Because ducks need to float and cows don't. If there was a densely fat duck it wouldn't float or fly very well and it wouldn't survive to reproduce.
To answer your question, the composition of fat varies because of the different conditions in which the organism needs to thrive. Fur is different as well. Bear in mind nature is a cruel place and any tiny edge you can get is vital for your survival.
My answer is a bit general but I hope it addresses the question.
According to a heavily-cited paper (below), homocysteine reduces the expression of thrombomodulin on the surface of endothelial cells.
Thrombomodulin binds to thrombin, and the resulting complex does not promote coagulation, but instead activates protein C. Protein C has an anticoagulant effect. Thus reduced levels of thrombomodulin will result in increased levels of free thrombin (promoting coagulation) and in reduced levels of protein C (also promoting coagulation).
I haven't found any evidence that homocysteine has an effect upon thrombin formation directly.
Lentz,SR and Sadler, JE (1991)Inhibition of thrombomodulin surface expression and protein-c activation by the thrombogenic agent homocysteine. J. Clin. Invest. 88:1906-1914
Abstract Elevated levels of plasma homocysteine are associated with both venous and arterial thrombosis. Homocysteine inhibits the function of thrombomodulin, an anticoagulant glycoprotein on the endothelial surface that serves as a cofactor for the activation of protein C by thrombin. The effects of homocysteine on thrombomodulin expression and protein C activation were investigated in cultured human umbilical vein endothelial cells and CV-1(18A) cells that express recombinant human thrombomodulin. Addition of 5 mM homocysteine to endothelial cells produced slight increases in thrombomodulin mRNA and thrombomodulin synthesis without affecting cell viability. In both cell types, thrombomodulin synthesized in the presence of homocysteine remained sensitive to digestion with endoglycosidase H and failed to appear on the cell surface, suggesting impaired transit along the secretory pathway. In a cell-free protein C activation assay, homocysteine irreversibly inactivated both thrombomodulin and protein C in a process that required free thiol groups and was inhibited by the oxidizing agents diamide or N-ethylmaleimide. By inhibiting both thrombomodulin surface expression and protein C activation, homocysteine may contribute to the development of thrombosis in patients with cystathionine beta-synthase deficiency.
Have you read the Wikipedia article on Fat? It has literally all of the answers you are seeking. However...
1: Every single thing is bad for you if you get too much of it. Animal fat, sugar, water, you can over-do it on anything. Fat can be bad for you but it is definitely required. In particular, "Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement." Fat does a host of other things, as mentioned in the article.
2: Fat is indeed a concentrated store of energy, but there's more to life than just energy. Protein, like other nutrients, are required for life. Protein happens to be particularly important, providing the structure for all our cells, is required for muscle growth, and provides amino acids, which are needed to make other proteins in your body. Proteins are used as hormones, cellular messengers, immune receptors, so on and so forth. You couldn't live without protein. Energy, while concentrated in fat, could come from elsewhere.
3: It worked just the same for them as for us. I will add, however, that our ancestors did not necessarily use every part from every animal, and these days, we actually use every part of many animals, just not always for food.
4: Sure? Energy is good, but protein is probably better. "Athlete" is a vague term, as strength-training and endurance activities are very different from each other. Protein is probably better for strength, carbohydrates are probably better for endurance. But you can ask over at http://fitness.stackexchange.com/.
I've been unable to find anything on the Google resembling this bird. I took the photo in Virginia Beach, VA around 2010, October, I think...
It appears to be between winter and summer plumage but I'm not sure. I tried looking on whatbird.com but couldn't find anything that really seemed to match up well.
Edit
I've added some more photos since people seem to question whether or not the white is snow, for some reason. Also note that most seem to have a red bill with a black tip, while the one with more white on its breast has a largely black bill with just a red band. Do bills change colors when plumage does, is that a thing, or perhaps it's just an anomaly or a gender trait?
Imagine the iris like a shutter in front of a focussing lens (which, in fact, it is; see the diagram).
This means that any light going through the iris will be focussed on a very small point on the retina, and your eye is wonderfully developed in a way that this exact spot is the fovea, the only spot in the retina that allows you to see colour and high-resolution.
The iris does not modify the focussing function, it merely changes the amount of light going through into the lens to then be focussed onto the fovea. Imagine that every single object in your field of view reflects/radiates light in every possible direction - narrowing the shutter won't exclude parts of the field of vision, it will only exclude some of the rays coming in at very flat angles and thereby reduce intensity.
Only if your lens is deformed, focussing (adaptation) will malfunction (directing the gathered light to the wrong spot; or focussing the incoming light in front of or behind the retina) and blur your vision.
Swallowing food requires muscle strength to force the food down the oesophagus, which is a soft tube that collapses when empty, simply because the body is very crowded (space-efficient) and empty spaces collapse unless forced open. Only when you swallow, the oesophageal muscles force space to be made for food coming through.
In contrast, the trachea and bronchi are covered in almost-circular or C-shaped cartilage which holds them open and stable for air to flow through. You can see it here: http://en.wikipedia.org/wiki/Bronchi.
Concluding, air does not enter the oesophagus because it is always closed. Additionally, when the chest expands for breathing, the lungs expand and create suction down the trachea and not into the stomach (simply because this is where they connect).
The exception of course is if air is trapped in the swallowing motion with (or without) food. In this case it will enter the oesophagus and cause you to burp.
Just to expand slightly on the answer by Jack Aidley:
Have a look at this section from Stryer's Biochemistry text book, particularly Fig 10.17, where you can see that haemoglobin has evolved to have a high affinity for oxygen at the O2 concentrations present in the lungs, but a low affinity at the O2 concentrations present in the peripheral tissues. This is achieved by binding oxygen co-operatively. This means that haemoglobin can release 60-70% of its bound oxygen. Under the same conditions myoglobin, were it be used in red blood cells as an oxygen carrier, would release much less.
Incidentally the Figure linked to shows a comparison between haemoglobin and a hypothetical protein which shows 50% saturation at the same concentration of oxygen but which binds oxygen non-cooperatively (like myoglobin).
A more direct comparison of haemoglobin and myoglobin - found here - is shown below:
edit added to respond to shigeta's response
I don't understand some of the statements from shigeta so here are my views - if I am wrong, I would (genuinely) like to be corrected, since I have to teach this stuff.
..."what is particularly useful about Hb's cooperativity is that the last oxygen is harder to pull off the Hb tetramer than the first."
This statement contradicts my understanding of the oxygen-binding behaviour of haemoglobin. In the deoxygenated state the protein is in the conformation known as the T (for tense) state, and this is a low affinity state. The binding of an oxygen molecule to one of the haem groups in one of the globin subunits of the tetramer increases the affinity, so that subsequent binding of oxygen becomes easier. The details of how this happens are still debated, but I think what I have said so far is accepted by everyone.
Here is an equation to represent the binding of the first oxygen molecule to the haemoglobin tetramer:
O2 + [Hb]4 <--> [Hb4]O2
If deoxygenated Hb has a low affinity for oxygen then that equilibrium must lie to the left hand side - in other words the right to left reaction (release) is faster than the right to left reaction (binding). This is not consistent with the idea that haemoglobin hangs on to its last oxygen.
"The heart, which is the first organ in the blood cycle after the lungs uses a lot of oxygen - if hemoglobin were not cooperative, it might take all the oxygen from hemoglobin just after the beat when it uses oxygen when in distress, creating a block of hemoglobin which is completely without bound oxygen."
This is based on an erroneous view of the circulation - it implies that all of the blood passes through the coronary artery before getting to the rest of the body. Oxygenated blood leaves the heart via the aorta. Although it is true that the first branch off the aorta is the coronary artery, most of the blood doesn't enter this branch, but proceeds into the remainder of the circulation. In this sense the coronary circulation (by which I mean coronary artery>coronary veins - the heart's own blood supply) is in parallel with the rest of the circulatory system, not in series with it. At rest, just 5% of the heart's output goes into the coronary circulation.
According to this review, Regulation of Coronary Blood Flow During Exercise, (I am simplifying a lot here, but this statement does appear in the review and is not taken out of context): "Increased myocardial oxygen demands during exercise are met principally by augmenting coronary blood flow." At rest the heart is already extracting most of the oxygen from its blood supply (see here for some interesting data) so again there is no question of the heart extracting much more - it simply needs more blood, and of course the increased heart rate will contribute to this. There is also scope for directing a greater proportion of heart output through the coronary circulation, but I have been unable to find any quantitative statements about that. Interestingly, if you take a look at the data in the 1st table of the data here you will see that, at rest, 22% of the heart's output goes into the renal circulation, but that much less oxygen is extracted from that blood (about one ninth of how much is extracted from the blood going through the cardiac circulation). This represents a source of potential increased blood to be diverted to the heart at the expense of a reduction in renal filtration.
"Also - Hemoglobin is pretty clearly an evolutionary adaptation where four myoglobins came together to form a cooperative oxygen binder, so at one time probably myoglobin was the oxygen carrier. There are some primitive animals which have no distinct hemoglobin, just myoglobin like carriers."
I agree it is clear that haemoglobin and myoglobin evolved from a monomeric myoglobin-like ancestor, and that the appearance of a tetrameric molecule created the potential for co-operative oxygen binding. I am not as convinced by the rest of the sentence. I think we have to agree first on what we mean by an oxygen carrier. What I mean is a protein that is a component of a circulatory system. I know of no evidence that a myoglobin like molecule could perform this function. This arises directly from the shape of a simple binding curve (a rectangular hyperbola). For the protein to be saturable at atmospheric oxygen concentrations it has to have a certain Kd, and this precludes significant release of oxygen at physiologically useful concentrations. You either have a protein which can unload effectively but will not ever become saturated with oxygen, or you have a molecule that is able to become saturated but cannot ever unload except at every low oxygen concentrations. That is the remarkable thing about haemoglobin - the appearance of cooperative binding allowed for a more switch-like interconversion between a high affinity state, for loading up, and a low-affinity state, for unloading.
Now, if you wish to include intracellular oxygen transport in your definition of "carrier" then we enter a whole other debate about the role of myoglobin, but I have gone on for far too long already, so I'll stop there.
The social insects consist of the ants, the bees, and the termites, which live in colonies rather than living solitary.
But I've heard that there are some species of bee which are solitary and don't live in colonies.
Are there also any species anywhere of either ants or termites which are solitary?
I would like to use MultiPipMaker for testing a genome alignment between two sequences, each sequence is in .fasta format, but the problem is that when I submit the couples of file that I need, the web browser sends an email that the blastz has timed out. Does anybody know why is the that?
The address of the program is:
http://pipmaker.bx.psu.edu/cgi-bin/multipipmaker
thanks
When using a preculture with Ampicillin in my protein expression, I have to get rid of the preculture medium to avoid carrying over too much beta-lactamases that will destroy the ampicillin in the main culture. To do this I pellet the cells and resuspend.
Which methods of resuspension are best suited if you need the bacteria alive afterwards? I'm not sure how much force I can apply without harming the bacteria, and resuspending very gently takes a very, very long time.
Which methods can be used to resuspend bacteria alive, and which ones are the fastest?
Regarding dimensions:
As per this image the length and breadth seems to be ~30-50 μm (area should be roughly around 900 μm²). The third dimension (thickness) as per this article can be assumed to be around 3-7 μm.
Regarding cell attachment:
Cells attach to extracellular matrix via integrins, which attach to ECM proteins like collagen and fibronectin. The matrix is a net of fibres and the cell is not specifically attached to a single fibre but rather "sits"(as you said) on the matrix [see the below image]. A single cell also simultaneously interacts with two different types of ECM proteins such as fibronectin and collagen.
During migration they move along the matrix using lammelipodia (actin filament polymerization in the direction of motion).
Fibroblast express ICAM1/VCAM1 (Inter/Vascular Cell Adhesion Molecules) under certain conditions such as inflammation and bind to T-cells and endothelial cells.
I found a a few of these guys on my composter, so they could have easily been eating bugs or decaying organics (or both):
To me it looks like a stink bug with oversized legs, not like the ones I'm used to seeing. His body measures just under 3cm, and I haven't pulled on his legs to get a measurement (I haven't pulled on it at all). The legs seem to be at least 1.5 times the body length as do the antenna. The body is grayish brown and the antenna and parts of the leg seem reddish brown.
I'm a microbiologist, so things big enough to see in a jar are not really my specialty. That said, here's info that I've been trying to use ID it:
Wingless Normal compound forelimbs (don't seem to have any kind of prey modification)
Segments filiform antenna (I think)
2 Tarsomeres (I think)
In the middle of South East US
Have had (unusually) heavy rains
Underside of the limbs and antenna seem red, but to seems gray
I've never seen it before! (and I usually notice such things).
Update: Despite my 4 year old putting other bugs and some leaves in with it, the bug died. I took the opportunity to get some much better photos, and low and behold when I started manipulating it I was able to pull out a substantial rostrum that I missed! These guys are good at hiding those. So going back to assassin bugs, can anyone id which assassin bug it is?
More photos: [I would add more but I think this should be plenty]
I at least think it's quite a pretty specimen (to betray my mammalian aversion to bugs).
Not being an opthalmologist, if one happens along and gives a better/correct answer, listen to them.
Otherwise, let's take a moment to look at the eye:
What is not pictured here is the saline-like solution that keeps the conjuctiva moist. If we include the lubrication in all of the surfaces which interact with light, our list would look like this:
Out of that list, the Iris, Retina, and Fovea are designed to absorb light; not reflect it. The Vitreous humour merely serves as a medium for light to pass through and probably would not reflect light on its own. The same is true of both aqueous humours - they do not modify the light so much as serve the eye structurally.
That leaves us with the Lubrication, Conjuctiva, Cornea, and Lens - surfaces which also interact with light, but act to some extent to reflect or modify it as well. The Cornea is what's actually operated on when a person undergoes corrective surgery; a pattern is etched into the Cornea which redirects light similar to the person's previous prescription and giving them better vision.
Now, because you mention the difference between an excited person and presumably someone at their normal state, it's worth to note (when dealing specifically with the eye) a very common side-effect of psycho-active drugs and emotional states (particularly fear and interest/curiosity) is the change in pupil size when lighting conditions don't change:
The reflection is different depending on the size of the pupil, and I would venture to guess the pupil size difference between someone who's excited or manic (whose system is flooded with endorphins) and the person at normality is part of what you define as 'gleam.'
The other situation you draw a difference between is a dead person vs. a living person. Before rigor mortis sets in, the relaxed state of the ciliary body is to stress the suspensory ligaments - resulting in pupil dilation. In addition, and I think this is the most important distinction: dead people don't blink. The act of blinking spreads the lubrication on the surface of the conjuctiva, and can be mimicked with tear-drops for people with dry eyes. Because the lubrication acts as another surface to reflect light (similar to having a thin layer of water on a surface), the dead person's eyes will have less of a "gleam" than a living person's.
So, to sum up: The "gleam" in a person's eye is probably due to hydration and/or pupil dilation. Pupils will dilate at lower light levels, under the influence of certain drugs, or when showing interest. Hydration is constant, except when the lubrication is not produced in the quantities necessary or when the person is unable to blink ('dead' in your example).
I think LuketheDuke's answer is an oversimplification of the biological species concept (possibly resulting from the dictionary having a poor definition). The definition he gives is one of many which are in current use, and is made redundant by many types of organism.
It is important to recognise that because reproduction is not the same process in all organisms, genetic differentiation between individuals occurs in different ways for different groups.
Let's take the definition given in LuketheDuke's answer...
The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.
Under this definition, lions and tigers (see ligers and tiglons, which are sterile hybrids between the two) would be considered one species, as would donkeys and horses (see mules and hinnys, again sterile hybrids). There are hundreds of other examples of pairs of animal species which can hybridise to produce sterile offspring.
However, these animal hybrids usually only take place with human intervention, by delibrate breeding efforts. Thus we could extend the previous definition to include them...
The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild.
That last part takes care of the ligers and tiglons. But what if we consider plants? Under the definition I just gave, most grasses (around 11,000 species) would have to be considered as one species. In the wild, most grasses will freely pollinate related species and produce hybrid seed, which germinates. You might then think we could just modify the definition to specify that the offspring must be fertile (i.e. able to reproduce with one another)...
The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild to produce fertile progeny.
Unfortunately, the situation is still more complicated (we've barely started!). Often wild hybridisation events between plants lead to healthy, fertile offspring. In fact common wheat (Triticum aestivum) is a natural hybrid between three related species of grass. The offspring are able to breed freely with one another.
Perhaps we could account for this by taking into account whether the populations usually interbreed, and whether they form distinct populations...
The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of populations or meta-populations of related individuals that resemble one another, are able to breed among themselves, but do tend not to breed freely with members of another species in the wild to produce fertile progeny.
This accounts for the grasses, but it still leaves a messy area when you have a hybridisation which establishes - until the hybrid population is segregated away from the parent populations it is unclear whether they still count as the same species.
We could probably live with this situation, except for the fact that bacteria refuse to conform to it at all. Bacteria of the same species, or even very different species, can freely transfer genes from one to the other in conjugation, which combined with fission can result in perfectly replicable hybrids. This is such a common occurence that it breaks even the 'tend to' part of the previous definition, and members of a population can be doing this almost constantly, which negates the segregation requirement.
Richard Dawkins had a go at defining around this, by stating that...
two organisms are conspecific if and only if they have the same number of chromosomes and, for each chromosome, both organisms have the same number of nucleotides
This partly gets around the bacterial problem and means that bacteria which result from conjugation are a new species. Unfortunately under this definition we might as well not ever bother trying to classify bacteria as billions of new species would be created every day - something which the medical profession might have something to say about. This definition would also mean that those with genetic diseases like trisomy 21 are not human. The final nail in the coffin of this attempt is that there are many species, including frogs and plants, which are very certainly considered a single species by taxonomists but which have some variety in the presence of small accessory chromosomes, which occur in different combinations between individuals.
Let's consider one last option. We now live in the era of genomics where data about genomes of thousands of organisms is accumulating rapidly. We could try to use that data to build a species definition based upon similarity at the nucleotide level. This is often used for bacteria, by considering organisms with less than 97% nucleotide similarity to be different species.
The major point I've been trying to make, though, is that species is not a natural concept. Humans need to be able to classify organisms in order to be able to structure our knowledge about them and make it accessible to people trying to link ideas together. But the natural world doesn't care about our definitions. Ultimately the species concept is different for different groups of organisms and will continue to change over time as our analytical methods and the requirements of our knowledge change. Note that I've deliberately skipped over many historical species concept ideas.
The direct answer to your horse question is "it depends how you want to define a horse".
Although both involve DNA fragmentation, the pattern produced is very different. During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern. Necrosis, on the other hand, is a more stochastic process, and will produce a smear. This details the difference rather nicely, including different ways to assay for either one in table 18.3.1 such as morphological staining or flow cytometry.
Here's a nifty image from the link. Figure 18.3.2. M is the marker, and in panel A, a conventional gel, lane 1 is apoptotic DNA, lane 2 is unprocessed DNA, and lane 3 is necrotic DNA. In panel B, a pulsed-field gel, lanes 1 2 and 3 are untreated, apoptotic, and necrotic, respectively.
As I know:
One of the most important chemical mediators are prostaglandins that in vivo act on different cell receptors and have different effects on the body. Prostaglandins are twenty-carbon lipid molecules and structurally similar to cholesterol. Prostaglandins have different types, such as F2, E2 alpha, PGI2, and so on.
A phospholipase enzyme converts phospholipids of cell membranes into arachidonic acid. The arachidonic acid within the cyclooxygenase enzyme or Cox (both type 1 and 2) can be converted to prostaglandins.
PGF2alpha has functions in uterus contraction and bronchoconstriction, so I think both uterus and lung cells produce it.
I have no special information about production of PGF2alpha in men.
Oddly enough it is a bit difficult to find good field studies where the diet of spiders was studied. I have a feeling it's a hard thing to get funding for. Luckily some do exist.
Peucetia viridans has been shown to eat from the Chrysididae family and Lepidoptera order, but I didn't find an explicit statement that it ate the larvae out of the caterpillar. Likewise Oxyopes globifer was found to have eaten from the Braconidae family and Lepidotera.
At this point you might be wondering why I'm looking for spiders that have been shown to eat both parasitoids (Chrysididae and Braconidae) and caterpillars (Lepidotera). It my assumption that in the scenario you describe a spider that would normal eat ether the caterpillar or the larvae would be just as happy to eat them both if it was lucky enough to find them.
I could find one example where it seems wolf spiders under the right conditions might seek out larvae, and I found a fun photo of a wolf spider eating larvae (though not the kind in the study).
I never saw the video you were talking about, and I too could not find it. It is not unreasonable to assume that an opportunistic spider wouldn't just take the opportunity to feed on both, or that it might find the larvae more tasty and just eat them. I've not found a spider seeking caterpillar as of yet.
Probably development, in particular transcriptional regulation. To quote each link in turn,
They are found in clusters across the human genome, principally around genes that are implicated in the regulation of development, including many transcription factors. These highly conserved non-coding sequences are likely to form part of the genomic circuitry that uniquely defines vertebrate development.
and
[Highly conserved non-coding sequences] are significantly associated with transcription factors showing specific functions fundamental to animal development, such as multicellular organism development and sequence-specific DNA binding. The majority of these regions map onto ultraconserved elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments
Here we report that 45% of these sequences functioned reproducibly as tissue-specific enhancers of gene expression at embryonic day 11.5. While directing expression in a broad range of anatomical structures in the embryo, the majority of the 75 enhancers directed expression to various regions of the developing nervous system.
These regions tend to be highly clustered in around 200 areas, and most of them are non-coding. ncRNA is often regulatory, and those UCE clusters are associated closely with developmental genes. That being said, not all of them are clustered near known genic regions, which might be a good indicator that there are heretofore unknown genes in those areas; UCEs might be useful for discovery. And here's a paper trying to give a role to one in cancer.
Preface:
Any question about adaptation on macro-level has very little meaning and no precise answer.
There are two types of larvae in invertebrates: primary ("original") and secondary (evolved from post-larval stages). Not digging into the details, nauplius (together with metanauplius) is the only type of primary larvae in Crustacea and it never has a carapace.
"Majority" is by far too strong term, even if we are talking about all larval types. If we just take the largest crustacean orders with species numbers > 1000, together comprising 92% of crustacean species (species numbers are from Ahyong et al, 2011, they seem to be largely correct):
So, "majority" could be applied to Decapoda only.
Fabula:
If we substitute "adaptation" with "main biological function" (as you have done) or more correctly "main physiological role":
I would prefer the (a), because carapace does function as a protective structure in those decapod larvae which don't rely on behavioral anti-predatory defenses: see Morgan: "Fishes quickly learned to avoid spined prey, which ... may also increase the rate of evolution of the character". Non-carapaced larvae rely principally on behavior only.
The only contribution of carapace to planktonic life-style in zoea is participation of its spines [when they are pronounced] in parachuting (Chia et al).
[The above should be largely true also for the cypris larva of the cirripeadians, which are enclosed in a non-spined bivalve carapace.]
From the morphological point of view, [at least in adult forms of decapods] carapace creates a chamber for gills, so a morphologist would argue that this is the "main function" of carapace.
I think the explanation for this description of fish oils as "easily oxidised" can be found in the Introduction to the actual paper (Nutrition 27 (2011) 334–337) that is cited in the article linked to in the question.
Fish oil contains high levels of eicosapentaenoic acid (EPA; 20:5 omega-3) and docosahexaenoic acid (DHA; 22:6 omega-3), which are omega-3 polyunsaturated fatty acids. EPA, DHA, and fish oil have been shown to have protective effects against coronary heart disease, thrombosis, inflammatory processes, carcinomatosis, and metabolic syndrome. Therefore, fish oils and components of the oils are marketed as health supplements. However, the effects of omega-3 polyunsaturated fatty acids on aging and lifespan are unclear compared with those of omega-6 polyunsaturated fatty acids contained in safflower oil and soybean oil. EPA and DHA are oxidized easily compared with linoleic acid (18:2 omega-6) and oleic acid (18:1 omega-9) in vitro .
In other words, the fish oil omega-3 fatty acids EPA and DHA have, respectively, 5 and 6 double bonds, whereas the omega-6 fatty acids in safflower oil, linoleic acid and oleic acid have, respectively, just 2 and 1 double bonds. So the fatty acids in fish oil are more prone to oxidation simply because they have so many more double bonds.
Incidentally, as you can see from the two structures below, both of the omega-3 fatty acids, EPA and DHA, also have an omega-6 double bond.
EPA:
DHA:
Yes, this is most certainly possible and already being done. As long as the visual cortex of the brain (in the occipital lobe, i.e. at the back of your head) is functional, the correct stimulation will produce visual perception.
In cases of blindness caused by malfunction of the retina, meaning that the rest of the visual pathway is functional, this is the most promising approach to restoring vision. See Visual prosthesis and the TED talk on it.
"Virtual vision" as in projecting a whole field of vision (reflecting the real surroundings) is the big ideal target that this technology is aiming for. Of course as soon as they manage to make a working prosthesis for blind people, someone will probably try to make it non-invasive and easily usable for commercial exploitation.
It is! Here is an amazing review from 2011 that literally has all the answers. I'm not kidding, all of them. I would marry this review if I could.1 It also includes information on other animals.
The main takeaway is that IgA from milk is not readily absorbed by the infant body. Secreted IgA is mainly to provide a protective coating for the mucosa while the infant is developing its own nascent immune system. IgG passed along from the placenta (your other question) provides the main source of absorbed antibodies. As it says in the review:
Milk sIgA is not taken up by the infant’s intestinal mucosa. In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth. However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine... Secretory IgA is considered to be the primary immunoglobulin responsible for immune protection of mucosal surfaces such as the intestine.
In terms of enzymatic activity, the digestive system will in indeed chomp up the antibodies; that's part of the reason breast feeding should continue as needed. That's okay, because there's plenty to go around:
Much of the immunoglobulin consumed in an immune milk can be expected to be partially or completely digested, however some portion of the immunoglobulin will remain intact or at least partially intact and capable of binding to an antigen.
It turns out that immunoglobulins are moderately resistant to digestion, at least more so than other milk proteins. There's a section in there detailing some experiments where Ab was given to individuals:
In adult humans consuming a bovine whey protein concentrate, approximately 59% of IgG and IgM was detected by radial immunodiffusion from effluents from the jejunum, while 19% was detected in the ileum. These estimates of digestion of immunoglobulin compare with estimates of digestion of milk proteins in adult humans which are approximately 42% complete at the end of the jejunum and 93% complete by the end of the ileum, again underscoring the relative resistance of immunoglobulins to digestion in the gastrointestinal tract.
Digestive enzymes vary as to which antibody they prefer to digest, but at least some of them will technically digest the antibody, but still leave functional Fab fragments, which are still immunologically active and useful to the infant immune system.
1: Did I mention I love this review? I love it.
Broad question. Summary:
The innate immune system processes everything. When it senses that something is dangerous it tells the adaptive immune system, that is T and B cells, that this thing I'm holding is dangerous (via coreceptors and cytokines).
T and B cells that are specific for this dangerous protein (or sometimes non-protein) are activated.
Ideally T and B cells that react to self proteins are deleted. These are from central tolerance mechanisms when the cells are developing (T and B cells are tested against self proteins; if they react they die) and in the periphery (once they're mature) by them only getting activated by the innate immune system and other mechanisms. There's also T regs which regulate the immune system by preventing any cells that react to self proteins from being activated.
Autoimmune disorders are caused by a break down of these mechanisms.
I remember doing this experiment many years ago in an undergraduate practical where we used vigorous vortexing of culture samples in glass tubes to achieve interruption and separation.
According to Griffiths AJF, Gelbart WM, Miller JH, et al. Modern Genetic Analysis. Bacterial Conjugation:
... sampling is accomplished by using a kitchen blender to separate
the joined cells, resulting in interrupted conjugation.
