Attaching suspension cells to coverslip during mycoplasma contamination detection

If you are working with suspension cells, it's always easier to use Flow cytometry but if you want to use microscopy then I would suggest using chamber slides. You just have to put your cell suspension inside the chamber and then stick the cells to the microscope slide. After that you can do whatever treatment you want just by putting in the chamber the proper solution and wash afterwards. The more the steps the more cells you'll lose mostly because of pipetting so try to pipette always at the same corner and be gentle. To stick the cells to the slide your best option is to centrifuge the slide. Unfortunately in my lab that wasn't an option so I just fixed the cells with methanol while there were suspended in PBS and it worked very well. Most of the cells were attached to the slide and the staining was perfect.
Hope I helped. Good luck!


Cellular and Molecular Immunology by Abul Abbas et al. is pretty good, and you can't beat Charlie Janeway's Immunobiology either. Both will give a good introduction to B-cells, antibodies, BCR signaling, and how they fit in to the immune system's structure and function. I own earlier editions of both, and their different perspectives are good for getting a more holistic understanding of the field. Good luck in your studies, it's a fascinating subject!


Why does affinity of Hemoglobin increases for Oxygen in carbon monoxide poisoning?

Affinity for any ligand to a protein is a function of the shape of the protein which provides some place for the ligand to bind/interact.

Hemoglobin typically exists in tetrameric form: it is a collection of 4 subunits that each bind 1 molecule of oxygen.

The shape of hemoglobin is affected by CO2/pH, which is important for having high affinity for oxygen in the lungs and lower affinity for oxygen in tissues where a lot of CO2 is released (i.e., where there is a high rate of metabolism).

The shape is also affected by binding oxygen itself: binding oxygen to one subunit causes conformational change in the other subunits of the tetramer, increasing their affinity for oxygen. This is called "cooperative binding."

So, how does any of this relate to CO? Well, it turns out that not only does CO bind very tightly to hemoglobin in the place oxygen would normally bind, taking up space and reducing the capacity for oxygen, it also very strongly increases the affinity of the other subunits for oxygen. It increases the affinity enough that even in the low-oxygen high-CO2 environment of the capillaries, carboxyhemoglobin (hemoglobin bound to CO) continues to hang on to rather than release oxygen. This is represented by a shift in the dissociation curve to the left: oxygen stays bound even when the concentration is low.

This means that fewer CO molecules are necessary to cause deficits in oxygen transport than would be needed if it was only taking up space: one CO molecule binding to a hemoglobin tetramer effectively prevents transport of up to 4 molecules of oxygen.

As a quick caveat, I believe some of the biophysics here are still incompletely understood, so please consider this answer to be an approximation and an explanation of experimental findings to a level of precision sufficient to understand the pathophysiology of CO poisoning. More depth is necessary for a biophysical approach.

Roughton, F. J. W., & Darling, R. C. (1944). The effect of carbon monoxide on the oxyhemoglobin dissociation curve. American Journal of Physiology-Legacy Content, 141(1), 17-31.

Eaton, W. A., Henry, E. R., Hofrichter, J., & Mozzarelli, A. (1999). Is cooperative oxygen binding by hemoglobin really understood?. Nature Structural & Molecular Biology, 6(4), 351.


Why aren't human babies considered larvae?

For animals with a clear larval stage, the presence of such a stage indicates that there is a metamorphosis, a change in body morphology at some point in development.

Metamorphosis does not necessarily refer to an 'instant' transformation or one that requires a pupation step or something similar; gradual change can still be metamorphosis, as long as there is a clear 'before' and 'after.'

Human infants, on the other hand, don't go through much of a metamorphosis: sure, they grow quite a bit, but their general body plan does not change. Contrast this with insects, or your tadpole example, and it is clear there are major body plan changes from larvae to adult stages.

The Wikipedia page on larvae describes the characteristics of larvae fairly clearly. Like most traits in biology that vary across taxa, you are likely to find some intermediate creatures where the presence of a larval stage is somewhat controversial or depends on opinion. There could be a difference of opinion on how much of a change is sufficient to describe a juvenile form as a larvae. Humans don't have a postnatal stage that approaches that potential boundary.

The part in your question about people who are "anti-baby" sounds a bit judgmental, but I think what you are describing is just a phrasing meant to be somewhat humorous and to evoke images of "gross" larvae; I wouldn't take that for any biological meaning and I wouldn't focus your time on proving it "wrong" - the actual difference of opinion you have is something entirely different.


Can food swallowed when a person is upside down reach the stomach?

The eminent @JanDvorak has basically provided the full answer, but yes, it is possible.  You can easily try this yourself, just lean off a bed and swallow something (small) and see what happens.  Peristalsis in the esophagus is responsible for moving food down into the stomach.  The big proof of this is that astronauts can eat when in space, when weightless.  Their food is moved into the stomach just fine.

It's easier to do it upright (peristalsis + gravity) as opposed to upside down (peristalsis - gravity) but definitely quite possible.


How to validate the regulatory interactions inferred from gene expression data?

You can validate the interactions by knockding down (KD) or overexpressing (OE) a gene and checking the change in expression levels of the downstream nodes. You can do this in a high throughput fashion using microarray or RNAseq. For protein you can do an LC-MS. However this method cannot help you in:

Differentiating direct vs indirect interactions
Finding regulation in case of loops and other non-linear interactions in the network

Loops are tricky but sampling at multiple time intervals can let you know if oscillations exist or not. For most usual cases this approach works out.

Usually this is followed by another round of validation using a relatively low throughput but sensitive technique such as

Real-time PCR (KD vs OE)
Western blots (KD vs OE)
Reporter assays (KD vs OE) would detect direct interactions. For e.g. possible promoter for a (Transcription Factor) TF (upstream of gene-Y) is used to express GFP to see if GFP responds to the TF; thereby validating the effect of TF on Gene-Y via the promoter.

In some cases you may have to do ChIP-seq to find out if a gene has binding sites for a TF in its promoter/enhancer. You may also use predictions for TF binding sites. For finding regulation by miRNAs you can see this post.

For finding complex dynamics such as pulses and oscillations you have to collect time-course data.

  how to quantify their expression levels as over or under expressed?

For that you first need to define your control (up/down regulated wrt what?). Having done that you can compare the expression and use right statistical tests to check differential regulation. If you have just one sample then most tests won't work. For RNAseq,  EM algorithms are used which use a bayesian model to obtain likelihoods and p-value (I have used cufflinks and eXpress). Then a FDR correction can be performed when comparing the test vs control. I am not very sure about algorithms used for comparing LC-MS data for proteins.


Blood and hair follicles from 25 people put on the Moon; enough to regenerate a human population?

If we assume for a moment that the samples could be successfully cloned, 25 individuals is probably not enough to maintain a stable human population for more than a few hundred year without experiencing severe inbreeding depression and eventual extinction.

In population biology, there's a general rule of 50/500 for minimum viable population sizes. Essentially, a minimum population of 50 is needed to prevent inbreeding depression, and 500 to stabilize genetic drift. Of course that's a generalization used in management situations, and lots of factors go into making a calculation like this with any amount of precision.

One estimate gives a minimum viable human population (for generational space travel and permanent colonization) of ~40,000 humans in order to maintain genetic diversity. But that only applies to a population carefully screened and selected to maximize the effective population size. Another suggests 160 people could be enough for a stable population, as long as they return home to mix it up with the rest of humanity every 200 years or so.


The color you perceive is ultimately dependent on the relative contributions of the color photoreceptors in the retina, namely the red, green and blue cones. The sensation of color, therefore, is physically determined by the wavelengths in the light source and the absorbance spectra of the cones. Thereafter, the neurophysiological wirings of the retina and the brain take over and these paths are pretty well defined too. However, one cannot say anything about the qualitative perception of someone observing a light source. This is the big difference between sensation (peripheral processes including the retina) and perception (central processes).

To quote the late Bach-y-Rita: 'You see with your brain, not with your eyes.'

Everything we perceive ('see') is a subjective construct devised by our brains. No red dwarf star is necessary to pose the possibility that you perceive my perceived red as green, or vice versa. No experiments can be conducted to prove or disprove a hypothesis like this.

In terms of experiments: we can test stuff like 'up' versus 'down', as with the prisms mentioned in the question. This, because a subject can qualitatively point out where an object is perceived relative to others, and that can be objectively measured. However, we cannot test the subjective quality of color. We can test relative color contributions through color matching experiments (Kalloniatis & Luu, 2012). These experiments will tell you which contributions the red, green and blue cones have in a certain color mixture, but they will not tell the researcher anything about the subjectively perceived color by the test subject in a qualitative way.

Reference
- Kalloniatis & Luu. Color Perception. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


Can I use multiple bicistronic RBS sequences in a synthetic biological circuit?

That’s a great question and has lot of opportunities to explore. I am not sure anyone has followed up on this original BCD work systematically. We did try cloning these elements on a medium copy plasmids, in an operon design, driving multiple genes, and now I think about it, that was not a smart thing to do. Cloning was very challenging, probably due to toxicity you mention. Didn’t have time to investigate this in depth (that it self is a cool project), but I think the toxicity is due to too much resources (ribosomes?) titrated out on these units. But that’s a hand-wavy explanation. Need mechanistic study to investigate. I think Tom Ellis’s group and others have done some beautiful work on toxicity associated with protein expression. Personally I think the toxicity is not related to the inert peptide (1st gene in a BCD operon) that’s produced. Another story we tried was to replace this first gene with something functional but not published.
Coming back to using BCDs for driving multiple genes, I would say if you clone these directly on genomes they should work like charm. We did try this and works good. Not published much (oh god, that’s so much work unpublished!) Bacterial operons have these junctions and elements of different strengths. Happy to discuss more if you have a follow up question!!
Thanks for your interest in this work. Really proud of our work on this system. Of course happy that we did this work as there were so many early effort on these BCD type elements. And love this open discussion SE platform! Don’t know how synbio survived without this system of sharing knowledge and experiences. Best wishes
Vivek Mutalik


Main mechanism of the evolution of sexual dimorphism

Sexual dimorphism evolves, as you suspect, via natural selection, specifically sexual selection (which I view as a form of natural selection).  Genetic drift, by definition, is random. Random changes of allele frequencies are extremely unlikely to lead to the consistent evolution of phenotypic differences between males and females.

Sexual selection on the other hand can lead to rapid evolution of secondary sexual characteristics (sexual dimorphism). If you consider natural selection in the broad sense, an organism's traits affect survivorship but do not guarantee reproduction. Individuals that live longer have an increased chance of reproducing more frequently but this does not mean the organism actually will reproduce more often than any other individual. In contrast, sexual selection acts directly on mating success. If a female chooses a male based on his secondary sexual characters, then that male will mate. His fitness (offspring produced) will be increased relative to males that are not chosen and do not mate. This can lead to runaway sexual selection for male traits and even speciation.

You are correct that sexual selection results from sexual conflict. Such conflict can arise because females invest considerable energy into relatively few eggs. Thus, it benefits her to be selective for her mates. If she chooses poorly, her fitness can be decreased quite a bit. On the other hand, males can produce copious quantities of sperm rapidly and with little energy cost. If a male wastes sperm on a genetically-poor female, his fitness is not really reduced. He can quickly mate with other females at little cost.

References

Any evolutionary text. They cover the basics of sexual selection in some detail.

Gavrilets, S. 2000. Rapid evolution of reproductive barriers driven by sexual conflict. Nature 403: 886-889.

Hosken, D.J. and P. Stockley. 2005. Sexual conflict. Current Biology 15: R535-R536.

Lande, R. 1981. Models of speciation by sexual selection on polygenic traits. Proceeedings of the National Academy of Sciences USA 78: 3721-3725.


What does vitamin B6 and B12 absorption depend upon?

Vitamin B12 (cobalamin) is a water-soluble vitamin required for homocysteine methyltransferase. In order to be absorbed, it must bind to intrinsic factor (IF), which is produced by the parietal cells of the stomach. The absorption of the vitamin B12-IF complex occurs in the terminal ileum (of the small intestine). The quote just means that if there isn't enough IF, then you can't absorb vitamin B12.

There are many things that limit absorption of vitamins, and even vitamin B12. Because vitamin B12 is found in animal products, vegetarians and vegans may need to supplement it. Pernicious anemia is an autoimmune disease that destroys IF or the parietal cells, Gastric bypass surgery can lead to vitamin B12 deficiency. Anything that affects vitamin B12 absorption in the terminal ileum, such as in Crohn's, celiac disease, or enteritis, can lead to deficiency.

To answer your question, no. Yes, it will use some IF (provided you have IF), but that would allow your body to absorb vitamin B12. For people who have diseases mentioned above, they can take vitamin B12 via injections, subligually (under the tongue), or intranasal gels, according to the fact sheet you cited.

Because all the B vitamins and vitamin C are water-soluble, they are easily absorbed through the intestinal wall. Excess amounts are usually excreted in urine. I believe vitamin B12 is the only vitamin that needs to be bound to a factor, due to its larger size. It can be stored in the liver for several years. Fat-soluble vitamins (A, D, E, K) are absorbed with lipids.


Evolutionarily, why do male rats and horses lack nipples?

Male mice lack nipples too. Mice are frequently used for embryonic research as they are small and reproduce quickly. It is thought that male mice do develop nipples, but that they regress during development (Wysolmerski, 1998).

In general, it is thought that mammalian organisms develop as females by default when there is no male (Y) chromosome present (Hughes, 2004). Notably, X_ individuals and XY individuals with certain Y-chromosome deletions also develop as females. Basically, it is testosterone that suppresses female features. Hence, also boys with testosterone production, but without the appropriate receptors also develop as females.

Hence, men have nipples because females do (Simons, 2003).

The development of nipples is a pretty complex process (Wysolmerski, 1998). Disruptions in the process cause regression. Indeed, in mice, the tissues typical for nipples do develop in males during embryogenesis, but degenerate within a few days, leaving no trace of nipples at birth.

Hence, given the mouse example, I think that every mammalian male species develops by default nipples somewhere in development like mice, but that development is halted at various stages across species. The later in development it halts, the more it resembles female nipples. When it is stopped very early after gestation, they regress completely, like in mice.

Why is there a difference between species as to when the nipple development halts? Because the nipple developmental sequence is complex (Wysolmerski, 1998), and because evolution typically prefers losing things over gaining them, it is likely that by happenstance one of many crucial genes was lost in males, but selective pressure was simply too small to be of any significant advantage over males with slightly better-developed nipples. But from here on, it is guessing.

References
- Hughes, N Engl J Med (2004); 351(8): 248-50
- Lawrence, Nature News, August 1999
- Simons, Sci Am, September 2003
- Wysolmerski et al., Development (1998); 125: 1285-94


Electrical currents stimulate neurons aspecifically. For example, the BrainPort artificial vision device conveys visual information through electrical stimulation of mechanoreceptors in the tongue. Similarly, cochlear implants and retinal implants convey acoustic and visual information through electrical stimulation of the inner ear and retina, respectively. The list goes on. Bottom line is, none of these organs (tongue, ear or eye) evolved to process electrical stimuli. And in fact, there are no specific current or voltage sensors in man. Electric currents aspecifically stimulate neurons, causing them to fire. When sensory afferents are activated in this way, sensory perceptions are generated.

In case of lightning (electrical shock to the skin) it is mainly pain and heat receptors that mediate the sensation. In the case of the BrainPort, it is the tactile receptors on the tongue that are mainly stimulated (taste perceptions are rare). In case of cochlear implants it is auditory nerve fibers and in retinal implants it is optic nerve fibers that are stimulated. Hence, various, and in fact all, neurons can be stimulated by electric current.

Note that sharks feature Ampullae of Lorenzini. These sensory organs are electroreceptors, which allow sharks to sense the bio-electrical fields of prey under water.


Suitable introductory book on Bioinformatics for a computer scientist?

Systems biology and bioinformatics are quite diverse subjects, but here are some options:

Biological Sequence Analysis by Durbin et al.: the classic bioinformatics text for people with a CS background. Does not deal with networks.
An Introduction to Systems Biology by Uri Alon: A physicist's view of systems biology, focusing on design principles and networks. Interesting concepts and some math (no algorithms). Doesn't really deal with methodology.
Physical Biology of the Cell by Phillips et al.: Nice introduction to biophysics and quantitative biology (no algorithms). Many parts are relevant for systems biology.
Any diverse Machine Learning text will be relevant and many have examples from biology/bioinformatics.
Probabilistic Graphical Models are also quite popular in bioinformatics (e.g. Hidden Markov Models, Expectation-Maximization, Bayesian Networks). Probabilistic Graphical Models by Koller et al. is a very comprehensive CS book on the subject.

Another suggestion is to look for primers/reviews in relevant journals. This is important because the field is new, so once a new technology is developed, it takes time until the appropriate computational methodology is developed enough to make it into a text book. Also, they can point you to relevant research papers. For example, PLoS Computational Biology has an Education Collection which features a large variety of such reviews.


A blood clot can nearly completely or completely block an artery, in which case the blood flow will be reduced or stopped.

How do we know this?

Pulmonary Embolism (Merck Manuals):

  Pulmonary infarction is when some of the lung tissue does not receive
  enough blood flow and oxygen and appears on imaging studies to die due
  to blockage of a lung blood vessel by a pulmonary embolus.

An embolus is a blood clot that usually develops in the leg veins in individuals with deep venous thrombosis, detaches and travels to a certain pulmonary artery and blocks it.

Similarly, atheroma (atherosclerotic plaque) that builds up within the artery and only partially blocks it, can reduce the blood flow to the target organ. For example, a partial blockage of a coronary artery can result in decreased blood supply to the heart and consequently in angina pectoris or myocardial infarction. It is then the investigation called coronary angiography that can show that a certain coronary artery is partially blocked.

When a clot interferes with blood flow (Harvard.edu):

  In venous thromboembolism, a blood clot slows or stops the flow of
  blood through the veins...


Why do microarrays require a priori knowledge of the genome?

If the query genome is unknown, a microarray cannot be made for a target species. Microarrays have DNA fragments of what you want to amplify on them. Those fragments must be known.
From nature:

DNA microarrays are microscope slides that are printed with thousands
of tiny spots in defined positions, with each spot containing a known
DNA sequence or gene.

From wikipedia:

Scientists use DNA microarrays to measure the expression levels of
large numbers of genes simultaneously or to genotype multiple regions
of a genome. Each DNA spot contains picomoles (${10^{−12}}$ moles) of a
specific DNA sequence, known as probes (or reporters or oligos). These
can be a short section of a gene or other DNA element that are used to
hybridize a cDNA or cRNA (also called anti-sense RNA) sample (called
target) under high-stringency conditions.


The article and published work here and here respectively, reveals that E. coli replication is close to thermodynamic limits of efficiency having modelled this process using mathematical equations. However an interesting article and published work here and here, respectively reports a bacteria (homologous to Thermobrachium celere and Caloramator indicus, which are closely related) with doubling times as short as 10 minutes have been discovered in areas of hot water emissions in Lake Tanganyika.

  Small chimneys emitting hot water at temperatures of 66 to 103 degrees Celsius (150 to 217 degrees Fahrenheit) have been discovered at the shallow lake bottom of Lake Tanganyika, East Africa. In a study searching for thermophilic sulfate reducing bacteria in this extreme environment, a spore-forming bacterium was discovered that grew with a doubling time as short as 10 minutes. In theory, a single cell of this bacterium in this environment can multiply to 500 million in less than 5 hours under optimal conditions (60 degrees Celcius).

EDIT: If the question is exclusively about E. coli and it takes into account laboratory conditions then I also came across this references page claiming tha E. coli doubling time is between 4-20 minutes. Based on this paper the page reports that

  Internationally renowned researcher Bernhard Palsson and other researchers from the University of California San Diego led a team of scientists from PNNL, the University of Heidelberg, and the German Cancer Research Center to study how E. coli bacteria changed and evolved from one environment to another in a laboratory setting. The team then compared proteomics, genomic, and metabolic data from the study with a computational model for bacterial growth.

The page then goes on to say

  Using high-performance liquid chromatography coupled to mass spectrometry, the team gathered data on how the bacteria changed their protein profile as they grew and reproduced in different mediums. The scientists found that the data and model were correlated to a surprising degree (more than 98% in some cases), validating the model's ability to predict the growth of E. coli bacteria under specific conditions.

This confirms the comments above that the growth rate of E. coli depends on the specific conditions in which it is in and furthermore its growth rate under specific conditions can be predicted based on the devised model.


What is the difference between orthologs, paralogs and homologs?

First, a note on spelling. Both "ortholog" and "orthologue" are correct, one is the American and the other the British spelling. The same is true for homolog and paralog.

On to the biology. Homology is the blanket term, both ortho- and paralogs are homologs. So, when in doubt use "homologs". However:

Orthologs are homologous genes that are the result of a speciation event.
Paralogs are homologous genes that are the result of a duplication event.

The following image, adapted (slightly) from [1], illustrates the differences:

Part (a) of the diagram above shows a hypothetical evolutionary history of a gene. The ancestral genome had two copies of this gene (A and B) which were paralogs. At some point, the ancestral species split into two daughter species, each of whose genome contains two copies of the ancestral duplicated gene (A1,A2 and B1,B2).

These genes are all homologous to one another but are they paralogs or orthologs? Since the duplication event that created genes A and B occurred before the speciation event that created species 1 and 2, A genes will be paralogs of B genes and 1 genes will be orthologs of 2 genes:

A1 and B1 are paralogs
A1 and B2 are paralogs.
A2 and B1 are paralogs.
A2 and B2 are paralogs.
A1 and A2 are orthologs.
B1 and B2 are orthologs

This however, is a very simple case. What happens when a duplication occurs after a speciation event? In part (b) of the above diagram, the ancestral gene was duplicated only in species 2's lineage. Therefore, in (b):

A2 and B2 are orthologs of A1.
A2 and B2 are paralogs of each other.

A common misconception is that paralogous genes are those homologous genes that are in the same genome while orthologous genes are those that are in different genomes. As you can see in the example above, this is absolutely not true. While it can happen that way, ortho- vs paralogy depends exclusively on the evolutionary history of the genes involved. If you do not know whether a particular homology relationship is the result of a gene duplication or a speciation event, then you cannot know if it is a case of paralogy or orthology.

References

R.A. Jensen, Orthologs and paralogs - we need to get it right, Genome Biology, 2(8), 2001

Suggested reading:

I highly recommend the Jensen article referenced above. I read it when I was first starting to work on comparative  genomics and evolution and it is a wonderfully clear and succinct explanation of the terms. Some of the articles referenced therein are also worth a read:

Koonin EV: An apology for orthologs - or brave new memes. Genome Biol, 2001, 2:comment1005.1-1005.2.
Petsko GA: Homologuephobia. Genome Biol 2001, 2:comment1002.1-1002.2.
Fitch WM: Distinguishing homologous from analogous proteins. Syst Zool 1970, 19:99-113. (of historical interest, the terms were first used here)
Fitch WM: Homology a personal view on some of the problems. Trends Genet
2000, 16:227-31.


Why does the DSC peak have a bell shape?

This is just a guess, but it's probably because the heat measurement is actually measuring the sum of many, many molecules reactions. It is a fact of mathematics, rather than natural science, that forces such phenomena to approximately follow bell curves (i.e., Gaussian functions). Basically, the central limit theorem states that if you have many instances of the same (random) variables and average them together, then the result will look like a bell curve. Here, the local thermodynamic change induced by a single individual protein molecule, as a function of the temperature, is presumably that random variable, since the thermodynamic behaviour of each protein is roughly similarly distributed. The randomness comes from the essentially chaotic random movements of the molecules.

See here or here for more.


Hill-Roberston effects and effective population size

Hopefully this syllogism will answer your question.

Given the following premises:

In the absence of selection, fitness of individuals are at a theoretical maximum.
If a theoretical maximum fitness is achieved then effective population size is maximum.
If there is an allele that confers both increased and decreased fitness you have a genetic conflict (e.g. an allele that turns you green gives you good woodland camouflage but is un-attractive).
If a deleterious allele is linked to a beneficial allele this is similar to having a genetic conflict.

The conclusion follows:

Strong linkage between beneficial alleles and deleterious alleles (Hill Robertson effects, i.e. 3. and 4.) prevents a theoretically maximum fitness to be attained (1.) and thus a reduced effective population size (2.). Which can only be overcome by high levels of recombination and mating (i.e. by separating deleterious and beneficial alleles).


What is the philosophical definition of life?

They ask different questions. Philosophy may ask what is life, is there a purpose behind it, etc. Biology asks how does it work, chemistry what are the chemical reactions that drive it, physics maybe how does physics allow for life and how life utilizes and impacts physics, and mathematics how can life and its components be described mathematically.

It is good to remember that all scientific disciplines branched off from philosophy (and religious philosophy) and that they are interconnected.

This is the answer to the part of your question that includes biology. If you want to discuss the meaning of life philosophically, you are welcome to come to do it on the philosophy page!


What is meant by "50% related to sibling" versus "95% related to chimpanzee"?

50% related to sibling means that, out of the portion of the genome that vary in humans, you share half of them with your sibling. (if you compared total genetic match not just ones that actually vary in humans you are looking at something closer to  ~99.95% match)  Now because because variations are not evenly distributed and your parents likely came from the same source population you usually share more with a sibling, but recombinations has a random aspect, and sex chromosomes have a large effect as well. So 50% would be the average using the most common methods of comparison, and even then it is only shorthand. It is a calculation more than a conclusion, if you are 50% related to your parents and so is your sibling then the probability calculation is [0.5 X 0.5 = 0.25]  Note this is in humans, other animals use different chromosome distributions which can result in different numbers, bees for instance have haploid males making females siblings far more closely related.

95% identical to chimpanzee means out of all the genetic elements only 5% of human ones are unique to humans (or chimps) and not shared by chimps and humans while 95% is shared by both. 95% is a lower estimate because they are using the strictest comparison.

One important thing to consider is there are many ways to compare genetic variance, consider a book as an example, if I switch 2 chapters is that one change, two changes, or hundreds of changes (by the number of letters or words in the chapters). because criteria are different you get slightly different estimates of difference. In the case of the 95% estimate that would be using the "hundreds of differences" method of comparing. Deleting the sentence "Mary had a little lamb" would be 21 changes using this method. Other methods would consider it only one difference since it is the product of a single mutation.


If this is in comparison to humans, the animals are more or less free from the two common dental diseases by which teeth are lost in humans. These are dental caries (dental decay)  and periodontal disease (gum disease).

Common to both the diseases is the biofilm which forms on the teeth known as dental plaque.

If the plaque is colonised by acidogenic (acid producing) micro organisms cavities are produced in the presence of refined carbohydrates.

The gum disease is produced by bacterial toxins from the plaque causing inflammation of the surrounding gum resulting in loss of supporting structures of the tooth including bone resulting in loosening and loss of teeth.

In animals in the wild, plaque accumulation is effectively controlled by the coarse unprocessed diet which has a very good scrubbing effect. Besides wild animals are not exposed to refined carbohydrates like sugars.

Hence wild animals do not have these two diseases. However domesticated animals on human diet are prone to similar diseases.

In wild animals severe attrition (wear) and fracture of teeth are more common.

Wild animals will not survive long without adequate number of functional teeth.


Could cancer be in itself a evolutionary process?

Interesting question. I believe it definitely is an evolutionary process. unicellularity breaking away from a multicellular life.

There are two examples that I can think of, which can support this argument:

Hela cells: Hela cells have been classified as a different organism because they have the ability to grow outside the host indefinitely and their genome is different from Homo sapiens. Hela cells also have a new scientific name- Helacyton gartleri
Transmissible tumors: two tumors have been known to infect other hosts and therefore can be called obligate pathogenic lifeforms. One is Devil Facial Tumor Disease which infects Tasmanian devils and gets transmitted by biting. Another is Canine Transmissible Venereal Tumor which infects dogs and spreads via sexual route.

  Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Cancer as of now has a pathogenic identity. It is a simplistic process which in a thermodynamic point of view can be described as maximization of entropy(disorder) and thereby increasing the stability [like the way solutes diffuse]. If a cancer has to give rise to a new functional organ then it has to be supportive of the ordered lifestyle which it is trying to break away from in the first place. It may adopt a pathogenic lifestyle initially and then may redevelop order. I don't know of any such evolutionary event but it may nonetheless be possible.


Factors on which one compound transforming to another compound depend

From my answer on chemistry:

After looking at the website I found the reaction is based off of an enzyme called: phosphoribulokinase. In biological systems many reactions occur under the auspice of enzymes or proteins. These are incredibly large molecules made of an extremely long chain of amino acids which are a set of 26 or so small molecules that can 'hook' into the chain structure of a protein. Each amino acid has different properties and thus experiences different forces pulling it towards and away from other amino acids on the chain. What this means is the whole chain folds up into an extremely complex structure. For a protein to allow a reaction to occur it has a small region that the reacting molecule can hook into. There are then sets of atoms and molecules that act as scaffolds that allow atoms in the reacting molecule to be moved without the need for nearly as much energy as would be required without the scaffold. Now this is how it changes structure. Now whilst the protein can just as easily allow the molecule produced to be converted back to the original, this may be less energetically favourable which brings us to equilibrium chemistry involving dynamic forward and backward reactions. What makes this more complicated is that proteins often have separate 'hooks' for molecules to disable them. That is if a lot of substance A is around then the protein will be disabled and no longer convert B into A until more A is consumed and thus stops inhibiting the protein.


Is there a model perennial plant species?

To my knowledge, Populus is one of the main model species when it comes to perennials and trees. It is for instance used in several sequencing projects, and to study accelerated breeding in strains that are promoted to flower at a very early age.

Excluding trees, other perennial species that has been described as model species are Panicum virgatum (Switchgrass) (see Lu et al. 2013. Plos Genetics) and Solanum lycopersicum (Tomato) (see Sato et al. 2012. Nature.

For a closer description, and arguments for Populus as a model species, see e.g. Taylor (2002. Populus: Arabidopsis for Forestry. Do We Need a Model Tree?. Ann. Bot.) or Jansson & Douglas (2007. Populus: A Model System for Plant Biology. Ann. Rev. Plant Bot).

  Here it is argued that Populus is rapidly becoming accepted as the ‘model’ woody plant and that such a ‘model’ tree is necessary to complement the genetic resource being developed in arabidopsis. The genus Populus (poplars, cottonwoods and aspens) contains approx. 30 species of woody plant, all found in the Northern hemisphere and exhibiting some of the fastest growth rates observed in temperate trees. Populus is fulfilling the ‘model’ role for a number of reasons. First, and most important, is the very recent commitment to sequence the Populus genome, a project initiated in February 2002. This will be the first woody plant to be sequenced. Other reasons include the relatively small genome size (450–550 Mbp) of Populus, the large number of molecular genetic maps and the ease of genetic transformation. Populus may also be propagated vegetatively, making mapping populations immortal and facilitating the production of large amounts of clonal material for experimentation. Hybridization occurs routinely and, in these respects, Populus has many similarities to arabidopsis.

(from Taylor, 2002))

  With the completion of the Populus trichocarpa genome sequence and the development of various genetic, genomic, and biochemical tools, Populus now offers many possibilities to study questions that cannot be as easily addressed in Arabidopsis and rice, the two prime model systems of plant biology and genomics. Tree-specific traits such as wood formation, long-term perennial growth, and seasonality are obvious areas of research, but research in other areas such as control of flowering, biotic interactions, and evolution of adaptive traits is enriched by adding a tree to the suite of model systems.
  ...
  The development of Populus as a model system for tree and woody perennial plant biology has been largely driven by the rapid development of genomic and molecular biology resources for this genus, as discussed below, culminating in the completion of a draft sequence of the Populus trichocarpa (black cottonwood) genome (106). This information will facilitate studies on the comparative biology of Arabidopsis and Populus as representatives of two angiosperm extremes, enabling discovery of mechanisms conserved among eudicots.

(from Jansson & Douglas, 2007)


Breeding season

Chances to see nests will be higher during breeding season which normally occurs once a year. Eggs will be laid in early May but they will be built in the previous months.

Area

In densely populated urban areas gulls may build their nests on rooftops instead of ground nesting. In the case of New Jersey I found the following brochure:

https://www.nj.gov/dep/fgw/ensp/pdf/bnb_brochure.pdf

If you mean seagulls as in all Laridae, then you have two members of that family (black skimmer and least tern) in that brochure that actually use NJ's beaches and even have their own designated space for that.

Googling 'seagull rooftop nests' brings a decent amount of pictures of rooftop nests. 'Seagull nests' brings a lot of cliff-placed nests, rooftop and ground nests. I assume the choice depends mostly on food availability and predator population density. I remember in Spain a few years ago there was a big enough problem to appear on local TV news related to seagulls attacking people. They would nest on every roof and attack people that would go out on the balcony with a sandwich.

Sources:

Habitat Selection and Nesting Biology of Roof-Nesting Glaucous-Winged Gulls
Kees Vermeer, Damian Power and G. E. John Smith
Colonial Waterbirds
Vol. 11, No. 2 (1988), pp. 189-201 https://www.jstor.org/stable/1521000?seq=1


To measure acuity, it's important to have a measure that considers visual space rather than physical world space (it doesn't make any sense to talk about "millimeters" because that says nothing about how far away the object is), so one would normally talk in terms of "degrees or arc" where 360 degrees is a whole field in all directions. Within degrees of arc, you can refer to "arcminutes" which are 1/60th of a degree of arc. If you could see everything in front of you, but nothing behind you, then you have 180 degrees of visual field in both horizontal and vertical dimensions (humans actually have a much smaller visual field than this), or 10,800 minutes of arc.

Your visual acuity greatly depends on where on the retina an image falls; the 'fovea' is the center of the retina where your vision is most sensitive. In the fovea, the maximum acuity is somewhere around 0.5-1.0 minutes of arc (see for example Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.), which corresponds nearly to cone density in the fovea.

A good "rule of thumb" (no pun intended, since we won't be using the thumb here...) is that the width of your fist at arms length is about 10 degrees of arc, your pinky finger is about 1 degree of arc. To get 0.5 arcminute resolution, then, you would need a screen the size of your fist (600 arcminutes) held at arms length to be 1200 pixels wide. Modern cellphones held at a moderate distance likely come near this limit, whereas TVs and monitors typically do not; however, you probably view your phone much closer than arms length and your TV much further.

Realistically, however, pixel counts far below this are sufficient for most scenes, because acuity measured this way is referring to the ability to separate points of light. In real natural vision, we aren't usually separating points of light, but rather organizing visual representations into salient objects, so the actual pixel density required to get a smooth image is less. Pixel limitations are more likely to be apparent when displaying text, since contrast is much higher with text than with natural scenes.

References

Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.


NMDA receptor mediated plasticity figure reference

One of the "Boss references" (nearly 11000 citations right now) for this is Bliss and Collingridge, A Synaptic Model of Memory: Long-Term Potentiation in the Hippocampus.
Being from 1993, it has references to some of the earlier work in this field (if that's what you're looking for).
It notes the different forms of NMDA-dependent and independent plasticity.
Another paper, also from 1993, on this topic is Malenka and Nicoll, NMDA-receptor-dependent synaptic plasticity: multiple forms and mechanisms

Some nice reviews with more recent work, focusing on the NMDAR itself include:

Paoletti et al, NMDA  Receptor Subunit Diversity:
Impact on Receptor Properties,
Synaptic Plasticity and Disease
Lau & Zukin, NMDA Receptor Trafficking in Synaptic Plasticity and Neuropsychiatric Disorders

and their references.


Ravens and other corvids are among the most intelligent birds. Of note, crows and ravens are known for their ability to solve problems that require tool use, memory, and delayed rewards (patience).

Many animals play, and ravens and crows are no exception. (A study entirely on raven nestling play.) The evolutionary purpose of play activity is thought to improve coordination/dexterity, provide exercise, strengthen muscles (such as wing-flapping by young birds that have yet to fledge), and develop social skills.

As to what type of objects ravens find most interesting to play with, I'm unsure of a definitive answer. Some birds, particularly the satin bowerbird, even collect colorful objects. My hypothesis is that the choice of object is likely due to simple availability (discarded) and conspicuous nature (color). In other words, ravens more easily find such objects because they are colorful, which in turn are frequently human-manufactured.


Is there a closed path through the circulatory system that never passes through the liver?

The liver gets blood from two sources: the hepatic artery and the portal system of venous drainage from the gastrointestinal tract.
As long as you don't follow one of these paths, you'd avoid the liver. Some examples would be circulating through any of the limbs or head, but any path that avoids those two paths will do. As you point out this is statistically unlikely without your magical navigation abilities.


Equation for accurate prediction of PCR yield

An expected efficiency for a typical PCR is 80%, meaning each cycle multiplies the copy number of the targeted DNA sequence 1.58 times.

Firstly, it makes more sense to refer to the amount of DNA in a polymerase chain reaction in terms of copy number or in terms of moles; the number of DNA molecules of interest is what the reaction is operating on, and the mass of product generated is a function of the length of the product (and, to a lesser degree, on the composition of the product).

The following discussion is sourced from this URL: https://www.csun.edu/~hcbio027/biotechnology/lec3/pcr/p.htm

According to Perkin-Elemer, copy-number amplification of 100,000 fold of the targeted sequence of DNA can be expected from a PCR with 0.1 ng of Lambda phage DNA (a well-characterized and standard DNA isolate) in a 100 µL reaction with > 25 cycles of denaturation, annealing, and extension.

In the above 100,000-fold amplification example, if the targeted amplicon were to be 500 bp in length, the estimated molecular-weight of duplex DNA of 500bp is 325,000 g/mol (based an average base-pair having a molecular mass of 650 g/mol).

The Lamdba Phage genome is 42,502 base-pairs in length.
42,502 bp × 650 grams/mol/bp = 2.762×10^7 grams/mol.

0.1 ng Lambda DNA -> 0.1×10^-9 grams.
0.1×10^-9 g ÷ 2.762×10^7 g/mol = 3.619 × 10^-18 moles.
3.619 × 10^-18 moles × NA (Avogradro's Number) = 2.179×10^6 copies, or 2,179,000 copies.

2.179×10^6 copies × 100,000 = 2.179×10^11 copies.
2.179×10^11 copies ÷ NA × 325,000 g/mol = 1.176×10^-7 grams of sequence.
1.176×10^-7 grams is equal to 0.117 µg or 117 ng.

An amplification yield of 100,000x after 25 cycles would mean at each cycle 1 template would yield 1.58 templates for the next round of synthesis.

How was this calculated? If c is the number of copies made per round of synthesis, then:

c^25 = 100,000 = 10^5
so c^5 = 10
and so 5(log c) = log 10 = 1
so log c = 0.2 and c = 1.58 (approximately)

(Or you could calculate the 25th root of 100,000 on a calculator, if you prefer.)

If we obtain 1.58 copies instead of the theoretical maximum of 2 copies, then the efficiency of the reaction could be said to be 79% (because 1.58/2.00 = 0.79).

One reason this calculation is important is that a slight loss of efficiency is magnified through the amplification. A reaction may appear to have not worked if the efficiency drops (in each cycle) by just a few percent. Optimization is critically important in the polymerase chain reaction.


Is there a program that simulates biology on a molecular level?

There is a recent paper that introduced the first molecular-level whole-cell simulation.

Karr, J.R., Sanghvi, J.C., Macklin, D.N., Gutschow, M.V., Jacobs, J.M., Bolival, B., Assad-Garcia, N., Glass, J.I., & Covert, M.W. (2012). A whole-cell computational model predicts phenotype from genotype. Cell 150:389-401 DOI: 10.1016/j.cell.2012.05.044

The authors combined 28 different sub-modules of various biological processes from the literature. Each one operates at the level of macromolecules, although models them in different ways: some by ODEs, some by logic; some by agent-based approaches. If you want to fool around their code is available online and I wrote a basic introduction/summary of the paper.

Here are some related bio.SE questions motivated by that model:

Short-term Lamarckism in asexual single cell organisms
Computational/mathematical models for predicting phenotype from genotype
Macromolecule levels in daughter cells after fission


Sequentially:

Yes. Up to the limit of what the mother's body can tolerate.  Of course, if the cells never aggregate, that suggests some sort of fundamental problem with the embryo's developmental process, and you will probably not get a viable organism.

Sort of and yes.  In utero, fertility drugs can cause multiple eggs to be released per cycle, which can cause fraternal twins when each egg is fertilized.  IVF can do the same thing, but you can also manually subdivide a single embryo into two (smaller) viable embryos, provided you perform the division before any cell differentiation occurs.

Yes, but good luck getting an ethics review board to approve that :D


Why have humans evolved much more quickly than other animals?

This question appears to address at least two distinct concepts:

the "speed" of evolution
whether there is some "end goal" that evolution seeks

I will provide an explanation of each separately below:
The Speed of Evolution
The speed at which a species evolves—that is, the speed at which it acquires new heritable characteristics—can be affected by numerous factors. Among the most obvious which come to mind are:

existing population size
reproductive cycle rate
number of offspring
offspring survival rate
environmental demands

That said, have humans evolved faster than other species?
On the whole, I do not feel that I could say without a doubt that humans have evolved significantly faster than other organisms. Considering the above factors (we have a slow reproductive cycle, few offspring, etc.), it seems unlikely but this is where a zoologist would know better. The answer provided by bobthejoe may provide insight as well.
I would just raise a word of caution before leaping to the conclusion that we have evolved rapidly without looking into it, because while we often study human evolution quite extensively in biology classes and thus are more aware of changes like upright walking and opposable thumbs and increased brain size, that doesn't mean other animals didn't evolve that much as well (we just don't learn about them in as much detail). Being a psychologist and not a zoologist, I do not have the knowledge to say with any surety that other species did not evolve in their own ways to the same magnitude as we have in the last 3-4 million years, so perhaps someone else can help you there.
But you ask whether we have a particular part of our brain that no other animal has; the answer to this is no, but the parts of our brains which we do share with animals are often much larger than as seen in those other species.
The "Goal" of evolution
I would like to point out here that human technology has nothing to do with evolution. Not only have all of our notable technological achievements occurred in the last couple hundreds years when human evolution was at its slowest (early human evolution as we know it today dates back at least 5-7 million years, and it was during this several million year period when all the genetic evolution you speak of happened), I would argue that human spaceships and computers are no more sophisticated to us than a mushroom garden and ventilation system are to a termite. I could be wrong here but it seems as if you are under the impression that evolution is striving towards something... That humans are somehow intrinsically better than lions or sharks or beetles. On the contrary, each of these creatures is not significantly more or less adapted to their environments as we are to our own, and in many ways these creatures possess features which are beyond our own.
I shall leave you with one of my favorite quotes:

"We need a wiser and perhaps a more mystical concept of animals. We
patronize them for their incompleteness, for their tragic fate having
taken form so far below ourselves. And therein we err, and greatly
err. For the animal shall not be measured by man. In a world older and
more complete than ours, they move finished and complete, gifted with
extensions of the senses we have lost or never attained, living by
voices we shall never hear. They are not brethren, they are not
underlings. They are other nations caught with ourselves in the net of
life and time, fellow prisoners of the splendor and travail of the
earth."

–Henry Beston, in The Outermost House
I don't have a dog in this fight, and I could very well be falsely assuming that you think this particular way when you in fact don't (you only wrote 4 lines after all, it's hard to glean much from that), but I wanted to make sure that these concepts were clear either way, particularly for any future visitors who might get the wrong impression. :)


Although "Virus" literally means "Poison" in Latin, it would be a great over-simplification to regard a Virus as a Poison.
Now, most poisons are chemical compounds that interfere in some chemical pathway in our body. For example:

Carbon Monoxide: Binds with Haemoglobin, rendering it unable to transport oxygen
Sarin: Indirectly inhibits degradation of the  neurotransmitter "Acetylcholine"
at the synaptic cleft.   Mechanism of action of Sarin

Hence most poisons are quite "simple" in their actions. However, viruses can be considered as a complex machinery of functions that interfere with a multitude of processes in our body including cell transcription, receptor-mediated endocytosis, et.c
Hence, the best analogy would be to consider a virus as a tactical poison.
Now, as for last question, viruses are fragile assembled structures.  Viral Self-Assembly

Environmental factors like heat, uv-light, oxygen, etc may damage the assembled structure. Hence, viruses have a self life, and so do may poisons.
  Sarin (self life)
However, poisons tend to have a longer self life because chemical compounds are more stable than the capsid of viral proteins with weak hydrogen bonds.
As per David 's suggestion, poison is defined as "...substances that cause death, injury or harm to organs, usually by chemical reactions or other activity on the molecular scales, when an organism is exposed to a sufficient quantity."  Wikipedia
Viruses do work at molecular level, but not in the same sense as poisons do. Hence, viruses do fit into the description of poisons but not precisely.
Hope you find this helpful.


Is "monosexual" still a valid term in biology?

I suspect "monosexual" is a term recruited in sociology, psychology and/or medicine. I haven't ever heard of it in application to biological questions. It's a behavioral habit and doesn't seem to be directly related to the (biological) opposition "separate sexes" vs "hermaphroditism".

In biology:

Animals can either be gonochoristic (separate sexes) or hermaphroditic. If an animal species reproduces without gametes it's called asexual (in animals asexual reproduction is rarely the only way of propagation), and if only females are present which give birth without fertilization, they are called parthenogenetic.

In some cases different modes of reproduction are utilized by different stages (alternate generations) or even phases (larva vs adult, young vs old). In other cases in populations coexist males and hermaphrodites or males and parthenogenetic females.

Mammals, including humans, are (nearly) perfect examples of gonochoristic animals: only a male and a female together can produce offspring. If someone is homosexual (it refers to behavior only), he is a dead end in this respect.


Multiple clones Sanger sequencing analysis

I haven't personally used it but seqtrace seems to be targeted for this purpose. It seems to be able to do alignments and facilitates multiple trace file analysis.
I worry a little bit about not visually inspecting trace files for sequencing of clones, but I may be a relative dinosaur (about sanger at least).
Here is the abstract:

Modern applications of Sanger DNA sequencing often require converting a large number of chromatogram trace files into high-quality DNA sequences for downstream analyses. Relatively few nonproprietary software tools are available to assist with this process. SeqTrace is a new, free, and open-source software application that is designed to automate the entire workflow by facilitating easy batch processing of large numbers of trace files. SeqTrace can identify, align, and compute consensus sequences from matching forward and reverse traces, filter low-quality base calls, and end-trim finished sequences. The software features a graphical interface that includes a full-featured chromatogram viewer and sequence editor. SeqTrace runs on most popular operating systems and is freely available, along with supporting documentation, at http://seqtrace. googlecode.com/.© 2012 ABRF.


Cell-autonomous viral defense involving oxidative burst?

So, the cell may trigger an oxidative burst in response to pathogen (not specifically virus).
In case of retroviruses, they are hard to detect for the cell (example HIV) as they use the cell machinery for replication and can also stay in inactive latent state thereby not triggering immune response.
Hope you found your answer. Thank you and good day.


If sexuality is genetic, how did asexuality evolve?

Update:
See @Bryan Krause comment. Just because something exists (or equally, doesn't exist) does not mean that it was selected for or has any evolutionary relevance. Imputing selection to any particular state of affairs is usually bad reasoning without a lot of evidence.
I didn't do a good job of coming out and saying this in my answer.
My answer is best understood as answering the question: how could asexuality evolve under selection?
It does not at all address the question: DID asexuality evolve under selection (in humans)?
This second question is one for which the answer is probably "no". Without more evidence, we cannot say whether asexuality has any evolutionary/selective relevance at all.
Original answer:
I would suggest looking more into the evolution of social animals for which large proportions of the population is non-reproductive (or sterile). There are many such examples, with insects as the obvious case:

Contrary to widespread belief based on heuristic arguments of genetic relatedness, non-reproductive workers can easily evolve in polyandrous species. The crucial quantity is the functional relationship between a colony’s reproductive rate and the fraction of non-reproductive workers present in that colony.

I would suggest looking more into that paper and citations therein. The question to answer is whether an individual's labor can be more important than their gonads to the continuation of their genes.
As suggested in the wikipedia article on homosexuality that you link to in your own comment, there is a positive effect on female fertility from having homosexual family members ("kin selection"). Granted, what causal mechanism is behind this is likely difficult to sort out.
It's quite plausible that asexuality behaves similarly to homosexuality in this regard. Those authors want it to be a genetic factor driving both sexuality and fertility. But to me it seems a bit more parsimonious to posit that it's good to have more warm adult bodies around to care for/support children.
From a practical perspective, if grandparents with non-functional gonads can help raise kids (i.e. increase effective fertility of kin), why not asexual relatives too?


History: Do evolutionary and ecological processes occur at the same timescales?

This doesn't directly answer your question but my current research is on building models that combine ecological and evolutionary processes. Thompson (1998) is one of the earliest papers to talk about rapid evolution on ecological time-scales. And also a recent paper highlighting the interactions was Schoener (2011).

Perhaps reading through these two papers and looking at their references will give you a better idea of when the shift in thought started.


What a timely question.

  Does DNA contain information beyond protein synthesis?

Yes. In fact, protein-coding genes only constitute a tiny part – less than 2% – of the whole DNA. There are of course many other genes which aren’t protein coding: there are genes for ribosomal RNA and we find more and more genes which code for small RNAs, such as tRNA. But even if we count all those genes we won’t come above maybe 10% of the total DNA.

Most of the DNA is instead devoted to the regulation of gene expression, most importantly via the binding of transcription factors (but the picture is much more complex than that). With the conclusion of the ENCODE project, a whole slew of papers were published which show that in fact most of the DNA is actively implicated in the binding of various factors (although it’s not known how much of that actually contributed to the cell’s fitness).

But I’ve hijacked your question a bit here. So let’s come back to what you’re actually interested in:

  What about higher levels, such as organelles, cells, tissue, organs?

There is no known mechanism (beyond the already mentioned regulation) which would encode such information in the DNA. Excluding its existence categorically may be hard but given that we haven’t found any machinery which would be necessary to read such information, we can be pretty confident that it doesn’t exist.

  If not, what guides those levels of structure?

The higher levels of organisation are to all appearances emergent. That is, they are a consequence of the lower level organisation. For instance, take the cytoskeleton which carries much of the cell’s physical structure. It is composed of different protein complexes which form spontaneously through assembly of globular proteins (such as actin). The are several ways in which the process can be guided but strikingly it’s largely stochastic – i.e. mostly unguided, and it still succeeds in building a stable skeleton, simply by virtue of molecular properties encoded in the proteins.

I think this is a common theme of cell organisation: the elementary building blocks are encoded by the DNA, and their abundance is tightly regulated. Everything else, i.e. higher-level organisation – follows from that: abundance and localisation of the right proteins.

  As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

In fact, much is known here, and it goes back to regulation on the level of DNA: we know that genes are differentially expressed depending on the cell type and stage of development (and the stage in the cell cycle). This regulation is highly complex and decoding it is a slow process. Nevertheless, the factors involved here are decoded one by one. This is the domain of developmental biology.


When you have your gallbladder removed, how does it affect bile flow into your small intestine?

Bile is stored, concentrated, and acidified in the gall bladder. Schwartz Principles of Surgery ch. 32 has a good section on this. After recovery from an uncomplicated surgery, the loss of the gall bladder does surprisingly little (other than, usually, resolve the symptoms of gallstones). This was a bit of a surprise to the medical community when the first cholecystectomy was performed in 1882, and it remained a controversial procedure for some time.

There are a number of studies on the effects on bile flow and the overall cyclic release, reabsorption, and return to the liver of bile via the portal vein called enterohepatic circulation.  Animal and human studies demonstrate compensation by the liver, bile duct, and the sphincter of Odie. Overall bile flow is reduced, there appears to be greater release into the intestine during fasting states, and there do appear to be changes in the composition of bile, but, most importantly, enterohepatic circulation is still pulsatile, in response to a meal, as you can see in the figure below.

Both solid lines are subsets of bile acids, measured in the serum of cholecystectomized patients in a classic 1978 study. The shaded areas represent control (not cholecystectomized) patients. These measurements suggest that enterohepatic circulation still follows a pulsatile pattern after cholecystectomy.


Why is it not advisable for humans to drink distilled water?

As you said, distilled water is completly out of minerals/ions. The principle of diffusion is that reagents diffuse from high-concentrated to low concentrated places to reach an equilibrium. So normally, ions from the erythrocytes would diffuse into the plasma to reach that equilibrium. However, it is quite difficult for ions to pass the cell membrane which is not the case for water. So what finally happens is that the distilled water wants to dilute the ions in your erythrocytes, passes the cell membrane and the cells explode because they are too full. As consequence, you die because there is no oxygen transport anymore.


How do we explain the white feathers of an albino peacock?

The surface structuresa that are responsible for the structural coloration of peacock feathers are actually barbules and rods made of the very same biopolymer that is responsible for pigmentation in many other animal species, namely melanin. Just as in other animals, melanin is produced in the melanocyte cells which reside in the skin's epidermis. The conditions of albinism or leucism are due to mutations to genes responsible for melanin expression in those cells, or their absence. So although structural coloration is resposible for the colorful peacock feather, it is the same mechanism that leads to colorless feathers as in other animals.

Reference

a Zi, Jian, et al. "Coloration strategies in peacock feathers." Proceedings of the National Academy of Sciences 100.22 (2003): 12576-12578. https://dx.doi.org/10.1073/pnas.2133313100


Do ants use something similar to the honey bee "waggle dance" to instruct the rest of the colony where to find a food source?

I can only help you on one question about if ants perform a similar communication such as the "waggle-dance" to tell other ants if there is food elsewhere?
Ants will send out scout ants or forages, which will go out in search for food. The ants will lay a pheromone trail, by tapping their abdomen on the ground, like breadcrumbs. If the ant has found a food source, they will taste the food and take part of the food and store it in their crop. The ant will take the food sample and re-trace her trail, making it more detectable when returning to the food source. Once the ant reached the nest and finds another ant, she will regurgitate the food from her crop and position it between her mandibles. She will go towards another ant and exchange the food and pass it on to the ant in a "kissing" motion. This is called trophallaxis, where there is a donor, the scout or forager ant, and a recipient, the ant back at the nest. The ants will then follow the trail the scout first put down and will eventually create a motoway of food going to the nest.
Look up people like Nigel Franks and John Sudd - The behavioural ecology of ants.
The lives of ants - Laurent Keller and Elisabeth Gordon
The Earth dwellers - Erich Hoyt
sciencedirect.com/science/article/pii/0003347295801405 about trophallaxis in solenopsis ants sciencedirect.com/science/article/pii/037663578290050X about trophallaxis in Myrmica ruba
Hope that helps.


What is the source of the electrons generated in the Krebs cycle?

The two electrons and a proton of NADH comes from a H$^-$ ion of a Krebs cycle intermediate during Isocitrate dehydrogenase reaction and Malate dehydrogenase reaction.

In the following reaction, Isocitrate is oxidised to Oxalosuccinate and in the process two Hydrogens are lost one as H$^-$ and the other as H+. This H$^-$ is accepted by NAD+ to form NADH.

Note: Oxalosuccinate is an intermediate formed during oxidative decarboxylation of Isocitrate.

Now coming to FADH$_2$ $-$

During oxidation of Succinate to Fumarate, Succinate looses a H$^-$ and a H+ ion which constitute the two protons and electrons of FADH$_2$  . Here's an image that illustrate the mechanism:

The alpha-ketoglutarate dehydrogenase complex reaction is similar to pyruvate dehydrogenase complex reaction(PDC).
PDC reaction is an oxidative decarboxylation reaction of Pyruvate in which the 2e$^-$ of NADH are derived from the electron shared between COO$^2-$ and C=O groups of Pyruvate.

The Hygrogen (H+) of NADH is either derived from the H+ of CoA-SH or from the medium. There's a series of complex reactions which need to be studied to fully understand the source of H of this NADH.

So you can understand that the 2 e$^-$ of NADH produced in Alpha-ketoglutarate dehydrogenase complex reaction are the electrons between COO$^2-$ and C=O groups of Alpha-ketoglutarate and the H is either from the medium or the H+ of CoA-SH.

Reference: Biochemistry by Berg


Why would you plate cells at different densities in a colormetric assay?

The comments you have given are some reasons, although they also depend on the confluency of the cells. Your teacher/professor/advisor is also making sure that you can see an effect at low levels of drug, as well as making sure that changes in the signal are visible - for example, does a 50% reduction in viability due to drug activity give the same drop in signal as reducing the number of cells by 50%? You don't say what kind of assay you're running, but a fairly common and inexpensive one is the MTT assay, with some kits nowadays switching to XTT for greater sensitivity and a reduction in the number of steps in the assay (example kit from Cell Signaling compared to an MTT assay kit from ThermoFisher), as the final colorimetric product does not require solubilization before reading. Finally, depending on the lab you're in, the conditions for the assay may not have been optimized yet, so your instructor wants you to test a couple of different densities to see what works best.


Characteristics of Araneus hui (an orb-weaving spider)

These pages cite papers that mention A.hui:
https://www.gbif.org/species/2160156
https://wsc.nmbe.ch/species/2910/Araneus_hui
The World Spider Catalog (WSC) offers papers to their users for free, and it is a free registration.
Browsing through the second pdf on the WSC, here is a sketch of the dorsal (top) view of the species:

The paper is primarily written in a language I cannot read.
The specific paper (book?) is:
Hu, J. L. (2001). Spiders in Qinghai-Tibet Plateau of China. Henan Science and Technology Publishing House, 658 pp.
658 pages is quite volumnous. The title of the paper suggests we limit our search to Tibet. Searching for Araneus images on iNaturalist in Tibet, there is a picture of one Araneus that has not been identified to species level, but it resembles the abdominal shape as in the drawing in the paper:
https://inaturalist.ca/observations/51273647
But the abdominal markings do not match at all. If you expand the geographical bounding box of the search around Tibet, you can browse a gallery of hundreds of possible pictures.


Does a DNA sequence has its own derivation tree or pattern?

From your example I guess that by "deriving" you mean something like decomposing into elements with diverse functions. Maybe we could apply this concept to DNA sequences: Some parts code proteins, which are decomposed into triplets, each of which codes an amino-acid. Other parts have regulatory functions: They can be motifs not coding a protein, but instead allowing a protein or something else to bind and modify the expression of nearby protein-coding parts. Other parts may contribute to the physical structure of the chromosome, or may have no function at all.


Can cerebrospinal fluid pass through the pia mater or ependymal cells of the ventricles?

Both the blood brain barrier and the blood CSF barrier tightly regulate the CNS fluid interstitial fluid environment of the CNS. You, however, are talking about a different barrier, the barrier formed by the pia mater, sometimes called the brain/CSF barrier. This barrier is less well studied. It does appear to prevent transport of particulate matter and red blood cells, but allow the passage of immune cells and small molecules. In addition to your professor's statement that the composition of CSF and brain interstitial fluid is similar, intrathecal injection directly into the CSF in the subarachnoid space provides an effective way to deliver drugs with CNS action, suggesting the pia mater does not effectively restrict small molecules (see Goodman and Gilman's The Pharmacological Basis of Therapeutics Ch 2).


Validity of the August Weismann mouse-detailing experiment refuting Lamarckism

If you are reading this after 31st July 2017 it will seem somewhat disconnected from the question. This is because the question has been extensively edited since I wrote this answer.

Anyone who is interested in the work of August Weismann should start by reading the corresponding Wikipedia page.

Ernst Mayr ranked him as the second most notable evolutionary theorist of the 19th century, after Charles Darwin.

As far as the mouse tail experiment is concerned, we learn that Weismann was concerned with disproving Lamarckianism, and that:

Weismann was aware of the limitations of this experiment, and made it clear that he embarked on the experiment precisely because, at the time, there were many claims of animals inheriting mutilations (he refers to a claim regarding a cat that had lost its tail having numerous tail-less offspring).

My grandfather used to claim that his mother was frightened by a bear whilst pregnant, which was was why he was born with bare feet but that's more likely to be due to an epigenetic effect I suppose.

Added later in response to Remi.b
I see that Charles has already addressed this to some extent, but since I have already done the research I'll post what I found:
from August Weismann, Essays Upon Heredity. Clarendon Press, Oxford, 1889
(Volume 1, Chapter 8, p. 431)

But now, after this little digression, let us return to the transmission of mutilations.
We have seen that the rudimentary tails of cats and dogs, as far as they can be submitted to scientific investigation, do not depend upon the transmission of artificial mutilation, but upon the spontaneous appearance of degeneration in the vertebral column of the tail. The opinion may, however, be still held that the customary artificial mutilation of the tail, in many races of dogs and cats, has at least produced a number of rudimentary tails, although, perhaps, not all of them. It might be maintained that the fact of the spontaneous appearance of rudimentary tails does not disprove the supposition that the character may also depend upon the transmission of artificial mutilation.
Obviously, such a question can only be decided by experiment: not, of course, experiments upon dogs and cats, as Bonnet rightly remarks, but experiments upon animals the tails of which are not already in a process of reduction. Bonnet proposes that the question should be investigated in white rats or mice, in which the length of the tail is very uniform, and the occurrence of rudimentary tails is unknown.
Before this suggestion was made, I had already attacked the
problem experimentally. Such a course might, perhaps, have been more natural to those who maintain the transmission of mutilations, to which I am opposed. Although I undertook the experiments expecting to obtain purely negative results, I thought that the latter would not be entirely valueless; and since the numerous supporters of the transmission of acquired characters do not seem to be willing to test their opinion experimentally, I have undertaken the not very large amount of trouble which is necessary in order to conduct such an experimental test.


If by "satellite chromosomes" you mean "satellite repeats", then:

Not always. There many types of satellites, such as telomeric, centromeric (like gamma, alpha, beta satellites), simple repeats (CT)n.
It is still an open question. Some say they are important for chromosome structure (e.g., centromeres). Sometimes satellites get transcribed as might act as lncRNAs. And of course, most of them are just junk DNA.
If there is T then there is A too.

Edit

Satellites contain telomeric repeats at their ends as all chromosomes do. But they are more about NOR repeats.
They are important for the nucleolus functioning. But shorts arms of acrocentric chromosomes are not crucial, take Robertsonian translocation as an example.


Is this plane indeed random?

Answer : I don't think so.

HUMAN CONE RESPONSE

Let's take a look back at human cone response curve.
This is cone response curve for normal people :

  But picture for deuteranopia is quite different. Confusion lines are intersecting at one point. But this is not a point nearby green color, it is opposite. Why?

In case for Deuteranopes, let's take a look at their cone response :

As you can see Deuteranopes have their green cone sensitivity shifted very close towards red.
This also why Protanopia and Deuteranopia is what we know as Red-Green color blindness, where they have difficulty in distinguishing shades of red from shades of green since its cones sensitivity is very close to each other (almost similar).

So for deuteranopia, why the intersecting point is it not green ? Well, despite the actual missing cone is green, its sensitivity is shifted towards red. Also, this "intersecting point" is called copunctal point.

CONFUSION LINE :

Now about confusion line, indeed each cones in our eyes is sensitive to each RGB primary (even though it's a little bit misleading). And yes, RGB color space is in 3-dimensional. But confusion line is mapped based on chromaticty diagram from CIE 1931, not RGB. Some specific transformation and normalization method need to be performed to convert 3-dimensional RGB into 2-dimensional chromaticity diagram.

As we know before, Protans and Deutans have their cone sensitivity close to each other, thus their copunctal point (point where the fundamental color is missing, point where all the lines converge) is also close to each other.

Here's the copunctal points (1) for all dichromats :

COPUNCTAL POINT     x         y
Protan             0.747     0.253
Deutan             1.080    -0.800
Tritan             0.171     0.000

CIE is quite tricky, they can have negative value as well (RGB can't have negative value). This copunctal point is very important since it's the fundamental information of the missing wavelength from colorblind, and this missing wavelength is converted into CIE colorspace and then mapped into the diagram. So, even though the deuteranopes confusion lines looks a bit confusing, it is the correct mapping from actual missing point in wavelength.

(1) Wyszecki & Stiles, Color Science (2nd ed.), 1982, Table 1 (5.14.2) p. 464


I write this as an answer instead of a comment because I don't have the reputation to do otherwise (frustrating!) even to edit my answer-which-is-now-a-comment

A weak vinegar solution (maybe 1:1 ratio water and vinegar) will solve your problem and will not stink up your home. Vinegar smell evaporates very quickly and are great for areas you can't reach easily to clean by hand. I promise your AC won't smell like egg salad.

Here's the first mold-cleaning with vinegar article I could find, there are plenty more where that came from


I assume there must be a maximum size for insects, and I atmospheric oxygen probably has something to do with it. Insects do not breath like vertebrates, they have a series of tubes call trachea that run through their bodies and open to the surface at spiracles. Air passes through these tubes and oxygen and CO2 passively diffuse through the tissues. Insects can force air through the trachea to increase the diffusion rate, but they just aren't as efficient as vertebrates with lungs and hemoglobin to carry oxygen around the body.

In the past, oxygen levels were much higher. Higher amounts of oxygen could allow for larger invertebrates, and there were 6 foot long millipedes and giant dragonflies. Their size probably was not entirely caused by the extra oxygen, this was before they faced competition from vertebrates, so increased competition probably had more to do with their size reduction than loss of oxygen.

I don't know what the maximum size for an insect is at modern oxygen levels, but you'd have to eliminate the other selective pressures such as competition and limits on food before an insect could reach that size.


Teens concerned about impregnation through clothes

If there has been an ejaculation by the male, and semen is present, there is a chance of getting pregnant. Period. Teens really need to know that.
I think you may have your terms confused - semen is the overall fluid released during an ejaculation, sperm are the cells with tails that are produced in the testes and fertilize the egg. At any rate, according to the WHO, a normal sperm count is over 15 million per milliliter, with some counts much higher (>50e6/ml ), and an average between 20 and 40 million. The volume of the ejeculate tends to be anywhere from 1-6 ml. If you take a healthy young male at the peak of his reproductive capabilities, this equates to a very large number of sperm being released during a sexual encounter. All it takes is for one to reach an egg and fertilize it. Sperm are very very small, much smaller than the pore size of average fabric, so clothing will do very little to stop them. The female is likely sexually aroused during this activity as well, and produces additional fluids and lubricants that promote the survival and motility of sperm, among other things.
So, it depends on many factors. If both parties are fully clothed (at least 4 layers of clothing between their respective reproductive organs) and there is a minumum of soaking through, the chances of pregnancy are correspondingly quite low. On the other hand, if only one partner is wearing just their underwear, it's essentially like there is no clothing present at all, and the relative chances go up significantly.
Safe sex practices can't be emphasized enough to young people, as education and awareness is so much better than ignorance and myths. Even aside from pregnancy, if condoms are not utilized properly to contain all the semen there is the chance of sexually-transmitted diseases, ranging from herpes and gonorrhea to AIDS. None of these require penetration to be passed along, and one might argue that the additional presence of potentially irritating fabrics could open up raw areas or cuts and enhance their transmittal.

Take home message
Now, all this being said, the chances of impregnation through clothing without direct penetration of the penis into the vagina is quite low compared to "typical" unprotected fully-penetrating intercourse, especially depending on where the female is in her fertility cycle. According to this study, a woman's most fertile day is two days before ovulation (as had been postulated before), and the chances of pregnancy on that day are about 25% (assuming penetrating intercourse). Overall, the chance of pregnancy throughout the month is about 5%.
I don't have any hard numbers on the pregnancy chances when one or both partners have at least some clothing on, as obviously it will vary greatly depending on who is wearing what, the volume of ejaculate, contact time after ejaculation, etc. Just for fun, let's assume it's 100 times lower. That means the chances of impregnation two days pre-ovulation would be 0.25%, or 1 in 400. While rather low, this is still a non-zero chance.
Condoms are about 98% effective if used properly during penetrative vaginal intercourse. Various other birth control methods such as contraceptive pills, intrauterine devices, implants and injections are quoted as being 99% effective on their own, although they do not protect against sexually transmitted diseases. I'm certainly not one for preaching abstinence, but done properly it should be 100% effective. Ultimately, it is up to both partners to decide what their risk tolerances are, together. It is much better to seriously talk about it beforehand than to be panicked and unsure afterwards.

Hopefully this addresses your concerns, please leave comments if you have additional questions.


Can the basement membrane of blood capillaries expand?

It's a good question.
Though there is hardly some evidence to answer your question.
However I will share what all I found.
So in capillary basement membrane, mostly collagen type 1 and 4 are  present.
Now collagen type 4 aids in elongation of the new capillaries-

in the ex vivo rat aortic model of angiogenesis using a type I collagen matrix, type IV collagen promoted new vessel elongation and survival in a dose-dependent manner compared with controls (no type IV collagen), which grew until day 9 and then regressed during the second and third week of culture (treatment with 3, 30, 300 g/ml of type IV collagen in 43, 57, 119% increase in microvascular length) [139]. In all then, type IV collagen seems important for stability of blood vessel formation.

The collagen in capillary basement membrane impart mechanical stability to the vessel.
Also elastin is a component of the basement membrane. Reference
Now though I couldn't find that it's the elastin of basement membrane only, but-

Comprising 50% of the dry weight of major arteries, elastin is the most prominent ECM protein in arteries [43]. In vessels, elastic lamina alternate with rings of smooth muscle forming a strong, flexible part of the arterial wall [43, 44].

Here is the article


How does the frequency of a visual stimulus affect the steady-state visually evoked potential?

Short answer
SSVEP frequency corresponds to stimulus frequency and SSVEP amplitude decreases with stimulus frequency.

Background
The simplest form of steady state visual-evoked potentials (SSVEPs) are those to flash stimuli. Herrmann (2001) studied the SSVEP by recording the EEG from the visual cortex at various flash frequencies. He found that SSVEPs occurred at a frequency corresponding to the flicker stimulus. Amplitudes decreased steadily with frequency and SSVEPs could be recorded up to ~90 Hz flicker frequencies. The shape and frequency following of SSVEPs are shown in Fig. 1.

Fig. 1. SSVEPs and FFT spectra at various frequencies. Source: Herrmann (2001)

Interestingly, SSVEPs in response to some frequencies showed resonance phenomena, indicating a selective frequency preference of the neural oscillators. Specifically, SSVEPs at around 10, 20, 40 and 80 Hz resulted in higher amplitudes than stimuli flickering at adjacent frequencies (Fig. 2).

Fig. 2. SSVEPs showing resonance at 80 Hz. Source: Herrmann (2001)

Reference
Herrmann, Exp Brain Res (2001); 137: 346–353


Interesting question. Indeed it is related to the working of cardiac muscles. First of all, lets have a look at the structure of a sarcomere of a cardiac muscle from here:

Here, what we can see is that the t-tubule is a depression formed in myocyte. It is important to know this fact here. Why? See this:

  In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction.

First, cardiac muscles don't work by external action potentials, they work on a cycle governed by themselves, known as the cardiac cell cycle.

Second, as is clear from above paragraph, these cells depend on extracellular Ca2+ ions for initiating contraction, a clear difference from skeletal muscles which need Ca2+ stored in SR. Hence, they require t-tubule at a place where a sarcomere ends. Obviously, having a depression in the middle of a sarcomere (i.e. between I- and A-band) would not work here.

Also, the structure of t-tubules is also different between the two. Compare my first image with the image below from here:

In the second one (from skeletal muscle), t-tubule seems like a mere little pit covering the muscle cell in 360° like a duct tape. In the first image, the t-tubule is more like a double wall dividing 2 sarcomeres. It is so because in skeletal muscles, t-tubules have to just transfer the action potential to SR while in cardiac muscle, they have to transfer calcium ions into the cell. So, at the end, the difference is not in efficiency, but in function.

If we look at non-mammalian muscles, then the cause of presence of t-tubules at z-lines couls be associated with presence of large amount of sarcoplasmic reticulum at z-lines. See this article:

  Electron microscopic examination of developing myofibrils in regenerating skeletal muscle of Rana pipiens tadpole tails reveals that SR is in regular and close association with Z-lines of young sarcomeres before t-tubules have formed alongside the myofibrils. SR is also associated with M-lines of young sarcomeres but on a less regular basis than with Z-lines...This suggests the formation of a specific bond between SR and Z- and M-lines...These observations support the conclusion that SR does not initiate formation of Z-line precursor elements, but rather associates with Z-lines as they condense from more diffuse Z-bodies.

Since SR is thought to be bonded with z-lines during their formation from z-bodies, hence large amount of SR should be present at the site of association. Hence, it might be beneficial for t-tubules to be present at z-lines to efficiently transfer action potential to SR. However, such association might be absent in mammalian muscles, which can partly answer your next question.

EDIT 1: As you asked in comments

what it would have been if duct like to tubules of skeletal muscle would were present at z line instead of a-i junction?

Now we head towards evolution aspect. Yes, it might have been more effective for skeletal muscles to have t-tubules at z-line instead of A-I junction, but it would not be effective enough to create an evolutionary pressure. Both of these could have same effectiveness too, but during the course of evolution, only those traits which have much greater and direct benefit to an organism's survival and fitness are selected. There is no specific answer for 'why we have 5 fingers instead of 6 or 4', the answer is just that there is no such benefit in having 6 or 4 fingers which would cause it to be selected against 5 fingers.

EDIT 2: Obviously, its exact cause can never be known, but following might also be partly helpful. In mammalian muscles, close communication between SR and mitochondria has been observed. Such so- called "through-space" communication is an important feedback system for effiecient muscle functioning. See this article:

  the SR and mitochondrial function in muscle are not independent as calcium uptake into the mitochondria increases ATP production by stimulating oxidative phosphorylation and mitochondrial ATP production and production/detoxification of ROS/RNS, in turn modulates SR calcium release and reuptake...The resultant anchoring of mitochondria to the Calcium Release Units provides a structural basis for maintaining bi-directional SR-mitochondrial “through-space” communication during vigorous contraction.

Now, for such critical communication, SR, t-tubule and mitochondrion need to be as close as possible for fastest & direct communication. Hence, SR & t-tubules need to be as near mitochondrion as possible.

  Ogata and Yamasaki used electron microscopy to provide the first detailed description of mitochondrial localization in adult mammalian skeletal muscle (Ogata and Yamasaki, 1985). These studies revealed that mitochondria are located within the I-band, adjacent to the CRU on either side of the Z-line. Precise localization of mitochondria adjacent to the CRU at the A-I band junction was subsequently confirmed in non-fixed rat skeletal and cardiac muscle (Vendelin et al., 2005). Juxtapositioning of mitochondria adjacent to sites of Ca2+ release that occur during EC coupling provides a structural basis for potential local or privileged communication between these two organelles (Rossi et al., 2009).

Thus, presence of mitochondrion at A-I junction and of a "through-space" communication also tend to answer this question.


Anti-antibodies for preventing transplant rejection

Within an organism, antibodies which bind to other antibodies in the body would be eliminated during clonal selection.  They are not made by the body after that period, which is in the first few months of life.

Such antibodies would have to be introduced from the outside.  Many have been designed or engineered for biotech and as therapeutics.


That is a tortoise beetle (Family Chrysomelidae (Leaf beetle), subfamily Cassidinae). It looks very much like the Indian Green Tortoise Beetle Chiridopsis bipunctata. https://indiabiodiversity.org/observation/show/338651
I am almost sure it is in the genus Chiridopsis.


Do presynaptic neurons and postsynaptic neurons have different compositions of neurotransmitter receptors and transporters?

Typical bouton-spine synapses are formed as an interactive process between the pre- and post-synaptic cells (Scheiffele, 2003). There is communication between pre- and post-synaptic cell through guidance cues, growth factors, and structural proteins, as well as neurotransmitter release itself. Therefore, as part of the normal developmental process, postsynaptic cells will usually have receptors for the major neurotransmitter released by the presynaptic cells: they find each other rather than connecting at random.

Synapses that become inactive or have lower activity than their neighbors can also degrade and disappear entirely (Purves and Lichtman, 1980) by a competitive process (Balice-Gordon and Lichtman, 1994). Because of this process, I would expect that even if some developmental fluke led to a formation of a synapse between mismatched pre/post neurotransmitter release/receptors, the result would be that the synapse would get no stimulation and would be pruned according to the normal process.

However, some neurotransmitters can be released more broadly into the extracellular space rather than at highly specialized synapses (including serotonin, dopamine, and acetylcholine - note: these neurotransmitters can also be released at synapses) (De-Miguel and Trueta, 2005; Trueta and De-Miguel, 2012) and call also 'leak' from synapses into the extrasynaptic space: in these cases, the neurotransmitter is not likely to have an effect (or the same effect) on all nearby dendrites, only those that express fairly high-affinity receptors that can detect the neurotransmitter at an extrasynaptic concentration.

References:

Balice-Gordon, R. J., & Lichtman, J. W. (1994). Long-term synapse loss induced by focal blockade of postsynaptlc receptors. Nature, 372(6506), 519.

De-Miguel, F. F., & Trueta, C. (2005). Synaptic and extrasynaptic secretion of serotonin. Cellular and molecular neurobiology, 25(2), 297-312.

Purves, D., & Lichtman, J. W. (1980). Elimination of synapses in the developing nervous system. Science, 210(4466), 153-157.

Scheiffele, P. (2003). Cell-cell signaling during synapse formation in the CNS. Annual review of neuroscience, 26(1), 485-508.

Trueta, C., & De-Miguel, F. F. (2012). Extrasynaptic exocytosis and its mechanisms: a source of molecules mediating volume transmission in the nervous system. Frontiers in physiology, 3, 319.