plate as a blank. Glucose stock solution is added to the wells and the plate is immediately read in a spectrophotometer every 10 seconds over three minutes, with the results recorded.

Results:

See appendix for all absorbance values and relevant calculations. Using the absorbance values determined from the spectrophotographic readings, and using the extinction coefficient given in the lab of 19000/M/cm, and the pathlength of 1cm, the concentration of the product (D-gluconolactone) can be calculated. Taking the change in product concentration over a time interval yields a reaction velocity, and plotting this vs. the glucose concentration yields the plot below.

Figure 1.1: Michealis-Menten plot of initial reaction velocity vs. substrate concentration, showing the location of Vmax, Vmax/2, and Km values.

By taking the reciprocals of the reaction velocities determined above and plotting them against the reciprocal of the glucose concentration, a Lineweaver-Burk plot may be constructed. From this plot, using the equation of the best fit line, the x and y-intercepts may be calculated, and thus Km can be found by -1/(x-intercept), and Vmax¬ can be found by 1/(y-intercept). This plot is shown on the next page in Figure 2.1.

Figure 2.1: Lineweaver – Burk plot showing the relationship between reaction rate and glucose concentration.

Using the absorbance values determined from the second part of the lab, a Lineweaver-Burk plot may be constructed using the same principles as used on the previous graph. This plot is shown below along with the values from the previous figure, without an inhibitor. The relationship shown can help to determine whether D-glucal is a competitive or non-competitive inhibitor as well as it shows how the rate of reaction is affected by an inhibitor of the glucose oxidase reaction.

Figure 3.1: Lineweaver-Burk plot showing reaction with and without D-glucal, showing that D-glucal is a competitive inhibitor.

By using the absorbance values for varying pH from part three of the lab, as well as the extinction coefficient of 19000 M-1cm-1, the concentrations of the resulting product can be determined. Plotting these concentrations vs. the time taken for their formation yields the plot below. Based on this curve, it is possible to determine at exactly what pH value the enzyme glucose oxidase reacts optimally.

Figure 4.1: Concentration vs. time for varying pH values. The pH 5 line did not yield any change in concentration, possibly due to the accidental omission of glucose oxidase from the well.

Discussion and Conclusions

Plotting the reaction rate vs. glucose concentration as shown in Figure 1.1 gives a curve that follows Michaelis-Menten kinetics because it follows the standard curve for a Michaelis-Menten graph. The Lineweaver-Burk plot (Figure 2.1) was constructed by plotting 1/Vi vs. 1/[glucose]. Using the Lineweaver-Burk plot shows the K¬M value to be .1796, and the Vmax value to be -1.609*10-6. Having a negative value for Vmax is not accurate, and shows there was some experimental error in completing this part of the experiment.

Based on Figure 3.1, the Lineweaver Burk plot showing the reaction with the inhibitor and without the inhibitor, D-glucal is shown to be a competitive inhibitor, because it has a Vmax value that is close to that of the reaction without the inhibitor. The intersection of the two best fit lines occurs close to the y-axis, which is characteristic of competitive inhibition, and not close to the x-axis, which is characteristic of non-competitive inhibition. The results do not show the intersection of the two lines at the y-axis exactly due to the inaccurate absorbance values for the 0.05M glucose concentration data point on the inhibited graph. The absorbance value was lower than anticipated. Possible error in the preparation of the glucose solution, such as insufficient mixing of reactants, could have contributed to this problem. Still, competitive inhibitors do not affect Vmax, and thus D-glucal is a competitive inhibitor.

Based on Figure 4.1 of absorbance vs. time for the differing pH values, the optimal pH for glucose oxidase is pH 6. This is because the best fit line for pH 6 had the greatest value of slope of all the equations for the differing pH values, showing pH 6 to be the most favorable. The greater the slope of the best fit line, the faster the reaction rate. However, we cannot be certain about this value because pH 5 did not yield any absorbance values for our experiment. A possible explanation for the inaccuracy of pH 5 would be the accidental omission of glucose oxidase from the solution.

The enzyme glucose oxidase has many uses outside the laboratory. Commercial uses of glucose oxidase include the following: diabetes monitoring, biofuel cells, food and beverage additive, wine production, oral hygiene, and is also a commercial source of gluconic acid (#3).

Lineweaver-Burk utilizes reciprocals for both the x and y value data points. This distorts the results extrapolated from the plot, because the double reciprocal of the Lineweaver-Burk plot amplifies any experimental error, giving a high error for determining Km and Vmax (#4).

For this experiment, the reactants combine in a similar way to the Cell cycle and ELISA lab. This is because glucose oxidase is similar to the primary antibody used in previous labs. Because glucose oxidase is an enzyme for glucose, it binds to it and in that way it acts like a primary antibody in that it binds to the molecule of interest. Horseradish peroxidase is similar to the secondary antibody from previous labs in that it is bound to the primary antibody (glucose oxidase) and it acts as a bridge to the color changing substrate which in this case is ABTS.

Based on the Lineweaver-Burk plot of the data shown in Figure 8.1 in Appendix 3, the inhibition between the ACE inhibitor peptide and the biologically engineered ACE inhibitor is non-competitive. This data does not support the finding that the biologically engineered inhibitor and the naturally occurring inhibitor are equally capable of inhibiting ACE activity. The reason for this is the difference in the reaction velocities between the engineered and natural inhibitors. The engineered ACE inhibitor is found to be less effective than the natural inhibitor, because the engineered ACE inhibitor has a faster reaction velocity, and is closer to the control, which shows no inhibition.


Appendix 1

Table 1.1: Raw data from kinetic reads from the spectrophotometer for all three parts of the laboratory.

Appendix 2
From Lineweaver-Burk:
Vmax: y-int. = -621502
1/Vmax = -621502
Vmax = 1/-621502
Vmax = -1.609*10-6
KM: x-int. = 1/KM
x-int. = 5.5686152
5.5686152 = 1/KM
KM = 1/5.5686152 = .1796


Appendix 3

Figure 8.1: Lineweaver-Burk plot of initial reaction rates of engineered ACE Inhibitor and Natural ACE Inhibitor Peptide, showing the relationship to be non-competitive inhibition.






Appendix 4:
Sample calculation for changing absorbance into concentration for MM graphs:
Absorbance = ε*c*b
ε = extinction coefficient = 19000 M-1cm-1
b = pathlength = 1cm
c = concentration


Ex:

Kinetic read 2 (10 sec) of Part 1, 0.1M glucose concentration:
A = 1.476
c = A/ε/b
c = 1.476 / 19000 / 1
c = 7.768*10-5

Appendix 5:
Sample calculation for Vi for Part 1, 0.1M glucose concentration, over time interval between 10 seconds and 20 seconds, (same calculations also used in Part 2).

Ex:

Δt = change in time = 10 seconds
Concentration at 10 seconds: 7.768*10-5
Concentration at 20 seconds: 8.479*10-5
Difference = Conc20 - Conc10 = 7.105*10-6
Vi = Difference / Δt = 7.105*10-6 / 10 seconds = 7.105*10-7

1/Vi was used for Lineweaver Burk plots, while Vi itself was used for Michaelis-Menten plots


References

#1: “Enzyme Kinetics.” Basic Enzyme Reactions. Worthington-Biochem. 27 Oct 2006 .

#2: “Competitive and Noncompetitive Inhibition.” MIT. 27 Oct 2006 .

#3: “Glucose Oxidase and Biosensors.” From Biosensors to Food Preservative. InterPro. 27 Oct 2006 .

#4: “A complete guide to nonlinear regression.” Displaying enzyme kinetic data on a Lineweaver- Burk plot . 1999. GraphPad Software. 27 Oct 2006 .

What to Blog About?

Sorry for the lack of posts lately, but I am trying to decide what direction to go with this blog.  I figured it would be easy, because I could just blog about what I have interest or experience in.  But this is such a broad area, and I am having difficulty narrowing it down.  I have experience in mechanical, biomedical, and electrical engineering.  I work on cars a lot, have the knowledge of a mechanic, and know how to do autobody work and paint cars.  I also have an extensive collection of tools and am constantly building things.  I have a pet bullmastiff that my wife blogs about.  I keep a saltwater reef tank as a hobby, and have various corals.  I designed the lighting and filtration systems for the reef tank myself.  I do secret work at a research institute that I am not allowed to talk about.  I have cut up cadavers for research before.  I have written numerous journal articles, and many more papers and review articles.  I have invented several medical devices, two of which have been patented and are in varied stages of development.  I have designed waste treatment systems for chemical plants, designed mechanical robots for building batteries, designed new age lead-acid batteries, designed glucose testing devices for diabetic patients, helped develop new treatments for early detection of retinoblastoma (eye cancer) in children, and numerous other things, some of which are not patented yet, so I can't talk about them.  These are some of my interests, but I am not sure where to go with it yet in this blog.  I have other blogs as well, and my wife does, so I will try not to overlap too much.  If you have any requests or interests, let me know.  I could share some of my research from grad school or from undergrad as well, if nothing else seems to be of interest.

What Kind of Car Should I Buy?

So I am in the market for a new car.  I've had several Fords, and I have been happy with them so far.  I had a Honda Accord, and I liked it a lot too, until it got totaled.  I currently have a Ford Contour, a Ford Mustang and a Chevy Malibu.  I hate the Malibu.  It is always having problems and breaking down.  So the question is:  Foreign or Domestic?  I don't want to spend a lot of money on the car, preferably less than $3,000, so it will be a used car.  Just something I can drive to and from work to put less miles on the Mustang.  So what kind of car should I buy?  I'll have to look around a bit, but comment below if you have any input.  Also, if you know of a good online method for buying cars, I would be interested.  I've tried ebay motors, and craigslist with some small success. 

Social Cognitive Theory of Human Development

Social cognitive learning theory focuses on the idea that people can learn through observation of others around them.  This learning can occur without the stimulation of reinforcement, but can occur through imitation as well.  However, this theory indicates that imitation is a somewhat complex mechanism, and involves the internal cognition of whether or not an action is desirable to imitate.  Albert Bandura, the champion of the social cognitive theory, indicates that experience of different behaviors helps people to develop a sense of self-efficacy, which helps the person to determine their own abilities and then allow them to choose which behaviors to imitate accordingly (Vail & Cavanaugh, 2010).

Social cognitive learning theory mainly addresses the sociocultural aspect of human development, with outside influences playing the chief role in determining what is learned by the person involved.   However, this theory of human development also addresses psychological factors, as the person has to actively interpret the events going on around them in order to learn through observation and imitation, as well as to determine which actions to imitate (Bee, 2000).

Social cognitive theory emphasizes nurture as prevailing over nature in the recurring issue of nature vs. nurture.  Involved within this theory is the belief that it is outside influences that determine what is learned through observation (Hockenbury, 2002).  This is the embodiment of nurture, and does not have much to do with the idea of nature as it pertains to human development through observational learning and imitation.

One strength of the social cognitive theory is that it is scientifically testable, with results that can be operationally measured (Hockenbury, 2002).  Another strength of the social cognitive theory is that it is practical in its ability to be applied.  Based on the conclusions attained by the experiment, adults can create an environment desirable to be imitated, and foster positive growth in nearby children. 

On the other hand, the social cognitive theory has its weaknesses.  One weakness of the social cognitive theory is that it tends to focus too much on a limited number of specific variables, when in actuality there may be a whole host of different influences on behavior other than those observed (Hockenbury, 2002).  Another weakness of the social cognitive theory is that it does not take into account the individual differences inherent in children, and thus cannot be applied universally (Bee, 2000).

Social cognitive theory can be used to address several research questions.  One such research question is posed as follows:  Will a person surrounded day in and day out by other people who all have similar education and career goals to each other be predisposed to pursue a similar education and career pathway to those said individuals?  This research question focuses on the influences of imitation and the recurring issue of nurture as it pertains to human development, and in this case, educational and career goals.  Based on the premises of the social cognitive theory, it can be hypothesized that a person will be predisposed to pursue similar goals to those which they are surrounded by.

References

Bee, H. (2000). The Developing Child (8^th edition). Needham Heights, MA: Allyn and Bacon.

Hockenbury, S. E. (2002). Psychology. New York: Worth Publishers.

Vail, R. V., & Cavanaugh, J. C. (2010). Human Development: A Life-Span View. Belmont, CA: Wadsworth Publishing.

So Today I was Stuck in an Elevator

So today I was stuck in an elevator. I work on the 7th floor of a research building in the downtown of a certain mid-south city. My first clue that something was wrong was that the power was out in the parking garage, and my key card would not lift the gate to let me in. However, that isn’t much of a problem if you remove the gate from the machine. So after the gate was taken off and set aside, I could pull my car in quite easily and park. Over one hurdle and on to the next. As I approached the building some woman came frantically derping out of the building calling for someone down the way telling them the power was out and the elevator wasn’t working. Okay, I thought. Who cares? Use the stairs - that is what they are there for. So I go into the building, which unfortunately has a charter school on the ground floor. Because the power was out, nobody knew what to do, so there were a couple hundred kids all milling about, calling me “sir” and asking what was going on. “I just got here” I replied, not knowing what to say to these inner city kids who went to a charter school so they wouldn’t get shot at the local schools. So I tried the stairs. I knew that when the power fails, the stairs are supposed to unlock in case of a fire hazard, so firefighters can get up, and employees and personnel can get out. Not the case today, however. So I tried swiping my card, and got the familiar beep, but then the green LED faded to dull. I tried the door, but alas, it was still locked. My assumption was that the sensor had just enough capacitance stored within it to read my card, beep, and then die. So I know that there is another set of smaller, single-file stairs within the building. So I go to the other set of stairs, and it is unlocked. I go inside, and under the dim glow of the emergency lights begin my ascent to the 7th floor. It is a long ascent, with each level taking three individual flights of stairs. However, I soon am disappoint. There is an emergency door between the third and fourth floors. It is like a chain-link fence gate that goes from floor to ceiling, and covered in plexiglass. Oh, and it was locked. I have no idea the purpose of the door, and I have no idea why it is called an “emergency door” when it prevents people from traversing either downward or upward on the emergency stairs. So while I was walking up the single-file stairs, I heard a lot of noise below me, and it was progressively getting louder. It seems as if the several hundred students from the charter school were all coming up the stairs because of the power outage. This took a long time… I don’t know why it took so long, other than the fact that the kids didn’t want to be in school and wanted to take as long as possible. It was kinda funny at one point. I could see down the stairs a little way, and this white woman came barging through yelling at the kids “TO THE RIGHT” and then they moved as far as they could and she barged through. She had nothing to do with the school, but worked on one of the upper floors, so it was funny to see her get exasperated. Some people here don’t like black kids. Oh well. So eventually I got downstairs, and when I did the power turned back on. So I got on the elevator. I had to press “7” a few times, but eventually the elevator started moving. I then got all the way up to just past the 6th floor, and the elevator stopped and the lights turned out. I stood in darkness cursing my luck for about 5 minutes, and then the backup power came on. The elevator took me down to the basement and the door opened. Not wanting to get stuck, I got out in the dark creepy basement. There is nothing down there. Just some walls and some storage and some electrical equipment. Only a couple of lights. So I am standing waiting for the power to come back on, and then the lights go out. So I get out my phone and use it for a light, thinking the devil is going to come kill me, and ten minutes later the power comes on. I then get in the elevator and go up to work. So that is the story of why it took me over half an hour to get from the parking garage to my office. Hope this was as entertaining for you as it was for everyone else I told this story to.

Retarded Dinosaurs

So my wife and I were bored one day and used Paint to draw some dinosaurs.  Somehow, the drawing became quite convoluted, and they turned out to look quite stupid, some would even say retarded.  I'm not saying "retarded" to offend anyone, and in fact I only use the term "retarded" to discuss individuals and things that are not really brain damaged, just stupid of their own accord.  Anyway, back on track:  the contrasting colors of the two dinosaurs make them interesting to look at.  They each have some sort of mane going down their backs, and have four legs and two arms each.  Would that make them insects?  I guess not.  They have retarded looking tails, and colored teeth.  The red one can probably not even close its mouth properly due to the immense overbite.  Their arms lack any distinguishing physiology that would allow them to be useful.  They also have udders, which is not reptilian at all, but a mammalian feature.  I guess all of this means that I would be a poor designer for a new life-form, if I did not use my training in genetic engineering, but rather used my creative skills on Paint.  Another point of contention with the drawing and real life is that the legs would not be strong enough to support the weight of the dinosaurs, based on their size, and do not have large enough feet to actively support the bumbling weight of the oversized retarded dinosaurs.  Hope you enjoyed this as much as I did.

I Got A Puppy!

So my wife and I got a brindle bullmastiff puppy.  She should get to be about 110lbs fully grown, based on her parents.  She is going to be big, but she will be fun.  She has had all of her shots and been de-wormed, so nothing to worry about there.  Here is a pic of her:

The Neuroscience of Autism

Autism Spectrum Disorders (ASDs) are classified as a wide range of developmental disorders that present early in life, consisting of a range of developmental disorders, including Asperger syndrome, Childhood Disintegrative Disorder, Rett syndrome, and, most commonly, autistic disorder (1). The phenotypes associated with ASDs are broad as well, including problems in communication, social interactions, and cognitive functioning, usually resulting in mental retardation (2). The incidence of these disorders has increased to approximately one child in every 166 born (3), which is a significant increase from studies performed in earlier years, resulting in a higher percentage of the population afflicted with this range of disorders. Several research groups have identified genetic roots to ASDs as well, meaning that it is passed on from one generation to subsequent ones to varying degrees (4). There is further evidence that ASDs result from an imbalance between the ratio of excitatory and inhibitory signals in sensory, mnemonic, and social systems (5). Because of the ever-increasing number of persons afflicted with this class of disorders, it is certainly a field of interest. However, the specific mechanism responsible for ASDs is not yet established, there is no animal model that is representative of ASDs, and there is no known cure or therapy to alleviate or reduce the negative effects associated with these disorders.

The primary focus of this paper is to investigate the work of Tabuchi et al, entitled “A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice”. The authors of this paper claim to have engineered a mutant mouse model of a phenotype similar to that of ASD patients, which could have further research implications in determining the cause for ASDs, as well as testing potential therapeutic treatments for this class of disorders. The model that Tabuchi et al utilized is the Arg451→Cys451 (R451C) mutation within neuroligin-3. This specific mutation has been found in a subset of human individuals afflicted with ASDs, and is one of the few genetic links that have been established for autistic behaviors. By knocking in the R451C mutation into the neuroligin-3 molecules of mice and comparing these mutant mice to control groups (wild-type mice), the authors investigated whether or not this specific mutation contributes to a phenotype in the mice similar to that seen in patients with ASDs.

Neuroligin-3 is a postsynaptic cell adhesion molecule, which is responsible for mediating synaptic signals. Neuroligin-1 and -2 have previously been investigated in mice, and result in changes to excitatory or inhibitory synaptic behavior (6), while neuroligin-3 has not been investigated in mouse models. Tabuchi et al, upon examining these neuroligin-3 mutant mice, found that this substitution significantly increases the levels of inhibitory synapse markers when compared to controls, as can be seen in their Figure 1. No change was found, however, in the levels of excitatory synapse markers, which is a significant result, demonstrating the potential imbalance that has been hypothesized to be responsible for ASDs. Whole cell recordings were performed on the mutant mice in the somatosensory cortex, as shown in their Figure 3, and they found that the mutant mice exhibited increased spontaneous inhibitory synaptic transmission when compared to KO mice or controls. They also found an increase in inhibitory synaptic strength in the presence of the R451C neuroligin-3 mutation. These results are all in agreement with the increase in inhibitory synapse markers from their Figure 1. This is important because it provides further evidence to the excitatory / inhibitory synaptic potential imbalance that has previously been suggested as the mechanism for ASDs.

Furthermore, Tabuchi et al compared the behavior and learning of the mutant mice to control mice. The mutant mice showed a lower propensity to interact with other mice, indicating decreased social behavior as compared to control mice. In order to test spatial learning, they employed the Morris water maze under both initial and reversal training. The mutant KI mice showed no difference in finding the visible platform, but performed significantly better than controls in finding the hidden platform. This indicates an increased spatial learning over wild type mice, which is a curious result. Most ASDs present with mental retardation and decreased cognitive functioning, but not these neuroligin-3 R451C mice. This could be due to the fact that some persons with ASDs exhibit the rare symptom of enhanced ability, such as the autistic savant, and this mutation tapped into that rare ability. It will be intriguing to see, as time progresses, whether any more research is performed on the enhancement of spatial learning associated with neuroligin mutation. Overall, Tabuchi et al have demonstrated that the R451C mutation acts as a gain of function substitution, resulting in increased inhibitory synaptic transmission in addition to behavior that is characteristic to ASDs.

It is interesting that the authors this paper attempts to develop a model for ASDs utilizing a mutation that is only found in a small percentage of individuals with ASDs. The R451C mutation was only found in two families that Tabuchi et al cited, whereas there have been hundreds of individuals with ASDs investigated. One author indicates that this Neuroligin-3 mutation has only found in 0.8% of individuals with ASDs that have been investigated prior to 2009 (7). This in itself is evidence that there is still much to be uncovered about this class of disorders, and raises the question: If the other classes of ASDs are not associated with a genetic mutation, then what is their cause? It is also a concern that if potential therapies were based off of this rare neuroligin-3 mutation, then the testing of potential therapies on this model may not be accurate beyond the scope of this specific mutation. For example, therapies that are found to be curative to these mutant knock-in mice may not be curative to the vast numbers of individuals with ASDs. However, it is a start, and can provide vital information to researchers who are trying to further understand the mechanisms involved with ASDs so that they can develop therapies to treat these debilitating disorders. Further testing should be performed to determine if there are any other mutations that are present in a greater percentage of those inflicted with ASDs. Also, it is important to note that the ASDs are very broad in their presentation in the population, and there could be many different potential causes that have not been investigated. The work of Tabuchi et al could very well provide the necessary tools needed to understand a subclass of ASDs, which is why its results are so compelling to the field of autism research.

Although this work provides legitimate evidence supporting their model, it is important to note another study that took place shortly after this work that claims a different perspective. In 2008, Chadman et al published a paper suggesting that the neuroligin-3 R451C mutation in a mouse model shows little to no behavioral characteristics similar to autism spectrum disorders (8). Furthermore, they advise that the results of Tabuchi et al are less than compelling, and that the Neuroligin-3 R451C KI mouse model is, in actuality, not one that is representative of ASDs. Chadman et al produced a R451C KI mouse in similar manner to Tabuchi. They subjected the mouse to numerous behavioral experiments as well as learning ones, and found no significant difference between the mutant mouse and littermate controls. They did admit, however, that there were minor differences between the mutant and control mice, just not ones that demonstrate the phenotype of ASDs.

This is further confounded by the publishing of another article by Radyushkin et al in June of 2009, who claim to have induced autistic behavior in neuroligin-3 deficient mice (9). Radyushkin et al found that knocking out neuroligin-3 in mice leads to behavior similar to ASDs, including reduced vocalization and lack of social interactions. They also found, interestingly, that there was a decreased olfactory sense available to these neuroligin-3 deficient mice. Similar olfactory loss has been found in humans with ASDs, giving further evidence that the neuroligin-3 mutant mouse could be a representative model of autistic phenotype. Although the mutation described by Radyushkin was not the same R451C mutation, they found similar behavior mechanisms to Tabuchi et al for the Morris Water Maze behavior. They found that the Neuroligin-3 KO mice showed normal performance for spatial learning and memory, and even showed some increase in spatial learning ability in reverse Morris Water Maze training when compared to controls. This is interesting, especially because it mirrors the increased spatial learning found in the R451C KI mice. Radyushkin’s work also supported Tabuchi’s findings in relation to socialability. Both the Neuroligin-3 R451C mutants and the Neuroligin-3 KO mice showed deficient sociability, and less time spent interacting socially with littermates. Also interesting is the lack of the increased inhibitory synaptic transmission in the Neuroligin-3 KO mice which was found in the R451C mutant ones. This could indicate that there is something more complex at play than just a single point mutation, or something more than simply an imbalance between inhibitory and excitatory synaptic transmission that contributes to the phenotype of ASDs. More likely, it is a combination of several different events working in conjunction to cause ASDs.

Tabuchi et al found that there was a 90% decrease in neuroligin-3 in the forebrain, as measured by immunoblotting and shown in their Figure 1. It could be the case that this downregulation was enough that it allowed for the behavioral patterns seen in their mutant mice to appear as if the neuroligin-3 was absent, as the behavior was similar in nature to the neuroligin-3 KO mice of Radyushkin’s group. This thought is pure speculation, however, and further studies could be performed to give more evidence of this. The work of Radyushkin et al, nonetheless, provides further evidence that neuroligin-3 can be modified in mice to produce a mouse with characteristics of ASDs, contrary to that which was demonstrated by Chadman et al.

The methods described by Tabuchi et al could provide potential therapeutic applications in the analysis and treatment of ASDs. Having access to a model that is a close homolog to the developmental disorder of ASDs, especially one as easy to manipulate and investigate as a mouse model, could yield a tool for further research in examining exactly what the mechanism is behind autistic behaviors, as well as the investigation of ways to reverse that mechanism. Tabuchi et al solidified the notion that that the inhibitory / excitatory synaptic transmission imbalance is a contributing factor to ASDs, and further testing can be performed based on this concept. For example, one potential examination that could be performed is the investigation of a way to rectify the inhibitory / excitatory synaptic potential imbalance, bringing the animal into balance, and possibly ameliorating the negative phenotypical effects associated with ASDs. Another question this raises is: Could this specific R451C mutation’s effects be reversed if the inhibitory synaptic transmission were to be downregulated to account for its unnatural increase?

Tabuchi et al have certainly brought to light some interesting and exciting new research in examining this broad class of disorders that are increasing in number. The potential for new research, the investigation of controversial results, and the unusual increase in spatial learning all would be potential topics of interest for future research.

References
1. E. DiCicco-Bloom et al., J. Neurosci. 26, 6897 (June 28, 2006, 2006).
2. K. Tabuchi et al., Science 318, 71 (Oct, 2007).
3. J. E. Carr, L. A. LeBlanc, Primary Care 34, 343 (Jun, 2007).
4. R. Muhle, S. V. Trentacoste, I. Rapin, Pediatrics 113, e472 (May 1, 2004, 2004).
5. J. L. R. Rubenstein, M. M. Merzenich, Genes Brain Behav. 2, 255 (Oct, 2003).
6. A. A. Chubykin et al., J. Biol. Chem. 280, 22365 (Jun, 2005).
7. C. Lintas, A. M. Persico, Journal of Medical Genetics 46, 1 (January 2009, 2009).
8. K. K. Chadman et al., Autism Res. 1, 147 (Jun, 2008).
9. K. Radyushkin et al., Genes Brain Behav. 8, 416 (Jun, 2009).

So Today I got a New Fish Tank

So I was looking around on Craigslist and found a guy who was selling a saltwater fish tank for $75.  I had fish as a kid, so I thought, why not?  I got this cool fish tank with a few rocks in it and a clownfish and a three stripe damselfish.  It came with a light and a filter and heater and stuff.  Pretty cool.  There are some worms and stuff in the gravel.  I decided to remove the gravel and put sand in it.  Maybe get some other cool stuff as well.  I'll post a pic of the fish tank what it looks like, and then over the next few weeks I'll post more pics as it gets fixed up.  There is a lot of algae to get rid of too.  You can't see it real clearly because the water is cloudy.  I'll take another pic when it clears up.

Technology Assessment for Electrocautery used in Conjunction with Pacemakers

Recommendation:
By utilizing emerging technology regarding electrocautery devices, and making modifications to that technology, an electrocautery device can be constructed that is safe for use on patients with pacemakers.

Introduction:
This report examines the both the existing technology as well as emerging technology regarding use of electrocauteries on patients with pacemakers. By comparing the technologies, recommendations can be made for the construction and implementation of an improved electrocautery safe to use on patients with pacemakers.
There is a medical need involving the inability to effectively use electrocautery devices on patients with pacemakers. Over three million people worldwide have pacemakers implanted into their body to regulate the rhythm of their heart [1]. The pacemaker produces a periodic electrical signal to stimulate the heart to keep its rhythm constant [2]. Because of the sensitivity of the pacemaker, it is susceptible to electromagnetic interference [2]. Electrocautery devices act by using high frequency electrical current through an electrode to cut through tissue, or seal blood vessels [3]. The issue at hand is that the signals from the electrocautery device can interfere with the pacemaker, causing problems with the patient such as: skipped beats, asystole, drained battery, pacemaker reprogramming, and fibrillation [3, 4, 5]. Thus, if a device were to be constructed that allows electrocautery without restriction on patients with pacemakers, many people could benefit.

Existing Technologies:
There are currently several existing ways to deal with electrosurgical devices when used on patients with pacemakers. These ways include only using electrocautery with bipolar signals [6, 7], not using electrocautery devices within a close proximity to the pacemaker location (about 15 cm) [6, 8], only using the device for short bursts, and not an extended period of time [6, 7], placing a magnet over the pacemaker to reset it and keep it in asynchronous mode [7, 8], and using an ultrasonic scalpel instead of a cautery for patients with pacemakers [6, 9]. A patent search also reveals a 1977 cautery protection circuit that was designed to be connected to the output of the pacemaker, absorbing induced electrical signals from electrocautery devices and protecting the pacemaker [10]. The alternative to any of the above ways of dealing with electrocauteries and pacemakers would be to not use electrocautery devices at all on patients implanted with pacemakers.

Emerging Technologies:
There are also two emerging new technologies that will be considered in this report, and compared to the existing technologies.
The first of these is described in a patent application as a device that is used in conjunction with an electrocautery device to protect tissue outside of the target area [11]. This device includes a stent implanted in nearby tissue, supplied with electrical power, which detects electrical fields generated by the cautery to the surrounding tissue. This stent then produces a signal that feeds back to the cautery probe, and regulates the electrical power supplied to the electrocautery, preventing the signal from being strong enough to get past the stent into surrounding tissue [11]. This is described in the flowchart Figure 1, taken from the patent application.




Figure 1: Flowchart of the operation of the stent and electrocautery probe [11].

The second new emerging technology that can be applied as a possible solution to this medical need is described in a 2004 patent. This device is a cardiac rhythm management system that includes a mode specific to electrosurgery [12]. This device is essentially a pacemaker that includes specific programming to counteract the effects of the electromagnetic interference caused by electrocauteries. This program can be activated from outside the body prior to surgery. When the program is activated, parameters such as the pacing of the heart, the AV delay, pulse, and amplitudes can all be controlled [12]. The program also filters out any electromagnetic interference that may be caused by the electrocautery device, making the device immune to electrosurgical interference [12]. A flow chart describing the electrosurgical mode is below, copied from the patent.

Figure 2: Flow chart illustrating electrosurgery mode of the pacemaker program [12].

Decision Criteria:
To best satisfy the medical need described above, the new solution should meet certain criteria. One criterion is that the solution should also not affect the function or operation of the pacemaker. The solution should work on all persons with pacemakers. Another criterion is that the solution should not be prohibitively expensive. The solution should also allow electrocautery in close proximity to the pacemaker without disrupting its function. Finally, the solution should allow electrocautery for an extended period of time on a patient. All of these decision criteria are shortcomings of the current solutions to this medical need, so if the alternatives satisfy these needs they are better equipped for this application.

Analysis of Alternatives:
Based on the above decision criteria, the alternative solutions can be evaluated as follows:
Electric field detecting stent:
Pros:
• Prevents electrical interference from traveling outside the target area, preventing pacemaker interference
• Can be used without resetting the pacemaker or changing pacemaker settings
• Circuitry could be simplified to be made inexpensive
• Would allow the cautery to be used within close proximity of the pacemaker, as long as the stent was there to prevent electrical signals from traveling
• The device could be used for an extended period of time, as long as the stent remains in place
Cons:
• The stent may be bulky and get in the way during surgery
• The device was not designed for use with pacemakers, so modification may be necessary
• If the stent were to fall out of place, signals from the cautery could travel to the pacemaker
• Increased complexity during procedures makes more room for error

Pacemaker with electrosurgery programming:
Pros:
• Prevents electromagnetic interference from disrupting the pacemaker function
• Allows electrocautery to be performed on any person with the programming in their pacemaker
• Would allow electrocautery for an extended period of time
• Would allow the cautery to be used within close proximity to the pacemaker
Cons:
• Would require either a new pacemaker, or a pacemaker modification, so it would not be ready to go on any person with a pacemaker
• Requires modification to the pacemaker program prior to surgery
• Expensive to replace a pacemaker with a modified version

Based on the analyses above, the electrical field detecting stent used in conjunction with the electrocautery satisfies the most criteria, and thus shows itself to be a good candidate to meet this medical need. The pacemaker with electrosurgery programming could meet future needs, but will not work on current pacemakers, and thus it is not as fit to satisfy this current need.

Conclusion:
The electrical field detecting stent combined with the electrocautery looks promising for allowing electrocauteries to be used on patients with pacemakers. However, further analysis and possible modification must be performed to test this device and its compatibility with pacemakers. Overall, this device shows vast improvements over the current technology, and could prove to be an important step forward in electrosurgery.

Actions Required
The cautery-stent apparatus was not designed specifically for use with pacemakers. For this reason, it must be vigorously tested to see if it is sufficient to block electrical signals from reaching and interfering with the pacemaker. Modification to the design of the device may also be necessary to improve the blocking of electromagnetic interference. Overall, it is recommended that this device be analyzed further as the most reasonable solution to this medical need.


References

[2]: DiFrancesco, D. Pacemaker Mechanisms in Cardiac Tissue. Annual Review of Physiology. 55: 455-472, 1993.

[5]: El-Gamal, H. M., R. G. Dufresne, and K. Saddler. Electrosurgery, pacemakers and ICDs: a survey of precautions and complications experienced by cutaneous surgeons. Dermatologic Surgery. 4: 385-390, 2001.

[9]: Epstein, Michael, J. E. Mayer, and B. W. Duncan. Use of an Ultrasonic Scalpel as an Alternative to Electrocautery in Patients With Pacemakers . The Annals of Thoracic Surgery. 65: 1802-1804, 1998.

[12]: Gilkerson, James O., et al. Cardiac Rhythm management System With Electrosurgical Mode. Cardiac Pacemakers, Inc., assignee. Patent 6,678,560. 13 Jan. 2004.

[11]: Kefer, John. Apparatus and method for protecting nontarget tissue of a patient during electrocautery surgery. The Cleveland Clinic Foundation, assignee. Patent Application: 11/502,700. 15 Feb. 2007.

[4]: Mangar, D., G M Atlas, and P B Kane. Electrocautery-induced pacemaker malfunction during surgery. Canadian Journal of Anesthesiology. 38: 616-618, 1991.

[6]: Okan, Erdogan. Electromagnetic Interference on Pacemakers. Indian Pacing Electrophysiology. 2: 74-78, 2002.

[8]: Petersen BT, Hussain N, Marine JE, Trohman RG, Carpenter S, Chuttani R, Croffie J, Disario J, Chotiprasidhi P, Liu J, Somogyi L, Technology Assessment Committee. Endoscopy in patients with implanted electronic devices. Gastrointest Endosc. 65(4):561-8, 2007.

[1]: Rozner, Marc A. The patient with a cardiac pacemaker or implanted defibrillator and management during anaesthesia. Current Opinion in Anaesthesiology. 20: 261-268, 2007.

[10]: Thompson, David L. Cautery protection circuit for a heart pacemaker. Medtronic, Inc., assignee. Patent 4,038,990. 12 Aug. 1977.

[3]: Tobias, Joseph D. Issues in Pediatric and Adult Outpatient Care. Audio-Digest Anesthesiology. 49.13: 1-5, 2007.

[7]: Wilson, Shurea, Steven Neustein, and Jorge Camunas. Rapid Ventricular Pacing due to Electrocautery: A Case Report and Review. The Mount Sinai Journal of Medicine. 73: 880-883, 2006.

Matlab Squid Axon Report

This is the write-up for the Matlab m-file for the squid model of axon signaling that I designed and created for my Bioelectricity course final project.

1. Variables:
m, h, and n are the three major variables for this model, and they vary according to the relationship set forth below in the differential equations. These variables are gating variables, and determine the values for the ionic currents, which are
then used to determine the voltage.

2. Input Signal:
Istimulation = 200uA/cm2 current stimulation for 0.05msec

3. Output Signal:

4. Differential equations:





B) Numerical Integration Method:
The 4th order Runge-Kutta method is a numerical integration method used to solve ordinary differential equations. It is a fourth order method with fifth order error. This method calculates slopes at the beginning of the interval, the midpoint of the interval, the midpoint a second time using the first slope to determine the value, and finally at the end of the interval. The weighted average of these four slopes are taken to determine the position of the next point on the curve of interest.




Initial Conditions


Choose step size, h, for n number
of steps from 0 to N


Calculate slope at beginning
of first step, k1


Calculate slope at midpoint, k2


Calculate slope at midpoint,
using k2


Calculate slope at end


Take weighted average of 4
slopes to find first point


Use the previous points, step size,
and previous k values to find next
point


Repeat until n = N
C) See attached m-file for Matlab code
D) Analysis Results:
1. Steady-state analysis:

Figure D1: Steady state values (m,h,n) of the gating variables as a function of membrane voltage in the range of -100mV to 150mV

2. Time constant analysis:

Figure D2: Time constants (Tau m, Tau h, Tau n) of the gating variables as a function of membrane voltage for the range of -100mV to 150mV

E) Simulation Results:

Figure E1: Plot of the membrane voltage versus time, showing the propagation of an action potential.


Figure E2: Plot of the ionic currents versus time.

Figure E3: Plot of the gating variables as a function of time.

The step size used for this project was h = 0.01. A smaller step size would probably produce more accurate plots, but would also slow down the program. If more computing power was available, it would be possible to have a smaller step size and still run the program reasonably fast. Truncation error is present to some degree due to the finite step size. This error is considered 5th order error, even though this is a 4th order numerical integration. Some data is lost, but the data obtained is still a faithful representation of the actual signal. Round off error is kept low for this program because of the larger step size. If the step size were to be much smaller, the round off error would increase. Numerical instability could be calculated by comparing the step size to α. Based on the resulting figures of this program, the numerical instability seems to be low.

F) Conclusion:
Overall, this project showed an accurate representation of the squid axon model through numerical integration of the Hodgkin Huxley equations. The action potential observed corresponds well to the action potential model learned in class. Therefore, the 4th order Runge-Kutta integration method is found to be valuable in solving differential equations.

Matlab Squid Axon Model of Hodgkin-Huxley

Here is Matlab code for 4th order Runge-Kutta solving of the squid axon model. To operate it, you must copy and paste into a Matlab m-file. It is self containing, and does not need any additional functions to work, other than the typical Matlab library of functions. To see how it works, look at my post entitled "Matlab Squid Axon Report".

Code:

clc %clears workspace
clear %clears any variables

%Model Constants:
Cm = 1.0; %(uF/cm^2) Membrane capacitance
ENa = 115; %(mV) Sodium Voltage
EK = -12; %(mV) Potassium Voltage
EL = 10.613; %(mV) Leakage Voltage
g_Na = 120; %(mS/cm^2) Sodium conductance
g_L = 0.3; %(mS/cm^2) Leakage conductance
g_K = 36; %(mS/cm^2) Potassium conductance
I_stim = 200; %(uA/cm^2) Amount of current stimulation for 0.05msec
Simul_time = 20; %(msec) Duration of the simulation

%Initial Conditions:
V(1) = 0; %(mV) Initial membrane voltage condition at time 0
m(1) = ((.1*25)/(exp(25/10)-1))/(((.1*25)/(exp(25/10)-1))+4); %initial value for the gating variable m
h(1) = 0.07/(0.07+1/(exp(30/10)+1)); %initial value for the gating variable h
n(1) = (.1/(exp(1)-1))/(.1/(exp(1)-1)+0.125); %initial value for the gating variable n

%Stepsize
step = 0.01; %(ms) Step size between points where slope is calculated
N = Simul_time/step; %Total number of points of data to be taken

time1(1) = 0; %initialization of time so time at t = 1 is 0 milliseconds
for num = 1:N %for loop initialization that contains calculation of all the data points
for i = 1:4 %embedded for loop to determine the variables necessary to calculate Hodgkin Huxley
if i == 1 %conditional statement for variables at the first slope
variable1 = V(num); %sets variable1 equal to the voltage at point num for the first slope
variable2 = m(num); %sets variable2 equal to the m value at point num for the first slope
variable3 = h(num); %sets variable3 equal to the h value at point num for the first slope
variable4 = n(num); %sets variable4 equal to the n value at point num for the first slope
end %end of the first slope conditional statement
if i<1 || i>4 %conditional statement for variables at the second and third slopes
variable1 = V(num)+(step/2)*K(i-1,1); %determines the voltage for the second and third slopes using the Runge-Kutta 4th order step increments
variable2 = m(num)+(step/2)*K(i-1,2); %determines the m value for the 2nd and 3rd slopes
variable3 = h(num)+(step/2)*K(i-1,3); %determines the h value for the 2nd and 3rd slopes
variable4 = n(num)+(step/2)*K(i-1,4); %determines the n value for the 2nd and 3rd slopes
end %end conditional statement for second and third slope
if i == 4 %conditional statement for variables at the fourth slope
variable1 = V(num)+step*K(i-1,1); %determines voltage for the fourth slope
variable2 = m(num)+step*K(i-1,2); %determines the m value for the fourth slope
variable3 = h(num)+step*K(i-1,3); %determines the h value for the fourth slope
variable4 = n(num)+step*K(i-1,4); %determines the n value for the fourth slope
end %end fourth slope conditional statement
for L = 1:4 %corresponds to slopes of points
if L == 1; %if for the first slope
if time1(num) > 0.05; %conditional statement accounting for the 0.05ms stimulation, so after 0.05ms, the stimulation current is zero
I_stim = 0; %current stimulation is zero after 0.05ms
I_Na(num) = g_Na*variable2^3*variable3*(variable1-ENa); %determines the value of the sodium current at point 1
I_K(num) = g_K*variable4^4*(variable1-EK); %determines the potassium current at point 1
I_L(num) = g_L*(variable1-EL); %determines the leakage current at point 1
K(i,L) = -(I_Na(num)+I_K(num)+I_L(num)-I_stim)/Cm; %determines the value of the dV/dt of the voltage equation

else %condition when time is less than 0.05msec
I_Na(num) = g_Na*variable2^3*variable3*(variable1-ENa); %determines the sodium current at point 1
I_K(num) = g_K*variable4^4*(variable1-EK); %determines the potassium current
I_L(num) = g_L*(variable1-EL); %determines the leakage current
K(i,L) = -(I_Na(num)+I_K(num)+I_L(num)-I_stim)/Cm; %determines the value of dV/dt (slope)
end %end conditional statements
end %end conditional statements
if L == 2; %if for the second slope
Alpha_m = 0.1*(25-variable1)/(exp((25-variable1)/10)-1); %finds the Alpha m H-H gating variable
Beta_m = 4*exp(-variable1/18); %finds the Beta m H-H gating variable
K(i,L) = Alpha_m*(1-variable2)-Beta_m*variable2; %finds the next K value slope
end %end condition
if L == 3; %if for the third slope
Alpha_h = 0.07*exp(-variable1/20); %finds the Alpha h HH gating variable
Beta_h = 1/(exp((30-variable1)/10)+1); %finds the Beta h HH gating variable
K(i,L) = Alpha_h*(1-variable3)-Beta_h*variable3; %finds the next slope
end %end condition
if L == 4; %4th slope
Alpha_n = 0.01*(10-variable1)/(exp((10-variable1)/10)-1); %HH gating variable
Beta_n = 0.125*exp(-variable1/80); %HH gating variable
K(i,L) = Alpha_n*(1-variable4)-Beta_n*variable4; %4th slope
end %end condition
end %end for loop
if i == 4; %conditional statement
for P = 1:4; %for loop to determine the values of k needed for finding the next points
kbar(P) = (1/6)*(K(1,P)+2*K(2,P)+2*K(3,P)+K(4,P)); %finds the weighted average of the slope voltage values
end %end for loop
V(num+1) = V(num)+step*kbar(1); %determines the value of the next voltage point
m(num+1) = m(num)+step*kbar(2); %determines the value of the next m
h(num+1) = h(num)+step*kbar(3); %determines the value of the next h
n(num+1) = n(num)+step*kbar(4); %determines the value of the next n
time1(num+1) = time1(num)+step; %increments the time so that it continues on
end %end conditional statement
end %end for loop
end %end initial for loop

I_Na(num+1) = g_Na*m(num+1)^3*h(num)*(V(num+1)-ENa); %sodium ionic current for the next point
I_K(num+1) = g_K*n(num+1)^4*(V(num+1)-EK); %potassium ionic current for the next point
I_L(num+1) = g_L*(V(num+1)-EL); %leakage current for the next point

Voltage = -100:.1:150; %voltage span for plotting

Alpha_m = 0.1.*(25-Voltage)./(exp((25-Voltage)./10)-1); %alpha m gating variable
Beta_m = 4.*exp(-Voltage./18); %beta m gating variable
Tao_m = 1./(Alpha_m+Beta_m); %Tm time constant

Alpha_h = 0.07.*exp(-Voltage./20); %alpha h gating variable
Beta_h = 1./(exp((30-Voltage)./10)+1); %beta h gating variable
Tao_h = 1./(Alpha_h+Beta_h); %Th time constant

Alpha_n = 0.01.*(10-Voltage)./(exp((10-Voltage)./10)-1); %alpha n gating variable
Beta_n = 0.125.*exp(-Voltage./80); %beta n gating variable
Tao_n = 1./(Alpha_n+Beta_n); %Tn time constant

m_bar = Alpha_m./(Alpha_m+Beta_m); %sodium current m value
h_bar = Alpha_h./(Alpha_h+Beta_h); %sodium current h value
n_bar = Alpha_n./(Alpha_n+Beta_n); %potassium current n value

figure(1) %produces the first figure
plot(time1,V) %plots voltage versus time, an action potential
xlabel('Time (ms)') %labels the x axis with time
ylabel('Membrane Voltage (mV)')%labels the y axis with voltage
title('Action Potential') %provides a title for the plot

figure(2) %produces the second figure
plot(Voltage,m_bar,Voltage,h_bar,Voltage,n_bar) %plots the voltage versus gating variables, all three on one plot
xlabel('Voltage (mV)') %labels the x axis with voltage
ylabel('Gating variables') %labels the y axis with gating variable values
title('Gating Variables vs Voltage') %provides a title for the plot
legend('m value','h value','n value') %produces a legend to label the plot curves

figure(3) %produces the third figure
plot(Voltage,Tao_m,Voltage,Tao_h,Voltage,Tao_n) %plots voltage versus time constants for all three time constants
xlabel('Membrane Voltage (mV)') %labels the x axis with voltage
ylabel('Time Constant Value') %labels the y axis with time constant values
title('Time Constants as a function of Membrane Voltage') %provides a title to the plot
legend('Tau m','Tau h','Tau n') %provides a legend to label the curves

figure(4) %produces the fourth figure
plot(time1,I_Na,time1,I_K,time1,I_L) %plots the ionic currents versus time
title('Ionic Currents vs Time') %adds a title to the plot
xlabel('Time (ms)') %labels the x axis with time
ylabel('Ionic Current (uA)') %labels the y axis with current
legend('Sodium Current','Potassium Current','Leakage Current') %provides a legend to label the plots

figure(5) %produces the final figure
plot(time1,m,time1,h,time1,n) %plots the gating variables versus time
xlabel('Time (ms)') %labels the x axis
ylabel('Gating variables') %labels the y axis
title('Gating Variables vs Time') %adds a title to the plot
legend('m value','h value','n value') %provides a legend to label the plots

Spanish Essay about Problems in the World

This is a Spanish essay that I had to write for my Spanish class a few years back:


Hay muchos problemas ne el mundo. La contaminacion es un problema de todo el mundo. La contaminacion es un problema importante de la civilizacion. Las industrias y los vehiculos producen contaminacion del aire. El cancer pulmonar y la bronquitis estan resultados de la contaminacion del aire en todo el mundo. La lluvia acida esta un otro resultado tambien de la contaminacion del aire, especialmente en los paises en vias de desarrollo.

La contaminacion es un peligro para muchas personas, animales, y para vegetales. El cigarrillo es un factor de la contaminacion ye tiene muchos enfermedades. Un otro factor de la contaminacion es que las fabricas estan quemandos las materias primas. La contaminacion es un problema grande y necisitamos tratar de controlar la contaminacion en el mundo.

El huracan es un evento reciente que dano mucho de los Estados Unidos. El huracan Katrina destruyo muchas casas y mata muchas personas. Katrina fue un acto del medio ambiente. A causa de Katrina, la cuidad Nueva Orleans fue destruida.

Muchas personas ayudaron a las victimas del huracan. Ahora, muchos personas estan rescatado de la contaminacion que Katrina hizo. A causa de Katrina fue inundacion del parto de los Estados Unidos.

El petroleo fue desperdicio en el huracan, y nosotros pagamos caro por la gasolina. El petroleo es danino al medio ambiente tambien. El petroleo contamina el aire.

El petroleo es necesario para la vida en los Estados Unidos. La gasolina es del petroleo, y necesitamos la gasolina para el combustible para los coches.

La inflacion es un problema tambien en los Estados Unidos. Un desastre como Katrina hace el precio aumentar mucho. El precio de la gasolina esta muy alto porque de la inflacion.

La inflacion es danina para la economia. Un poco de los Estados Unidos dicen que la inflacion es de George W. Bush, el presidente de los Estados Unidos. Los tres, el huracan, el petroleo, y la inflacion causen problemas por los Estados Unidos y tambien todo el mundo.

Por los anos pasados, algunas personas dicen que la temperatura tiene el aumento de 1 grado C. Las personas dicen que los humanos causen el aumento de la temperatura y no es la naturaleza. Tambien, algunas personas dicen que el aumento de la temperatura produce huracanes.

Otros personas dicen que la temperatura no tiene el aumento mucho, y los humanos no causen el aumento pero es la naturaleza.

El aumento de la temperatura es porque del efecto invernadero. El efecto invernadero es cuando el dioxido de carbono en la atmosfera se recalenta porque del sol. El dioxido de carbono en la atmosfera es nefasto al medio ambiente. Cuando el dioxido de carbono en la atmosfera se recalenta, todo el mundo tiene el aumento de la temperatura.

Algunas personas dicen que los humanos causen el aumento de la temperatura. Estos personas dicen que los humanos causen el dioxido de carbono aumentar. Los humanos queman la madera ye la materia prima. Tambien, queman el combustible para los coches. Con quemando, el nivel del dioxido de carbono en la atmosfera tiene el aumento. A causa del aumento de la temperatura, todo el mundo tiene el efecto invernadero y el aumento produce huracanes con perditos. Los huracanes son danino, como Katrina. En los Estados Unidos, tenemos muchos huracanes ese ano. Pero, los huracanes son naturalezas o de los humanos?

La destruccion de la selva y las materias primas producen mucho dioxido de carbono. El dioxido de carbono esta alrededor el mundo. La capa de ozono tambien es un problema de ahora. Quemando el combustible y el humo y la ceniza de las fabricas estan danino por la capa de ozono. El humo destruyo la capa de ozono. La capa de ozono es muy importante para la vida. Sin la capa de ozono, todo el mundo va a morir porque la capa de ozono es necesario prevenir el sol de quemando el mundo.

El aumento de la temperatura es un problema muy grave en el mundo ahora. El efecto invernadero es necesario para la vida, pero el aumento del nivel del dioxido de carbono causen el aumento de la temperatura. Una posibilidad es que el huracan Katrina fue un resultado del efecto invernadero.

La destruccion del huracan Katrina fue muy grande. Para prevenir los huracanes, necesitamos dejar del aumento de la temperatura. Necesitamos conservar las materias primas. Tambien, necesitamos reciclar y no destruir. La selva es muy importante ye necesitamos conservar la selva.

Algunas personas dicen que el aumento de la temperatura no es muy grande y es solo de la naturaleza. Estos personas dicen que no es necesario para conservar las materias primas y no necesitamos proteger la atmosfera. Estos personas dicen que no necesitamos reciclar, pero podemos usar las materias primas y podemos usar las fabricas y no es un problema.

Hay muchos problemas en el mundo. La contaminacion causa enfermedades. La contaminacion del aire causa el asma, la bronquitis, el enfisema, y el cancer pulmonar. La contaminacion es un peligro para muchas personas, animales, y para vegetales. El huracan Katrina es un evento reciente y el huracan destruyo muchas casas y mata muchas personas. La inflacion es un problema tambien en los Estados Unidos, y es danino por la economia. Un otro problema es el aumento de la temperatura porque del efecto invernadero. Hay muchos problemas en el mundo y necesitamos trabajar juntos para rescatar el mundo.

New Postings

You may have noticed some new postings from me that appear as if they could have come from an English assignment.  That is just what they are.  I have taken some of the literature that I have written for past courses in college, and published it online.  It is a way to get my ideas out there, and gives me new ideas to look ahead to.  I'll put some links up when I get a chance, but for now you can just look at my other postings for the posts that I am describing.  Have fun!

Ralph Waldo Emerson's "Nature" and "Language"

Ralph Waldo Emerson's "Nature" and "Language" From "Nature" explain in detail Emerson's view on what nature is and how it relates to the world. He also gives his views on how language is related to nature. Through nature, one may transcend the worldly and accomplish a rising up to a higher understanding of the world. Language is how nature is displayed and enables one to reach that heightened understanding.

According to Emerson, nature is the natural parts of this world, such as flowers, animals, mountains, or woods. Nature is what is untouched by humans and society, and one must leave his own room as well as society in order to go into solitude. Amidst solitude, one may come to realize nature and achieve a type of spiritual awakening. Emerson suggests looking at the stars as a way of being alone and then examining the natural things of this world in order to realize the wisdom of nature. When we view nature in this way, we see beyond what is apparent to the human eye. We are able to think of things in a “poetical sense in the mind,” where we make connections and have a better awareness of the beauty of nature and can better convey those thoughts. In nature, one loses all of his connections to society and becomes nothing, just a “transparent eyeball” that Emerson suggests is akin to having God’s presence flow through him. It is only in nature, among the untainted wilderness, that this spiritual event can occur. However, this is not always the case with nature. As our perceptions of the world around us change, so does our views of nature. If we are experiencing sadness, then nature may appear dull or resentful. Only when nature and man agree can one achieve a spiritual awakening.

Emerson describes language as the method in which nature conveys itself to mankind. Every word that is used can be traced back to something having to do with nature. The meaning of words used today goes back to the beginning of language, when all words came from things in nature, and it was over the years that these nature words transformed into our language today. The natural meaning of words in language is used to describe spiritual facts. Parallels are used between nature and the spiritual through words. Language in its beginnings was pure, represented only by nature itself. Men today can use the natural aspects of language to empower their conversation. If one really desires to communicate truth and nature without corruption, he can do so using the symbols of nature. Corruption of language occurs when nature is no longer used to convey truth. Excellent writers, through imagery, can display truth of almost a spiritual and transcending nature and create magnificent pieces of work. Emerson goes on to say that it is the will of God and godly ideas that are expressed through pure symbols of nature through words. Nature can effectively display the human mind without loss. Through words of a natural nature, one may effectively write or communicate aspects of a spiritual nature with a simplistic beauty that can only be found in the natural world.

Nature

Nature, according to me, is defined as the creation of God of all that is natural. This includes all life, the planet earth, the sun and moon and the entirety of the universe. Nature is seen in everyday life, and can be felt and experienced. It is a tangible truth, something open and free that can be seen by everyone living. Nature is in the very air we breathe, it is on the dirt and grass that we walk over every day, it is in the water we drink, it is in our blood, and it is all around us. Without nature, life would not exist. Nature, as vast and all encompassing as it is, is not able to be controlled by humans. The course of nature is controlled by the hand of God, and the wisest of man cannot begin to come up with a way to control nature. If controlling nature were in the hands of man, the life on this planet would surely die. There are an infinite number of processes and harmonies that have to be sustained in order for life to survive, and nature, as sustained by God, is what keeps life going on this planet. Nature is identifiable, and you can see nature and experience it just by looking around you at the natural aspects of the world. Watch an ant crawl across the ground and work together with thousands of other ant without argument, all working toward a common goal. Stand outside in a thunderstorm and see the magnificence and grandeur of nature in all her glory and power, uncontrollable and wild and yet with a purpose that is perfect. This is nature to me. It sustains life and is all around us and we get to experience it every day and stand by in awe at the magnificent wisdom intrinsic in all of this thing that we call nature.

Expository Thoughts about the Ozone Layer

The ozone layer has become a greatly discussed topic over the past several years, in both scientific and non scientific communities. It is important for one to realize exactly what ozone and the ozone layer are, and to understand the issues relating to them. If not for the ozone layer, life would not exist on the surface of the earth.

The ozone layer is important to everyone that lives on the earth. A cloud of invisible gas encompassing the planet, the ozone layer acts as a “global security blanket” for the earth, blocking out harmful ultraviolet rays, while letting other rays from the sun reach the earth (Fisher 13). Ultraviolet rays are damaging to life on earth, killing plant life and causing cancer in humans. This is the reason that sunblock has become so important in recent years.

The sun is the greatest source of energy for the earth. The temperature of the sun is about 6000 degrees centigrade, and it gives off great magnitudes of radiant energy (Schneider 13). This radiant energy spreads out from the sun and eventually reaches the earth. Some of this energy is reflected from earth’s atmosphere back into space. Some more of the sun’s radiant energy is reflected back into space from the surface of earth. But about 25% of the suns radiant energy is absorbed into the earth’s atmosphere (Schneider 14). The ozone layer is what determines exactly what is absorbed and what is reflected from the sun’s energy. Letting in wavelengths other than ultraviolet, the ozone layer allows enough radiation in to keep the earth warm and provide light (Fisher 13). The 25% of the radiant energy that is absorbed by the atmosphere is absorbed through greenhouse gases in the stratosphere, and the heat that results is enough to sustain life on earth. This is known as the “greenhouse effect,” and is called so because it is similar to the way a greenhouse works. The ozone layer holds in greenhouse gases in the stratosphere of the earth, just as glass panels of a greenhouse hold in heat. As the sun’s radiant energy beats down on the earth, the ozone layer allows some energy through to the greenhouse gases. These gases heat up and send their heat down to the atmosphere and the surface of the earth. According to Stephen Schneider, a Climatologist with the National Center for Atmospheric Research, “If it weren’t for the greenhouse effect, temperatures at the earth’s surface today would be some 33 degrees C colder than they are, and life as we know it would not exist” (13). This is a valid statement and agreed upon by most scientists. It is the ozone and stratospheric gases that hold in the heat from the sun to make earth habitable.

In order for one to understand the implications of the ozone layer, one must first understand what the ozone layer is. The oxygen breathed by humans is comprised of two atoms of oxygen, and it is written O2. Ozone, however, is also a molecule comprised of oxygen. But ozone is of a different nature. Ozone is comprised of three atoms of oxygen, and is written O3. Oxygen is needed for life and is found abundantly in the biosphere. Ozone in the biosphere, however, is a poison, and cannot be breathed by animals (Fisher 17). Ozone is found mainly only in the high stratosphere, about 12 to 20 miles above the surface of the earth, and it is here that the oxygen absorbs ultraviolet radiation form the sun and is turned into ozone (Fisher 18). There is one other place besides the stratosphere that ozone can be found. This is as a pollutant at ground level. Ozone at ground level results from oxides of nitrogen chemically reacting with volatile organic compounds in the sunlight (“Chief Causes for Concern”). So basically, ozone at the surface of the earth is from the sun reacting with pollution on earth. It is for this reason that ozone is a major constituent of smog. Automobile exhaust, industry emissions, gasoline vapors, and chemical solvents all react with sunlight to produce ozone in the biosphere (“Chief Causes for Concern”). This ozone at ground level is the worst during the hotter months of the year, when smog is most prevalent. Another problem with ozone at ground level is that it can be transported very far, even hundreds of miles away (“Chief Causes for Concern”). This pollutant is a poison both to plants and animals as well as humans, meaning that disease and sickness may occur as a result of exposure to ozone. Other possible results of ozone pollution in the biosphere could be the damaging of natural ecosystems and plant life within range of the ozone pollution.

While ozone in the biosphere is a bad thing, life on earth would not be possible without ozone in the stratosphere. The radiant energy emitted by the sun reaches the earth at all different wavelengths. As stated earlier, some wavelengths are allowed to pass through the ozone layer, and these are the longer wavelengths, and these provide heat and light for the earth. However, ultraviolet radiation from the sun also reaches the earth, and the wavelength of this radiant energy is extremely short, and “the shorter the wavelength, the higher its energy, or radiation, content and the more dangerous it is to life on earth” (Fisher 18). Ultraviolet radiation is harmful in varying degrees. UV-A is the longest wavelength ultraviolet radiation, and it is generally not considered harmful (Fisher 18). UV-B is the middle wavelength and it is destructive to life when it leaks through the ozone layer, causing cancer and other problems (Fisher 18). UV-C is the shortest wavelength ultraviolet ray and “would be an instant death ray were any of it to get through the ozone” (Fisher 18). UV-A rays escape through the ozone layer to the surface of the earth quite frequently, and they have something to do with the tanning of humans when they are out in the sun. UV-B rays escape much less frequently through the ozone layer, but are also much more powerful. These rays cause sunburn when humans are out in the sun, and they are also the major contributor to skin cancer. Sunscreen and sunblock have become much more popular in the recent years that the implications of these UV rays have been made known. UV-C rays are not allowed through the ozone layer into the lower atmosphere whatsoever.

There are more implications to ozone than it being a pollutant or blocking out UV rays, however. There is much controversy surrounding some issues dealing with the ozone layer. One such issue is that of ozone depletion. Research has shown that there is a possibility that the ozone layer is slowly being eroded away. The scientists in favor of this idea believe that the release of chlorofluorocarbons (CFCs) or other ozone-depleting substances are slowly eroding the ozone layer as they make their way up into the stratosphere (“Ozone Depletion”). If this suggestion is true, the repercussions could be very grave. If the ozone layer erodes, more UV rays will escape through the ozone into the biosphere, damaging plant and animal life and increasing the chances for humans to get skin cancer. The opposing idea to the erosion of the ozone layer is that the ozone layer is not really eroding at all, just going through periodic cycles of thinning. Regardless, the ozone layer is important to human life and health on earth.

A final controversy regarding the ozone layer is the idea of global warming. Global warming is the idea that the levels of carbon dioxide are rapidly increasing with human activity (such as the burning of fossil fuels), and that these increased levels will allow the atmosphere to absorb more of the sun’s radiant energy. Simultaneously, the erosion of the ozone layer will allow more radiant energy to escape to the atmospheric gases, such as carbon dioxide. According to this theory, this event will heat up the earth to an extent that life will no longer be able to exist. This theory has been under much speculation over the past several years, and it still remains an unproved theory. The opposite view to this theory is that there really is no global warming at all. Some people believe that global warming is an unscientific hoax, just to attract the media and scare people into being more environmentally-minded. Whether one believes in global warming or not is for one to decide, but it is apparent that the ozone layer is an important issue facing the world today.

The ozone layer is important to life and health for humans here on earth. While it is present as a pollutant here on the surface of earth, its presence in the stratosphere preserves life here on earth. Controversy surrounds the ozone layer in several ways, and it is for each person to decide their own views on the subject. The implications of the ozone layer are important no matter what one decides, however.

Works Cited
Chief Causes for Concern. U.S. Environmental Protection Agency. 03 Oct. 2005 .
Fisher, Marshall. The Ozone Layer. New York: Chelsea House Publishers, 1992.
Ozone Depletion. U.S. Environmental Protection Agency. 03 Oct. 2005 .
Schneider, Stephen H. Global Warming. San Francisco: Sierra Books Club, 1989.

Reviews of Books Pertaining to Genetic Engineering

The following are reviews of different articles/books related to genes and genetic engineering. Each review gives a basic summary and some general information about the book/article. Enjoy.


Aldridge, Susan. The thread of life: the story of genes and genetic engineering. New York: Cambridge University Press, 1996.
This book is all about genes and genetic engineering and the human genome project and everything that has to do with genetic technology. It is very in depth into the process that plants and animals go through in the genetic engineering process, even down to the cellular structure. This book is very informative, but I think that it may actually be too informative for my purposes, and thus may not be appropriate for my purposes. The bias of this book is definitely supportive of genetic engineering.

Caswell, Julie A. "Labeling Policy For GMOs: To Each His Own?." AgBioForum. (2000). 25 Oct 2005 .
This source is an online journal for agrobiotechnology and contains many articles dealing with topics pertaining to genetic engineering and biotechnology. This site contains much up-to-date information that is very useful. As far as labeling, I managed to find an entire article that explains in depth what labeling of genetic engineered food is and what is involved in that process. This site has proved to be very useful to me in my research and provides much needed background information. There is no bias in this website that I can see.

“Genetically Modified Foods and Organisms.” Human Genome Project Information. 17 Sept 2004. The Human Genome Program of the U.S. Department of Energy Office of Science. 27 Oct. 2005 .
This site is a government site sponsored by the United States. It contains a wealth of information about government policy regarding the labeling of genetically engineered food. The good thing about this site is that it does not have a bias either way in the issue, but rather presents government policy to the reader and allows him or her to make his or her own decision. This site is very useful to me in finding what the current government policy is regarding labeling.

Huffman, Wallace E., Jason F. Shogren, Matthew Rousu, and Abe Tegene. "The Value to Consumers of GM Food Labels in a Market with Asymmetric Information: Evidence from Experimental Auctions." 15 May 2001. 25 Oct 2005 .
This is an online published scholarly journal written by three different professors. It contains a lot of information about labeling and is very thorough. This journal effectively addresses both sides of the argument of labeling. It provides a lot of information supporting labeling, as well as a lot of information against it. However, after reading this article, I noticed a bias toward the side that labeling is excessive and should not be implemented. This journal is very helpful to me and helps me support my argument.

Reiss, Michael J. Improving nature? : the science and ethics of genetic engineering. New York: Cambridge University Press, 1996.
This book is mainly concerned with the morals and ethics of genetic engineering. As most books of its kind, it addresses both sides of the argument. This book does not really take a stance either way as to whether it is moral or not to genetically engineer nature. This book seems to be intended as an introduction to genetic engineering for the person who is not an expert on the issue. I rather like this book as it introduces theology into the issue and provides case studies of different relative issues. Overall, it didn’t really have a bias either way but was intended to inform, and did so.

Rifkin, Jeremy P. The Biotech Century. New York: Putnam, 1998.
This book is one of the only print sources that I’ve found to be biased towards genetic engineering. It is supporting genetic engineering. The book describes in quite a bit of detail the way that technology has advanced to the point that biotechnology can do lots of stuff never imagined, such as genetic engineering. The point of view of this book, however, talks a lot about computer and how they have impacted this technology. This is the only reason that this source may not be right for my topic.

Labeling Genetically Engineered Food

     We all have gone to the supermarket and bought groceries. Buying and eating food from the store is an important part of life here in the United States. Unbeknownst to you, some of the food that you have eaten has probably been genetically engineered. You most likely have not noticed it because it is not very much different than naturally grown food. Genetically engineered food is just as healthy for you, even more so in some cases, and it is usually better looking and tasting. Despite the obvious desirability of better looking and better tasting food, a growing controversy today in the agricultural world is that of the labeling of genetically engineered or modified produce. Should you be able to tell, when you go to the grocery store, whether or not your food has been genetically modified? Some may think that this is a good idea and that consumers need to know. However, why should we know if our food was genetically engineered or not? The food still tastes good and is just as healthy as naturally grown food. So what is the big issue? Why should we spend millions of dollars, raising the price of producing food as well as the price of the food itself, just to satisfy some people’s desires to know the process their food went through before it came to the store? The mandatory labeling of genetically engineered produce is cost ineffective, unnecessary, and should not be implemented.
     First of all, importance lies in an informed opinion, so we need to examine and find out what exactly constitutes genetically engineered food. And in doing so, we need to define what food we are dealing with. The topic at hand is the genetic engineering of produce, the crops and plants that farmers harvest and sell to the supermarkets and grocery stores. This is a different issue than injecting cows with growth hormones to make them produce more meat for the market. According to the United States Government, “Combining genes from different organisms is known as recombinant DNA technology, and the resulting organism is said to be ‘genetically modified,’ ‘genetically engineered,’ or ‘transgenic’” (“Genetically Modified Foods and Organisms”). So basically, a food product is considered one of these terms if someone combines some of its genes with those of another food product in order to produce a resultant product with a combination of the genes of the two parent products.
     Moreover, it is important to realize that much of the fear surrounding genetically modified foods is unfounded. The main reason for genetic engineering of produce is to produce desirable traits in the offspring. Some of the major traits that are produced in genetically engineered produce are: reduced time to plant maturity, increased nutrients and yields, better resistance to disease and pests, and improved taste and quality (“Genetically Modified Foods and Organisms”). These are all very legitimate goals and should be treated as such. They are not, on the other hand, damaging food or increasing health risks for the consumer. Conversely, genetically modified food is in development to benefit human health. For example, in development right now is a “sweet potato resistant to a virus that could decimate most of the African harvest, rice with increased iron and vitamins that may alleviate chronic malnutrition in Asian countries, and a variety of plants able to survive weather extremes” (“Genetically Modified Foods and Organisms”), showing that much good can be accomplished through the genetic engineering of produce.
     Mandatory labeling of genetically modified products has been implemented in several nations throughout the world, such as Japan as well as several countries of the European Union. Support for mandatory labeling in the United States has come about with growing anticipation as well. Currently in the United States, the policy is that no mandatory labeling system is implemented. Farmers may, at their wish, determine whether or not they label their produce as genetically engineered or not. This is a far better system than mandatory labeling. Some farmers may deem it more cost effective to label their products as genetically engineered, hoping that their product will be seen as better as and healthier than the other produce available. In this case, the farmer would do well to label his produce. Another policy currently in effect from the FDA is that products must be labeled as genetically modified if they are extremely different from the original product (Huffman 3). An example of this situation would be a giant tomato or corn with extremely large kernels. The issue at hand is different, however. The matter we are considering deals with the labeling of products that could not otherwise be determined by the consumer as being natural or genetically engineered.
     With mandatory labeling, however, as opposed to voluntary, there are many more factors to consider. The concern brought about is that everything would have to be labeled, whether it is genetically engineered or not. This imposes a very high cost both to the producer and also to the consumer. Along with the label telling whether or not a product is genetically engineered, it is necessary to explain to the consumer on the label just what exactly genetic engineering is and what it does to the product. Also, non – genetically engineered products cannot be labeled in such a way that designates that genetic engineering affects the product in an adverse way (Huffman 3), meaning that non genetically engineered food cannot delegate itself as being safer or healthier solely because it is not genetically engineered. An additional cost to the millions of dollars it will take to label every product put up for sale is the cost of verifying the claims made by the farmers as to whether or not their product is genetically engineered. According to Julie Caswell, an expert in the field of agrobiotechnology, “Labeling affects the entire supply chain for food products. It requires definition of the attribute to be labeled and segregation of products with and without the characteristics throughout the supply chain from seed inputs to the supermarket shelf” (Caswell). This brings into the picture a whole new set of problems. For example, if a field of corn that has been enhanced through genetic engineering is adjacent to a field of corn that grows naturally, the concept of labeling suggests that each farmer’s produce must be labeled accurately. This will involve painstakingly difficult scrutiny of each farmer and their fields. If the farmer with naturally grown corn has machinery that accidentally brushes up against his neighbor’s corn, the whole crop harvested by that machinery will be contaminated and cannot be labeled as free of genetic engineering. As you can imagine, the costs for monitoring the labeling of crops is very high. And where will this cost be passed on? To the consumers, of course. The prices of all produce in the supermarkets will increase as a result of mandatory labeling. This will effectively act similar to an increase in taxes. Lower income families, who spend more of their income on food anyway, will sink deeper into poverty with the heightened prices of produce as a result of mandatory labeling (Huffman 5). Thus we need to ask ourselves if these great costs are worth the small amount of knowledge to be gained from the labels on produce.
     In addition to the cost incurred as a result of mandatory labeling, the whole idea of mandatory labeling warrants the label itself as irrational and unnecessary. The FDA already requires labeling of products if alterations from their original state take place. This is all that should be needed. If no obvious alterations are present, then why does the consumer need to know? There is nothing dangerous about the genetic alteration of produce. It is certainly not adding anything such as poison or pesticides to the produce. For years, pesticide use on produce has been debated, but as of today no labeling system has been implemented regarding their use. And pesticides have been proven in some cases to be detrimental to human health. So why should genetic modifications be labeled, when no evidence is relevant concerning their harm to human health? All things considered, mandatory labeling just seems silly and there is no reason for it to be declared on labels for consumers to read. The government of the United States makes it priority for its citizens to be safe. The FDA has been doing its job correctly, and it would not let produce go out on shelves for us to buy if it was dangerous. It is time we put faith in our government and accept things the way that they are, genetically modified or not.

Works Cited
Caswell, Julie A. "Labeling Policy For GMOs: To Each His Own?." AgBioForum. (2000). 25 Oct 2005 . “Genetically Modified Foods and Organisms.” Human Genome Project Information. 17 Sept 2004. The Human Genome Program of the U.S. Department of Energy Office of Science. 27 Oct. 2005 .
Huffman, Wallace E., Jason F. Shogren, Matthew Rousu, and Abe Tegene. "The Value to Consumers of GM Food Labels in a Market with Asymmetric Information: Evidence from Experimental Auctions." 15 May     2001. 25 Oct 2005 .