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The author’s central argument is that killing a fetus is not as morally wrong as killing an adult or a person (contrasts with Marquis). Marquis stated that killing a fetus will deprive it of “a future like ours” which is false. This is because fetuses do not have plans or wishes to do things in its future. Adults have personhood, unlike fetuses. They are thought of as persons and not organisms. There personhood can change throughout their lives and they can develop into different persons. Therefore, an adult is a person and would not be identical to the fetus from which he or she was developed. Lastly, adults also have autonomy while Fetuses lack autonomy. Due to these important disanalogies between killing adults and fetuses, one should not assume that whatever is a sufficient condition for the prima facie serious moral wrongness of killing adults is also a sufficient condition for the prima facie serious moral wrongness of killing fetuses. Thus, the standoff continues between whether personhood is crucial to the morality of abortion or not.

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. In addition, the broad peak at 3000 cm^-1 indicated the presence of a carboxylic acid O-H bond and a broad peak with medium to strong intensity at 3300 cm^-1 indicating an alcohol O-H were not seen on IR spectroscopy. The odor and IR spectroscopy indicate successful completion of the esterification reaction to yield n-propyl propionate.

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

Another challenge when developing mathematical models with respect to data usage is the accessibility of specific data pertaining to the topic of simulation. Often times data necessary to simulate certain scenarios, such as number of deaths by a certain disease, is not accessible to the general public or researchers alike. This makes it impossible to accurately model certain scenarios, of which solutions could be offered with mathematical modeling. The WHO has proposed that “Raw data need to be made publicly accessible for research purposes. National health equity surveillance data need to be reported to, among others, national policymakers and WHO. Global health equity surveillance data need to be reported to the Economic and Social Council, other international bodies, and back to national governments” This would allow mathematical models to be more consistent, accurate, and faster and easier to develop. In turn, modeling done more efficiently allows for interventions to be made much sooner, and problems from the community to global level would be resolved relatively quicker.