Drafts

Phytochromes consist of a protein, covalently linked to a bilin chromophore. There is two types of them which divides into A and B. They both have PAs domain and GAF domain. The difference is that phytochrome A is etiolated, displays far red and labile light. B is just red. Phytochromes interact heavily with PIFs. PIFs are a subset of transcription factors that negatively regulate photomorphogenesis. COP1 forms a complex in the nuclues, functioning as an E3 ubiquitin ligase, making positive regulators of photomorphogenesis for degradation. There are many processes in this complex for an example, cryptochromes. Haven't learned much of cryptochromes yet though.

- low Thyroid v. high Thyroid symptoms associated w/ these levels
- hypothyroidism: excothalmose, bulging eyes, 30% of patients have them
- hyperthyroidism: diagnosing these disorders is difficult b/c symptoms are not the same for everybody even tho it’s the same H
- radioimmunoassay is a way to measure thyroid hormone in you by the doctor
- measurements of thyroid hormone in blood defines thyroid diseases, can have all these symptoms but unrelated to Thyroid hormone levels is the “normal” range “normal”? how is the range measured?
- studies of populations that are the same in many ways
- exclude those w/ signs of disease
- there is a lot of variation in the population but for each individual , variation is only about 10%, they only take one measurement for you
it could be a normal value for her but it could be outside the reference age, bc of varianve of the ind
- sub-clinical TH category?
- important for pregnancy because fetus require Thyroid for development and their's don't begin to function until later on
- t4 and t3 released from T gland, but t4 comes from liver also
- t3 levels in blood aren’t indicator of T function, good indicator of t4 metabolism instead
- t4 binds to R w/ low affinity, needs to be converted to t3 to be more active
- not very soluble in water and not soluble enough in membranes that in can cross membrane by itself
-specific transporter that actively transports TH across membrane across the cell
- genetic defect in this transporter = development of very few muscles
- neither brain or muscle could take it up during development, transport is very essential (case of boy in Berlin, couldn’t talk, hold head up and had very low IQ)

In this lab a Fischer esterification reaction was performed using the reagents n-propyl alcohol and propionic acid to produce an ester product of n-propyl propionate in the presence of sulfuric acid. The ester product was characterized using odor and IR spectroscopy and was retained with a yield of 68.9%. The odor of the starting reagent propionic acid was described as unpleasant and similar to body odor. The odor of the product was described as fruity and sweet, which is in agreement with the characteristic odor of an ester. This indicates that the reaction went to completion and yielded the desired ester. IR spectroscopy also indicated characteristics of the ester product. Esters are characterized by a sharp, strong peak at 1740 cm^-1, indicated a C=O, and one was seen at 1741 cm^-1. In addition, a sharp, strong peak was described at 2972 cm^-1 , which is typical of an alkyl C-H bond.

To a round-bottom flask add n-propyl alcohol (0.82mL, 11mmol) and propionic acid (0.97mL, 13 mmol). Add four drops of concentrated sulfuric acid and mix. Connect the rb-flask to a reflux condenser and heat to a gentle boil. Reflux the solution for 45 minutes. Cool the solution sufficiently. Transfer the cooled contents into a centrifuge tube containing water (1mL) and wash the solution. Perform two subsequent washes with saturated aqueous sodium bicarbonate (1mL) and saturated aqueous sodium chloride (1mL). Pipet organic layer into a vial and add anhydrous CaCl₂ (5 spheres) and swirl. Pipet contents into dry tared capped vial. An IR spectrometry was performed to determine properties of obtained product.

- hormones act thru receptors
- [ ] of free hormone and free receptor combine, need one for the other (the equation)
- will bind and dissociate so there is a rate constant (association rate constant and rate of dissociation constant)
- association constant * the product of free hormone and free receptor = dissociation constant * HR complex
K2/K1 = KD
- disocciation and association rates don’t have to be the same but they are very important
- smaller KD, smaller [ ] of hormone req’d to bind 50% of the receptors = more potent!! (the hormone itself, more effective)
- HR [ ] = hormone bound to receptor v. adding hormone graph
- the more you add, the more is bound to the receptor
- eventually receptor won’t bind anymore and you get receptor saturation (= provides no info at all)
KD: the concentration of hormones in which 50% of the receptor is bound (50% is arbituary %age, could be something else)
2 diff [ ]s of receptors, KD is the same so point at which 50% is saturated is the same but effect is very different
the 2 receptor populations are seeing the same [hormone] but the tissues respond differently
# of receptors dictates magnitude of response and sensitivity of response
- response is measured by cGMP generation, more in 100 than in 0.2
- more receptors = greater response
- the same response will occur at lower concentrations of hormones depending on # of receptors available
- more receptors available, the same response will be achieved at a lower of [H]
- affinity for the hormone of the recptor is not the most important factor attributing to the efficacy of the hormone, this is v. important for drugs
ex: why is propafol a classic agent used as an anesthetic and yet there is a 50-fold difference sensitivity b/w field
some are more sensitive that others (metabolism isn’t the only factor, basically)

feedback pathways to V1 carry mainly excitatory input and porject preferentially to pyramidal cells
- V1 is characterized by a unique layered appearance in Nissl stained tissye = striated
magnocellular pathway: associated w/ movement of the visual image, to upper parts of the layer 4B
parvocellular pathway: associated w/ form and color, to lower parts of layer 4
- M-cells from 4C project to layer 4B and have side projections to interblob cells and now you know how B responds to input from both sides (not just contralateral or ipsilateral)
- P-cells from 4C project to more superficial layers in 2 and 3 where you see ocular dominance columns cell can respond to either eye
- critical dev. period (12wks) req’d to set up ocular dominance columns, for high acuity, depth perception
- past a certain age, wiring becomes hard-wired, a lot less plasticity
- ex: lazy-eye, patch good eye to allow the bad eye develop
- visual deprivation experiments in cats, suture eyes and study ODCs, suturing causes loss of striation patterns
- neurons in primary visual cortex respond preferentially to oriented edges (all edge orientations equally represented in visual cortex)
- different orientations of a bar on a screen and recording from layer 2/3 of V1 of a specific neuron, up and down = max burst, can graph a tuning curve and see which stimulus responded it best to
- a given orientation in a visual scene seems to be encoded by the activity of a distinct population of orientation-selective neurons
- respond to same stimulus in the same position in the VF if recording up and down (“a column”) in the V1
- similar RFs, and orientation selectivity is similar
- BUT, if you go across (R to L of the cortex), they have different RFs and different responses to different orientations of the bar as you go across
- “orderly progression of RFs and orientation selectivity”

- in the mouse, everything crosses at the chiasm, in humans it’s not the case
- axons (of RGCs) of the optic tract terminate in 4 nuclei w/in the brain:
1.) LGN: of the thalamus – for visual perception
2.) superior colliculus: of the midbrain, non-image forming – for control of eye movements
3.) SCN: of the hypothalamus, non-image forming – for control of diurnal rhythms and hormonal changes
4.) pretectum: of the midbrain, non-image forming – for control of the pupillary reflex
- LGN has 6 layers, 3-6 are v. alike and 1+2 are similar to each other (Nissl stain of ER ribosomes)
1&2 = magnocellular layer, cells are larger, contain more Nissl stain substance
3-6 = parvocellular layer
- just a relay station, inputs = outputs of the ganglion cells that then project to the primary cortex/v1/striate cortex
- alternating layers get input from RGCs
- 18 types of RGCs (ON and OFF RGCs, ON/OFF center surround RGCs, etc)
- P&M ganglion cells are specific to the primate high visual acuity and color processing systems
- classes of ganglion cells called P and M ganglion cells in primates, encode two important features of vision
- P and M project to two different parts of the LGN
- size of RFs of P and M are very different, structure related to function
M cells: (like alpha cells in cats) are important for detecting motion
- M-cells project to magnocellular layers
- M-cells are color-blind, direction sensitive, adapt to a maintained stimulus, best for detecting movement across a RF
- much larger than P-ganglion cells
- synapses w/ many bipolar cells
- large concentric RF and more sensitive to small center-surround brightness differences
- responds w/ a transient, RA response to a maintained stimulus
- responds maximally, w/ high discharge rates, to stimuli moving across its RF
P cells – high acuity b/w neighboring points in the RFs/retinas, and color sensitive (sensitive to wavelengths of light), like beta cells in cats
- not direction selective (produce weak responses), midget RGCs
- pavocellular layer receive input from the P-cells
- out# the M-ganglion cells by ~100 to 1 in the primate retina
- make synaptic contact w/ one to a few cone BCs that are innervated by foveal cones
- small concentric RF
- produces a stustained, SA response that lasts as long as a stimulus is centere in its RF
- this type of response is best suited for singlaing the presence, color ad duration of a visual stimulus and is poor for signaling
stimulus movement

Solutions to prevent this loss of important data have been explored by communities around the globe. An example of this includes community-based monitoring, in which communities that are not in countries where health data is routinely collected record their own data. This has been seen in India, where a pattern in sex determination and abortion rates was observed after community-based data was collected. When the sex of the child was determined as female, it was seen that many women chose to terminate these pregnancies. This potentially detrimental pattern to the population would not have been caught without this data collection and analysis. Based on this, mathematical models can then be used to simulate interventions and policies to offer the best solution to this problem.

As previously stated the original hypothesis constructed before the experiment was, if there is predation by crabs present and the trait of shell thickness is being observed, then evolution by natural selection will occur and a shift to a larger average shell thickness in the experimental tanks containing the Dogwinkle snails can be expected. Based on the results it is fair to conclude that this hypothesis is supported and that when predation by crabs is present evolution by natural selection occurs. This can be concluded because in all trials the average shell thickness of the tanks with crabs, the experimental population, increased significantly from day zero to day 160. For example in Figure 1 the average shell thickness of tanks with crabs increased from 7.175mm on day 0 to 8.875mm on day 160, a total increase of 1.7mm. Meanwhile there was no trend within the tank without crabs, the control population, and the change of average shell thickness within the population was either random or insignificant. For example in Figure 1 the average shell thickness of the tanks without crabs in them change from 7.175mm to 7.4mm, a total increase of .225mm, a much less significant change than the 1.7mm observed in the tanks with crabs. This change in the experimental population proves that evolution by natural selection occurred when predation by crabs was present because the fact that the trait of shell thickness was heritable and variable was already known, but the significant change from thinner to thicker shells in populations where predation was present proves that there is a selection differential when discussing shell thickness, more specifically it can be concluded that thicker shells provide the organism a higher probability to survive and reproduce. This conclusion reiterates the three requirements needed for evolution by natural selection to occur being, heritability, variability and selection differential. Also the interval and duration of the experiment being only 160 days shows exactly how quickly and effectively natural selection can occur in and change a population.

I simply do not understand how memes can free themselves away from us and evolve away on their own. Memes aren't living things. Yes I feel they can evolve, but in ways that we cause them to evolve. Without us, how would they even come into existence in the first place? So without us, memes are nothing. We were the ones who led to Despacito being the most watched video on YouTube. How could the meme of Despacito itself exist on its own without us? 

The same concept goes for the tide pods. People tend to already eat things that aren't supposed to be eaten. Kids for example always eat things they shouldn't eat. We were the ones who turned the eating of tide pods into a thing. How would the meme of tide pods come into existence without some person starting it and then others copying them? Therefore I believe that we are using memes as a way to communicate. This is why memes go viral. It's because we are trying to use them to connect with others and communicate our ideas. The ideas came from our brains. The ideas did not just come into existence by itself. Successful mass communication is possible because memes tend to spread like diseases as stated in the Virality Prediction and Community Structure link. Memes share complex ideas in such short words without the use of scientific reasoning.