Does terminology for changes in membrane potential refer to additive or multiplicative change?

Note to others: this question appears to be about terminology rather than the biophysics behind the membrane potential.

When the terms "increase" and "decrease" are used relative to membrane potential, they refer to additive changes in potential, not to multiplicative change or effects on absolute value. The standard is to relate the potential inside to the potential outside of a cell (so a negative potential means the inside is more negative than the outside; potentials in biology are always relative, just like in physics).

Therefore, a membrane potential decrease means that the value of the potential becomes more negative, and a membrane potential increase means the value of the potential becomes more positive. The changes on the absolute value of the potential depend only on where you start from.

Other terms that are more clear to use are hyperpolarization and depolarization, where hyperpolarization always refers to the membrane potential becoming more negative than rest, and depolarization refers to the membrane potential becoming more positive than rest. Repolarization is also used, particularly in the context of action potentials, to refer to voltage changes in the direction of hyperpolarization when the cell is currently depolarized.


Why does migration distance depend on log of molecular weight in SDS-PAGE?

An SDS-PAGE standard curve of Rf vs LogMW is linear because the standard you're given is engineered to behave that way. An expanded SDS-PAGE curve would show that the actual graph is sigmoidal: Structues that are too large can't enter the matrix, and too small they pass right through. Your standard has taken into account the % composing the gel, and the size of the proteins which the standard consists of that ensure you get the linear data points on the semilog graph.

If we look at the raw data though plotted linearly, the graph isn't entirely linear. The data is much prettier, and trivial to convert back to MW if we log transform the MW. It's the same data, just mathematically transformed. Some more reading on it here.


Though a full body image would help a lot, I feel certain that it is the desert king snake scientifically known as Lampropeltis getula splendida. This species is seen in most parts of New Mexico and is not venomous. It primarily feeds on rodents, lizards, birds, snakes and eggs.
Here's a link to a website with more details on this species and other snake species of New Mexico: http://www.nmherpsociety.org/reptiles/snakes/lampropeltisgetulasplendida/index.html
Here's a variety of different photos of the desert king snake from different angles (but different ages, sizes and pattern varieties of the same species).


How many mutated genes from a complementation test?

There are 5 mutations being tested in these complementation test.

The first gene, carries mutation number 2.  In other words, mutation number 2 complements mutations, 1, 3, 4, and 5, and fails to complement itself.

The second gene, carries mutation number 4. In other words, mutation number 4 complements mutations 1, 2, 3, and 5, and fails to complement itself.

The third of the three genes, carries mutation 1, in one strain, mutation 3, in a second strain, and mutation 5, in a third strain.  In other words, mutations 1, 3, and 5 all fail to complement each other, yet all three complement mutations 2 and 4.

There are 5 different strains in this experiment, and there are five different mutations (one in each strain), but the five mutations only affect three different genes.


How does use an action potential from innervation selectively modify tropomyosin over time?

At the neuromuscular junction, motor neurons release acetylcholine which binds to nicotinic acetylcholine receptors on the muscle. These receptors are ligand-gated ion channels that are permeable to small cations.

Opening these channels depolarizes the muscle cell membrane, which causes the opening of calcium channels, primarily on the sarcoplasmic reticulum (SR) for skeletal muscle. The key channel is called the ryanodine receptor and is either mechanically coupled to a voltage-gated calcium channel (skeletal muscle) or activated by calcium released from voltage-gated calcium channels (smooth & cardiac muscle), but in both cases the change in voltage is the initial signal.

Calcium concentrations are very low in the muscle cell at rest, but high within the sarcoplasmic reticulum so calcium rushes through and some of it binds with troponin (not tropomyosin itself, but they are associated/attached with one another), which releases the hold of tropomyosin on the actin filament.

The calcium-bound tropomyosin doesn't go anywhere, but as calcium is quickly pumped into the SR or buffered up by calcium-binding proteins, troponin is no longer bound to calcium, allowing tropomyosin to block the myosin binding sites.

The increase in calcium concentration is transient, and travels in a wave down the muscle. If there are no further action potentials, the muscle will relax. Constant contraction requires a constant train of action potentials, and the overall strength of the contraction can be regulated by the firing rate of the motor neuron.

The Wikipedia pages for muscle contraction, tropomyosin, voltage-gated calcium channel, and ryanodine receptor can all be helpful. I'd also recommend a basic textbook on neuroscience, which typically covers neuron effects on muscles and some of the mechanics of muscle contraction. I typically recommend Purves, see https://neuroscience5e.sinauer.com/ or a library or anyplace you get books from (any edition is fine).


Is there are evolutionary explanation for why humans and primates are ticklish? How might it have evolved?

Tickling probably evolved from a defense mechanism but then gradually changed into a more social action, as explained in Provine, 2005 (PDF):

  The neurological mechanism of tickling probably evolved from a reﬂex defense mechanism that protects our body’s surface from external, moving stimuli, probably predators or parasites. Our response to tickle is more varied and complex than the typical reﬂex, but it has some stereotypic, reﬂex-like properties (i.e., we laugh when tickled, struggle to escape the tickler, huddle, fend off the tickling hand). Although you can be tickled to laughter by a machine (Harris, 1999) (PDF), most everyday tickle is yet another social context for laughter and a form of communication.


Why are truncations in Receptor Tyrosine Kinases so sommon in transformations?

As you said the simple overexpression can lead to transphosphorylation and activation of mitogenic signalling. This helps the cancerous cells to survive.

By truncation of the molecule the cell also gains a benefit, because it could prevent inhibition of the receptor from outside the cell.
The truncation furthermore could be induced by treating cancer with inhibitory antibodies against the receptor. For example a treatment with anti-EGFR antibodies could induce resistance by mutation and selection. One of this mutations could be the truncation of the receptor.


To answer point 1: The length of the unlinked strand is not represented accurately, it is shown shorter only because this is a schematic. In reality, the unlinked strand should be the same length, and would have the same number of bases as you have guessed.


It's not that people didn't want to use hemagglutinin as a target for antivirals, it's that they haven't been able to get the antivirals through the approval process yet. There are a number of experimental inhibitors (see for example Progress of small molecular inhibitors in the development of anti-influenza virus agents) but the approval and licensing process is slow and difficult.


How many neurons are stimulated by electrodes in memory engram experiments?

edit: More directly answering the initial question, thank you, I misread what you wondered and was mislead a bit by a previous comment and your response to that comment.

In these experiments, they are using optical, not electrical techniques. Therefore it is a bit difficult to estimate exactly the number of cells activated directly, because light will scatter in the tissue but also fall off with distance. Based on the density of labeled and affected cells (to be stimulated, the cell has to be both a) labeled by a virus injection, and b) active in the engram) pictured in the second link you included, it seems like no more than a few to a couple dozen cells would have been activated directly.

In your comment, you said "IOW, how finely can implanted electrodes read and stimulate neurons?" - this is a different question. Implanted electrodes can read from and stimulate single neurons, or populations, depending on the electrode and experiment. It is difficult to target particular neurons with electrodes without an additional optical technique.

In the experiments you reference, optogenetic tools are used to selectively label cells that were active earlier in an experiment, and then reactivate those same cells with light. These sorts of experiments have only become possible recently with the development of those tools.

(original answer below)

Standard answer of biology applies here: "it varies", probably by species, type of memory, brain structure, etc.

But, to give you some ideas, one area that has been studied a lot in this field is the dentate gyrus of the hippocampus (the second and third links you sent, for example). One paper showed that a given memory activated something like 2-4% of the cells in that structure in a mouse http://www.sciencedirect.com/science/article/pii/S0166432811006462 with something like 1,000,000 dentate gyrus cells total in a mouse. So, that's a lot of cells, but those cells might be doing something special (pattern separation), so maybe it isn't right to think of them as the "engram" itself, or maybe we should be counting them PLUS all the cells activated in CA1, PLUS all the cells activated in cortex, etc. Whatever the case, one thing that is clear is that cells are involved in many many different engrams - if you are familiar with pop neuroscience you might recall the excitement about "grandmother cells" and "Jennifer Aniston" cells from a few years back. That's almost certainly not how engrams work, but that out of the subset of neurons and stimuli they examined, there was only limited overlap in those cases.

For fMRI studies, it's pretty hard to get a handle on the number of cells involved, but it isn't really possible to measure from "small clusters of cells" in fMRI on the same scale as in other measurement techniques. What is going to be more important for the fMRI decoding studies is "variation within a brain region" where the total number of neurons is many many millions, but the exact number involved in any one engram can't be measured with current technology.


Percentage of genome devoted to regulating gene expression

Okay, I'll take this out of the comments and put in an answer for all of us to work on.

To directly answer your question:

  "Is there an estimate for the percentage of these genes whose primary
  function is related to regulation of gene expression?"

It depends on how you define "gene expression." And what cellular processes you want to include in that definition.

Larry's answer is the usual standard response, especially for people (such as me, ha) that have spent significant time studying transcription factors. About 1% of human genes have DNA binding domains and are thought to be directly involved in regulating the transcription of genes into mRNA - these are transcription factors (TFs). Closely related are cofactors, which regulate expression by binding to TFs or RNA polymerase machinery, but not directly to DNA.

Regulation of gene expression could also include modifications at the chromatin level - here you would include chromatin remodelers, histone acetylases, deacetylases, methylases and the histones themselves.

mRNA transcripts can also be regulated by miRNAs: post-transcriptional regulators that bind to complementary sequences on target mRNAs, which leads to translational repression or target degradation and gene silencing. So you would also include the proteins involved in this process, most notably the RNA-induced silencing complex, which includes Dicer.

There are also proteins involved in mRNA stabilization and turnover, which effects gene expression.

I'm not sure if anyone has added up all of the genes above to determine an overall percentage of the genome.

If you include in your definition of "gene regulation" post-transcriptional modification, folding chaperones, intra-cellular transport, extra-cellular and intra-cellular signaling, and so on - then Shigeta is right, you begin approaching 100%. In the most basic sense, life itself is gene regulation.


Are there differences in energy of glucose isomers?

The common hexoses do not differ much in energy content (meaning Gibb's energy of formation, $\Delta_f G$). But they have different structures and chemical properties. Glucose and galactose are aldehydes when present in linear form (they are tautomers), while fructose is a ketone, which gives somewhat different properties. They are also used in different macromolecules and other metabolic products. For example, galactose is a component of hemicellulose in plants, while glucose is used for glycoproteins in humans.

Glucose has evolved to be the main blood sugar in vertebrate animals, and other sugars from the diet are quickly converted into glucose. This arrangement is useful as it provides a "common currency" of carbohydrates that can be exchanged between cells of the body, and reduces the number of enzymes needed in central metabolism. The conversion of fructose and galactose into glucose has a small biochemical cost, so in this sense, these sugars afford slightly less energy to human cells than glucose. But again this is not because of an inherent difference in energy content, but rather due to how the metabolic network is structured, with glucose as a "central", preferred metabolite.

In general, though, isomers of chemical compounds can have different energy levels, because some configuration are more energetically favorable than others. The classic example is the difference between the trioses glyceraldehyde/dihydroxyacetone and their isomer lactate, which differ enough in energy to support the synthesis of 2 ATP in lower glycolysis.


Is there enough vitamin B12 in lakes, rivers and ponds, for humans not to need to take supplements?

Of course there is no evidence for the superiority of the vegan diet claim to begin with, so there is that, and there are plenty of vegan foods fortified with B12, even some from non-animal sources.

No, there is not enough B12 in treated water nor well water for a human. There can be enough B12 in untreated river/lake water because it contains high levels of fecal matter or algae which is high in B12 (b12 is manufactured by anaerobes).  Of course these are the things you want removed from your drinking water so reducing B12 is inevitable. Also can contain enough being the key phrase it depends on the water source, cleaner river contain less.

Evolutionarily speaking humans eat animals for the same reason every omnivore and many herbivores (deer, ect) do, because we can, it is generally a superior nutritional substrate which is more than enough for evolution to favor it.

source 1

Source 2

source 3


Recent classification for parasitoid (ecological relationships)

I think the wikipedia article defining parasitoids has it right on this one. The term is, and should be flexible and it's definition defined by context. i.e Case by case definitions are made obvious in the literature.

  Patently there is no point to trying to draw arbitrary lines of distinction between such vague, and often variable, life histories. In each ecological or ethological study, the terms applied should reflect the facts in the contexts relevant to the matter in question. Such studies need not in all cases use the identical terminology, and there is no reason they should.

This means that you should always describe the life cycle even if you call the organism a parasitoid. There is too much variation between seemingly similar organism life histories to use a strict and specific term.

For those struggling to see the link from the question, they suggest a parasitoid can be measured as a parasite that reduces host fitness to zero:

  ... they are also quite different from these other parasites,
  in that, similar to a predator, they must kill their host.

A recent (2015) review on Whiteflies refers to Hymenoptera as parasitoids of Whiteflies because the Hymenoptera are parasitoids as larvae as they kill the Whiteflies and then become free-living adults.


I did a few searches, just for fun, but all I came up with was:

  Yuhong Zuo and Murray P. Deutscher "Exoribonuclease superfamilies: structural analysis and phylogenetic distribution"
  (2001) Nucl. Acids Res. 29 (5): 1017-1026. doi: 10.1093/nar/29.5.1017

Not very recent, but it's open access. It might be possible to search for more recent papers that have cited this. Although I haven't tried it myself, I found suggestions for doing this at https://www.bc.edu/libraries/help/howdoi/howto/pubcitation.html.


What animal makes these spherical sand clusters?

Not sure what exact species it is, but those definitely look like crab holes. They create the holes in the sand to get away from the heat and predators. They clean their homes by depositing unwanted ~sand around their door (the hole).

So yes, you're totally right in assuming those were made by an animal.


Which part of human eyes is getting tired?

These symptoms have a name: Computer vision syndrome.
Basically our eyes are made to look at longer distances from 1-6 meters without much accommodation. Typically computer screens are located at a much closer distance (30-50cm), which requires constant accommodation by the eye. This leads to high stress on the muscles in the eye which subsequently get tired. Additionally less blinking leads to drier eyes.

One of the common recommendations against this is to regularly focus further located objects to give the eye the chance to relax. This is sometimes called the "20-20-20" rule, every 20 min focus on a 20 feet (about 6 m) far object for 20 seconds. See the article in the Wikipedia and here for more information (and probably also the linked references in the articles).


Is it theoretically possible to create two humans by splitting one human in two?

If you split a human early enough (in the first weeks after fertilization), you can get monozygotic twins.

Other than that, you are in the field of science fiction and we cannot safely answer such question on a science website. I am not sure your question will be accepted in its current format but you may try WorldBuilding.SE.

And if you like fantasy novels, I recommend The Cloven Viscount by Italo Calving! You will definitely not learn much about biology in this book though.


How do schistosomes find and attach to human skin?

Schistosoma recognize human skin by mechanical, thermal and chemical stimuli from host. Attachment of parasite to skin is  stimulated by L-arginine. Schistosomes specifically bind  to L -argine by chemotaxis. L-arginine guides this parasite towards site of penetration. The lipids on the human skin surface also serve as signal for host invasion.

It is also reported that parasite may use L-arginine to synthesize nitric oxide for blood vessel dilation so that it can easily penetrate into the host. Schistosoma may attach to L-arginine of surrounding tissues to escape the cellular immune response from host.

(Via: https://www.ncbi.nlm.nih.gov/pubmed/11860033)

These parasites enter the host through skin by producing several proteolytic enzymes to degarde the host tissue proteins including elastin, condromucoprotein, keratin, fibronectin, laminin and collagens.

Two distant serine proteases are responsible for digesting host tissue. One is Chymotrypsin-like protease which degrades protein with large hydrophobic side chains. And the second one is Trypsin-like protease which prefers proteins with positively charged side chains.

(Via: http://www.jbc.org/content/275/49/38667.full#ref-2)


What is meant by nucleated in this context?

Cytoskeletal nucleation refers to the de novo formation of cytoskeleton filaments. If microtubules are nucleating, that means microtubules are being polymerized from lit. "From the beginning" by α/ß-tubulin dimers. So literally, and we see in the image below, Arp2/3 complexes act as progenitor sites so to say for new actin filaments by the "nucleation" of actin:

From wikipedia for Nucleation: "Nucleation is the first step in the formation of either a new thermodynamic phase or a new structure via self-assembly or self-organisation."


Can pymol show cartoon (secondary structure) for a pdb of multiple frames?

It seems that if no HELIX record is present in the PDB, PyMol attempts to assign secondary structure itself. For whatever reason, it does not do this if multiple MODELs are present. You should be able to use the dss command to force PyMol to calculate secondary structure in a PDB with multiple MODELs.


Difference between 'Orbit' and 'Globe' in eye anatomy?

I've found a rough answer myself:

  The globe of the eye, or bulbus oculi, is the eyeball apart from its
  appendages

http://en.wikipedia.org/wiki/Globe_%28human_eye%29

  ... the orbit is the cavity or socket of the skull in which the eye and
  its appendages are situated. "Orbit" can refer to the bony socket, or it can also be used to imply the contents.

http://en.wikipedia.org/wiki/Orbit_%28anatomy%29


Number of genes required to sustain life

Depends on what kind of life you want!  The Database of Essential Genes lists genes essential for life for a number of species, although I would be wary of some of the numbers; bacterial results are probably more reliable but it lists 118 for humans and 2114 for mice.  There are a bunch of different numbers for different E. coli strains, with larger numbers being published earlier, go figure.

It of course varies by species.  In mid-August of this year, scientists reported the smallest genome yet: 112kb with only 137 protein-coding genes (predicted).  Crazy!  That doesn't mean it's the smallest number of genes though, just what we've found.  Some folks in 2006 predicted the smallest would be 113kb and 151 genes - pretty close close to the above, all in all.

For something a little more familiar and studied, though, Craig Venter has made synthetic biology his goal.  Part of trying to create life is knowing what the bare minimum is.  Working with Mycoplasma genitalium, he and his crew knocked out each gene and found that 381 were indeed essential.


Why is it harder to sequence plant genomes than animal genomes?

The authors of this 2012 review article summarize the problem well in their introduction:

  In contrast to the tremendous advances in throughput, assembling sequencing reads remains a substantial endeavor, much greater than the sequencing efforts alone would suggest [22-24]. Large complex plant genomes remain a particularly difficult challenge for de novo assembly for a variety of biological, computational and biomolecular reasons. Plant genomes can be nearly 100 times larger [25] than the currently sequenced bird [26], fish [27] or mammalian genomes [28]. In addition they can have much higher ploidy, which is estimated to occur in up to 80% of all plant species [29], and higher rates of heterozygosity and repeats [30] than their counterparts in other kingdoms. Furthermore, the gene content in plants can be very complex, as shown by the presence of large gene families and abundant pseudogenes with nearly identical sequences derived from recent whole genome duplication events and transposon activity [13]. Plants tend to have high copy chloroplasts and mitochondria organelles, which complicate assembly of their remnants in the nuclear genome and skew coverage levels [12]. Finally, it is often very difficult to extract large quantities of high-quality DNA from plant material, making it difficult to prepare proper libraries for sequencing.

From: Schatz, Witkowski and McCombie. "Current challenges in de novo plant genome sequencing and assembly". Genome Biology (2012). 13:243

As you can see, all of the key reasons have been touched on by the various people who have commented below your question.


How to measure quality and quantity of DNA?

You can run your DNA sample on agarose gel to see, whether you have significant degradation.

If you are interested in contamination, you can make a standard photometric analysis to assess the 260/280 and 260/230 ratios and absorbance at 320 nm on NanoDrop or even something similar to Eppendorf's BioPhotometer.

In case RNA may be an obstacle for some down-stream procedures, with Qubit you can also measure separately DNA and RNA concentrations and then decide if you have too much RNA and it's worth treating your sample with RNase.


What causes fingerprints to form and why is the pattern formed unique?

I would say genetic diversity is the primary reason which results in other reasons that you are looking for. At the lowest level, random crossing over at prophase I, random separation of homologous chromosomes at anaphase I, random separation of sister chromatids at anaphase II, and random fertilization: one sperm fertilizes one egg randomly.

The skin is developed from ectoderm so need to look at the formation of embryonic disc and specifically to the genesis of germ layers: ectoderm.

However, I would stick to the primary reasons, since it is extremely difficult to visualize the given formation - actually we do not have resources for it at the moment.

Very good question the last part. I have an intuition that skin develops randomly because of the above reasons. You would also need a lot of memory to make identical skins for twins! It has not been useful to have identical fingerprints between two people so evolution has not resulted into it.

Feeling surfaces and gripping are movements - not much space taken things, in contrast to the memory needed in storing the exact surfaces of skin from one generation to another. - Learning is a way to save resources here and it is a lot more efficient and than storing static information to species from one generation to another.


Yes. It is actually the case of most mutations that affect the phenotype!

Only 1.5% of the human genome codes for proteins. About 5-10% of the human genome are regulatory sequences which do not produce any protein but greatly impact the phenotype by regulating the expression of coding sequences. A mutation in a regulatory sequence does not directly impact the protein sequence but can have drastic impact on the phenotype (and fitness).

There are a lot of such mutations that have been identified. Here are a few quick examples

Variation in Vertebrate Cis-Regulatory Elements in Evolution and Disease
A cis-Regulatory Mutation of PDSS2 Causes Silky-Feather in Chickens
A regulatory mutation in IGF2 causes a major QTL effect on muscle growth in the pig
Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element [..]


Are epigenetic changes involved in evolution?

To start I will repost some of an answer I have previously posted, which will explain what evolution is:

Evolution is simply a process of change.  It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection.

  "Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage." - Ridley,
  Evolution

Your Answer:

Evolution depends on the inheritance of information from the ancestral population to the descendant population. Much of the time we talk about information in the form of genetic variation, the information contained within the DNA. However, more and more we are realising that other forms of information transmission can occur, including epigenetic effects, and that these can contribute to evolution.

  "Epigenetic modifications are a bit like ornaments on a Christmas
  tree; the tree (the DNA sequence) is still the same, but the
  decorations (epigenetic modifications) change how it's perceived." ...

  "Over the past few years, several studies have compared the epigenetic
  modifications of our genome with that of other great apes, leading to
  an emerging picture of the importance of epigenetics in our recent
  evolutionary history." ...

  "The role of epigenetics in evolution (particularly primate evolution)
  is an active and exciting area of research..." - Nature Scitable


Those arteries are (a) big enough for the catheters, (b) superficial enough (close enough to the surface of the skin) for catheterization. It would be quite a challenge to use the renal arteries, for a ridiculous example. There is also less of a risk of embolization than using an artery like the carotid, where embolism can cause stroke, which would be quite serious. An embolism in an arm or leg could be painful and cause damage, but unless it is massive it isn't going to significantly affect the patient over the long term.

Also note that those are fairly special cases of catheterization, such as when doing percutaneous interventional techniques targeting the peripheral or coronary arteries. Those approaches use fairly large devices so you need a large vessel, and you need to be in the portion of the vasculature that you are targeting (i.e., you can't access those targets through a vein). As @VanceLAlbaugh mentioned in a comment, other arteries are targeted for other purposes. And overall venous catheterization is much more common than arterial, such as when an IV line is established to deliver fluids/medicines.


At what point, when connected, do DNA strands become a helix?

In general, a single stranded nucleic acid is helical in the absence of other secondary structure. The base stacking that drives helix formation does occur  between adjacent bases in the same strand. Note, however, that such structures are dynamic and dependent on properties such as temperature and salt concentration. You can see an example of a single-stranded RNA helix in the following crystal structure (1MHK):

Note the blue helix at the bottom of the image is actually a duplex in the crystal.


Are Schwann cells the sole source of myelination in PNS?

Schwann cells seem to be the most common type of glial cells outside of CNS, and the myelinating Schwann cells are the only known source of myelin in PNS. Other types of neuroglia in PNS, for example non-myelinating Schwann cells and astrocytes-like cells do not seem to take part in myelination, neither in CNS nor in PNS.


Does the effect of light on melatonin release adapts to light level over long periods of time?

This paper, for example, shows that indeed, melatonin is suppressed more in the light after a week of dim light exposure compared to after a week of bright light exposure.

However, the authors note that although the result was statistically significant, the effects were fairly small compared to the overall variability in the data.


Lack of skin in a certain area of the body --- hypo[what]?

First, this is not an area where I have any education or experience. However, out of curiosity I consulted google and found two genetic castle diseases that should be relevant to your question:

Epitheliogenesis imperfecta (vetbook.org)
Ectodermal dysplasia

Both diseases are very serious, and Epitheliogenesis imperfecta is fatal (due to infections).

I chose not to include any pictures of the diseases in this answer since they often look quite horrible, and some people might find them unsettling. If you click the links there are pictures of the conditions though.

A "similar" condition in humans might be  Epidermolysis bullosa, which is caused by decreased anchoring between dermis and epidermis, which cause a very fragile skin:

  Epidermolysis bullosa (EB) is a group of mainly inherited connective tissue diseases that cause blisters in the skin and mucosal membranes, with an incidence of 20 per million newborns in the United States.[1] It is a result of a defect in anchoring between the epidermis and dermis, resulting in friction and skin fragility. Its severity ranges from mild to lethal.

(Wikipedia)


How many plants are needed to survive in an airtight chamber?

According to this news article, in a NASA experiment one man survived for 15 days in a sealed chamber containing 30,000 small wheat plants. If you read the article you will find that this did not produce a completely balanced system - some excess oxygen had to be removed, and some extra CO2 had to be pumped in.


What could humans do to "see" what dogs smell?

NMR spectroscopy is a technology that is used to identify molecules. So-called "NMR spectra catalogs" document the spectra of various known compounds. Acquiring these spectra requires purified samples, expensive equipment, and time. In addition to making next-generations of this technology into something that would be practical for realtime "smelling", you'd have to match up catalog entries with what dogs actually respond to. That's going to take a fair bit of work.

There's some literature online about growing olfactory sensory neurons in a Petri dish (with difficulty). If we can learn how the signaling pathways work for "odorant detection" for specific odorants or "fragrances" that we already know dogs perceive, perhaps we could genetically engineer a cultured neuron cell to "light up" a fluorescent marker or issue some other signal that is perceptible to humans, whenever some dog-specific odor wafts in. I suspect this would be more realistic than "tabletop NMR" in our lifetime.


It's called the Diving reflex, also known as the bradycardic response. It goes away around six months.

From https://www.breatheology.com/articles/mammalian-dive-response/

  Another action of the diving response can be observed in infants when they are under water. The windpipe by the vocal chords spontaneously closes to prevent water from entering the lungs. This reflex is initiated as soon as there is contact with water. However, it disappears when the child reaches the age of roughly six months.


It is German cockroach (Blattella germanica) with two dark parallel streaks on it's pronotum.
The one in your picture is a lady laying her ootheca.

It is a pest.
Here's it in different stages of life cycle.
Things you might like to know:

Blattella germanica occurs widely in human buildings, but is particularly associated with restaurants, food processing facilities, hotels, and institutional establishments such as nursing homes.
German cockroaches are omnivorous scavengers. They are attracted particularly to meats, starches, sugars, and fatty foods. Where a shortage of foodstuffs exists, they may eat household items such as soap, glue, and toothpaste.
The German cockroach reproduces faster than any other residential cockroach, growing from egg to reproductive adult in approximately 50 – 60 days.

Source: Wikipedia and different pest service websites.


What is the mechanism behind the F-Wave?

This is a great question, and I've had trouble finding any authoritative study; since F-waves are mostly used as a diagnostic tool it doesn't seem like they've been studied much at the mechanistic level. The only non-clinical usages seem to be in pharmacology experiments in intact organisms (in particular people) where people aren't going to be going in and doing whole-cell patch clamp in the spinal cord.

This paper:

Balbi, P., Martinoia, S., & Massobrio, P. (2015). Axon-somatic back-propagation in detailed models of spinal alpha motoneurons. Frontiers in computational neuroscience, 9, 15.

has some relevant simulations, though they don't entire answer your question. However, I think their results are sufficient to make some good guesses. Without developing my own simulations, though, I'll have to mostly hand-wave after establishing some key facts.

Axons are small, so it doesn't take that many ions to depolarize a stretch of axon to threshold. The axon hillock has a lot of sodium channels to sort of 'jump-start' the action potential down the axon, but that's in a context where the rest of the soma is already depolarized.
In a back-propagating action potential, the ions flowing into small compartments eventually meet the soma: the soma is big, and so the number of ions needed to depolarize the soma to threshold is large (lots of capacitance in the membrane to charge): the axon hillock may not immediately bring the soma to threshold. This is called "impedance mismatch" and is also important at synapses (where axon terminals are bigger than the axons).

And so now for the hand-waving component... I can't say for certain which channels are involved, but it's possible that the antidromic action potential depolarizes the soma just a little bit, enough to open some voltage-gated channels but few enough that it takes some time for the rising phase to occur. Could involve other ions that aren't sodium, like calcium; could involve the proximal dendrites as well. Because of the different voltage sensitivities of different channels in different compartments, by the time the whole soma depolarizes sufficiently, the proximal part of the axon has had time to recover enough that it can spike again.

One other piece of evidence in support of this mechanism is that the number of cells that fire an orthodromic spike in the F-wave after the antidromic spike is few and variable - that is, it's a small fraction and that fraction varies from pulse to pulse. That seems to suggest that the specific conditions of the soma and nearby processes matters, so there must be a fairly narrow range of parameters that allows an orthodromic spike to follow.


Why is ATP the preferred choice for energy carriers?

I really like this question as it is such a fundamental underpinning of all life on the planet, yet there is such sparsity of actual information on its origins and why selection rewarded ATP use over anything else. Here I am talking generally since no specific studies exist in ATP vs other candidates.
A lot of the below information is taken from a relatively old article mentioned in the comments by TomD that discusses: "Why nature chose phosphates." by Westheimer, 1987. The article is very influential and has been cited over a thousand times since publication. Another article that came out in the same year that this question was asked "Why nature really chose phosphate." by Kamerlin et al., 2013
Some of the below arguments are more convincing than others, but all of them should be thought of when attempting to answer this question.
Summary.

ATP has ancestral dominance. Most other reasons derive from this.

Alternative phosphate groups or other molecules may not provide enough energy.

Alternatives may be toxic.

Other molecules, particularly phosphates, are used for inefficient high energy bursts.

Pi is a "good" leaving group.

Phosphates are fundamentally able to be regulated through electrostatic manipulation.

ATP synthase can efficiently reattach the Pi to ADP.

Lots of Pi available to organisms because of it's ancestral dominance ("if it ain't broken, why fix it?" is at play).

ATP can provide more energy if needed; it's scalable to the situation. (ADP becomes AMP + Pi)

Easily usable by a variety of proteins.

Why ATP?
ATP is an efficient and relatively easily biosynthesised molecule that can fulfil multiple biochemical roles. Cells do have alternative energy carriers, some with more specialised roles, however, ATP is ubiquitous throughout our cells and inter-cellular spaces. There aren't a wealth of resources explaining why ATP is any better than other compounds, however, there is plenty of reasons why the phosphates are required.
Why not the alternatives?
Citric acids and their derivatives are a good candidate, with deductible groups and high bioavailability but they simply don't give enough energy to stabilise genetic material.
Another tribasic candidate is arsenic acid. This is a fundamentally toxic compound, though, which isn't particularly great for living things.
There are other phosphates too, and they are used in many organisms. In biology, they have specific functions, and not used as the general energy carrier. For example, creatine triphosphate provides a high energy phospho- anhydride bond, that is often used to quickly and anaerobically regenerate ATP, useful during high rate muscle activity for contraction.
GTP is structurally very similar to ATP. GTPases are used more to initiate cellular signalling pathways. It is sometimes used as an energy source. This is a good example of an alternative energy carrier.
Over the years, many proteins have specialised with a specific shape, and this chance is the primary reason behind ATP over GTP. In other words, the choice of ATP over GTP is primarily down to cellular preference of molecular shape. One of them had to emerge as being more widely used, and it was ATP that 'won'.
Efficiency and simplicity.
The reaction was once thought to be a relatively simple nucleophilic displacement. From the 2013 paper:

...this simplicity is deceptive, as, even in aqueous solution, the low-lying d-orbitals on the phosphorus atom allow for eight distinct mechanistic possibilities, before even introducing the complexities of the enzyme catalysed reactions.

Traditionally one will be taught that ATP is such a chemically efficient way of storing and transporting energy. This is due to the ATP->ADP & Pi hydrolysis reaction. The phosphate groups in ATP are full of negative charges and these are repelling one another. This means that the third phosphate is a great leaving group and breaking the phospho- anhydride bond is a favourable reaction. ...
...But the story is a lot more complicated than that. The above explanation isn't really satisfying because those same negative charge forces are repulsive of the nucleophile that is attempting to complete ATP->ADP & Pi. A more comprehensive explanation would go along the lines of 'although a negative charge repulsion exists between the nucleophile of the protein and the phosphate, that high energy barrier can be overcome by electrostatic manipulation'. This allows an "on-off switch" for the hydrolytic reaction by tweaking the electrostatic environment. This is another great regulatory tool that the phosphates provide. This regulatory feature is important for signal and metabolic/catabolic cascades.
When it comes to 'rebinding' the Pi to ADP, it is fairly easy since ADP seldom covalently binds to anything, which would require a lot of energy to recover the ADP. This also helps the bioavailability of free ADP to ATP synthase, an incredibly efficient enzyme, that uses membrane proton gradient to drive the production of ATP. Talking about actual numbers is difficult here as there is only data available from Rat hepatocytes. Who is to say mammals are representative of all organisms? The estimates of energy of hydrolysis range from ΔG˚ = -48 kJ mol-1 to -30.5 kJ mol-1. Note that these are considerable, but not exceptional values, so it's easy for many different proteins, that need not be very specialized, to break the bond all over the body. I couldn't even find the numbers for the synthase reaction per ATP, but a single ATP synthase can produce up to 600 ATP per minute.
The final point of this efficiency is that the elements in ATP are very abundant and established in the biosphere making it readily available. This makes the phosphates a convenient biomolecule.
Multi-functionality.
ATP is ubiquitous in the body, but in some cases more energy is needed than there are ATP available. In these times of need, ATP can be used to produce more energy, breaking another phosphoanhydride bond to become AMP+2Pi. AMP however is typically a signalling molecule.
With the low activation energy required to break the phosphoanhydride bond, a multitude of enzymes, far too many to list here, can make use of ATP in order to gain energy towards the activation energy for many other functions.


Mutation-drift equilibrium and among loci variance in heterozygosity

In The Distribution of Gene Frequencies in Populations, Sewall Wrights derivates a continuous approximation to the probability distribution for the frequency of an allele in a panmictic population under the pressure of drift and mutation on a bi-allelic locus. In his paper, he reports several version of the same equation. Below is one of them, where $\phi(q)$ is the probability density of the one specified allele to be at frequency $q$.

$$\phi(q) = C q^{4N\nu -1}(1-q)^{4N\mu -1}$$

, where $C=\frac{\Gamma(4N\mu+4N\nu)}{\Gamma (4N\mu) \cdot \Gamma (4N\nu)}$ is a constant, $\mu$ and $\nu$ and the forward and backward mutation rate The heterozygosity is then a simple one-to-one function of the allele frequency.


The question title and the question itself ask two slightly (but critically) different questions.

Can cancers caused due to viruses be contagious? NO
Are these oncoviruses infectious in nature? YES

The tumors caused by the viruses are not contagious.  You can't take the tumor and transfer it to a new host and see a new cancer.  The viruses that cause the tumor are contagious, but in many cases by the time the tumor has arisen the viruses are no longer in a contagious form.  A tumor that's caused by HPV doesn't have contagious virus in it (see explanation below), and you can't transplant the tumor into a new host.  There still may be contagious virus present in the patient, but the tumor itself is not contagious.

Explanation HPV causes cancer by having a part (and only a part) of its genome integrated into the host genome, so cancers associated with it inevitably have a defective virus genome. There could theoretically be infectious virus in the neighboring tissues, but the cancer is driven by non-contagious virus. See for example The role of integration in oncogenic progression of HPV-associated cancers for a fairly basic explanation


According to this study, both a high temperature wash (57C) and full spectrum sunlight will kill rotavirus.

It would appear that a washer with a sanitation cycle (newer models often have a cycle that hits or exceeds 165F) would be your best bet for treating bedding.

See Figure 2.


What is meant by single molecule sequencing?

For the classic Sanger sequencing you need quite large amounts of DNA to be able to run the sequence reaction. This is a problem when you want to sequence whole genome since the DNA needs to be amplified then, which for some sequences can cause problems, introduce errors or cause bias.

Single molecule sequencing is a huge step forward here, since only one molecule of DNA is used for sequencing. There are different sequencing technologies based on this principle.
The system of pacific biosciences uses a polymerase bound to a small well which binds a singlestranded DNA and begins to make the opposite strand, when nucleotides are present.
See the image below or this video, which explains the technique quite nicely.

Illumina binds singlestranded DNA molecules to the surface of the reaction chamber and starts amplifying them there. The use of fluorescently labelled nucleotide allows to monitor the reaction. This looks like the following (left side of the figure from the review mentioned below):

An illustration from Illumina which is more detailed, can be found here.
Although it is a bit older (and the technology develops fast), this review is a nice introduction: "Sequencing technologies - the next generation."


Are Gram negative bacteria classified as such because of their negative membrane potential?

Short answer
The distinction between Gram positive (Gram+) and negative bacteria (Gram-) has absolutely nothing to do with membrane potentials; it is all about the Gram staining procedure.

Background
The Gram staining was named after the Danish bacteriologist Hans Christian Gram, who originally devised it in 1882 (Gram, 1884). Gram staining is a common technique used to differentiate two large groups of bacteria based on their different cell wall constituents. The Gram stain procedure distinguishes between Gram+ and Gram- groups by coloring these cells violet or red, respectively (Fig. 1).

Gram+ bacteria stain violet due to the presence of a thick layer of peptidoglycan in their cell wall, which retains the crystal violet these cells are stained with. Gram-, on the other hand stain red, which is attributed to a thinner peptidoglycan wall, which does not retain the crystal violet during the decoloring process.

Gram staining procedure
The procedure involves staining the cells with a crystal violet dye. Next, an iodine solution (iodine and potassium iodide) is added to form a complex between the crystal violet and iodine, which is insoluble in water. Then, a decolorizer, such as ethyl alcohol, is added to the sample, which dehydrates the peptidoglycan layer, shrinking and tightening it. The crystal violet-iodine complex is not able to penetrate this tightened peptidoglycan layer, and is thus trapped in the cell in Gram+ bacteria. In Gram- bacteria, however, the thinner peptidoglycan layer does not retain the crystal violet-iodine complex and the color is lost. Lastly, a counterstain, such as the weakly water soluble safranin, is added to the sample, staining it red. Since the safranin is lighter of color than crystal violet, it does not disrupt the purple coloration in Gram+ cells, but it does stain the decolorized Gram- cells red.

Fig. 1. Gram+ bacteria (left) and Gram- on the right. source: Lab Tests Online

Reference
- Gram, Fortschritte der Medizin (1884)


Why do both the mango and the bee have "Indica" in their binomial name?

In short, we do not think about the uniqueness of the second part of the binomial (the species epithet) but about the uniqueness of the binomial itself (the genus and the species epithet). Thus, the unique binomial of mango is Mangifera indica and the unique binomial of bee is Apis indica. For more detail, see this question.

To complicate matters  slightly, plants and animals are governed by different nomenclatural codes. So it is possible for a plant to have the exact same binomial as an animal. These are called "hemihomonyms." For more detail, see this question. However, a plant cannot have the same binomial as another plant, and an animal cannot have the same binomial as another animal.

In this specific case, the authors probably chose to give both species the epithet indica because they are associated with the Indian subcontinent, which is the root of that word.


Melatonin production - requires nighttime, or just full darkness?

The immediate thought came to my mind was relation between Melatonin and Serotonin. Because both hormones have sleep related function. I read that both are light sensitive. Melatonin is produced by pineal gland in brain whereas Serotonin is at gut and CNS.

Light dependence(Wikipedia) of Melatonin is explained here where they say blue light produces more Melatonin and wavelength of light <530nm will have effect on Melatonin production. If the light intensity is more then Melatonin will not be produced. So what they say is if there is darkness(artificial) or dim light environment then this hormone will be produced and induces sleep. Almost everywhere they explain Melatonin whose production is sensitive to light.

(But even in the afternoon when there is bright light some of us feel sleepy which is mainly due to Serotonin released after heavy meal which is produced from tryptophan. This will again effect the sleep. It is obvious that without food we can not sleep at night. So Serotonin and Melatonin are interrelated as explained here Link1 and Link2).


How can I list genes present on a given series of bands?

There's a brief tutorial here on how to search by band. Here is a more extensive help document, and here is a human-specific help page, Basically:

Select the species and annotation release. We're Homo sapiens, by the way...
Select the chromosome you are interested in.
On the left side of the page, it says Region Shown: followed by two input boxes. You can search by band using standard cytogenetic nomenclature: 7q11 and 7q36. Enter these into the input fields and click Go. Here is 7q11:7q36.
There are various links to download data. Perhaps most relevant to you, there is a link on the left of the page which says Data As Table View. Here is said page, a list of genes at various levels of characterization.

Here is a table of different search queries you can use. There are a couple of ways to analyze the data:

Interactive Genome Browser:

Click on Genome Browser.
In the search field, enter the cytogenetic coordinates: 7q11;7q36. Press Go. Here is the resulting page.

Table Browser (for downloading data):

Click on Tools > Table Browser.
There are a lot of options. A tutorial can be found here. Most important for your search is region. Select the position radio button and enter your cytogenetic coordinates. I'll leave the rest of the options to you.


How are there multiple varieties of the potato?

You're missing that potatoes also reproduce sexually.

They're flowering plants, and they produce seeds that are not genetically identical to their parent plants.


Try this.

  cadnano simplifies and enhances the process of designing three-dimensional DNA origami nanostructures. Through its user-friendly 2D and 3D interfaces it accelerates the creation of arbitrary designs. The embedded rules within cadnano paired with the finite element analysis performed by cando, provide relative certainty of the stability of the structures.


This seems to be Scadoxus Puniceus, also known as the Paintbrush Lily (not to be confused with other species with the same common name). The dutch originally cultivated scadoxus puniceus, and your specimen could be one of several hybrids of the original.

Dave's Garden has plenty of pictures of the species. He didn't have any fruit at the same stage of ripeness as yours, but the likeness is still rather compelling.

For a slightly more reliable source (if a little older), the South African Medical Journal also identifies Scadoxus Puniceus in a study of accidental poisonings by herbal medicine. The flower might be a touch wider than yours, but you almost certainly still have a Scadoxus, and within-species variations can easily account for such a small difference.

Copyright Disclaimer: All included photos would typically fall under fair use due to their limited scope compared to the original work and due to their non-commercial use as a benefit to the public. If any of the copyright holders disagree, feel free to contact me so we can resolve the problem.


What is this spider hunting in the tree in the night?

It's look like Sac Spider (Clubiona lutescens) to me.

Source: http://ednieuw.home.xs4all.nl/Spiders/Clubionidae/Clubionidae.htm


Carrying or packaging capacity of SAD B19 dG rabies virus

I have gone through quite a number of papers using this virus, but I haven't found any definite answer on the maximum insert length. There is an indirect answer, though. The two articles cited below both report possible insert length of up to 3.7kb without any experimental problems. This insert length results in a viral genome which is about 1.9kb longer than naturally occurring. So at least 3.7kb insert length are possible, if longer inserts can also be used, needs to be tested.

References:

Design and generation of recombinant rabies virus vectors.
New rabies virus variants for monitoring and manipulating activity
and gene expression in defined neural circuits.


Does neural network in brain form cycles?

In general neural networks are a lot less simple and directed than ANNs or artificial circuitry - connections can be inhibitory or excitatory, vary widely in strength etc etc. So unsurprisingly yes, recurrence is observed in actual neural networks. I don't know of any statistics on the frequency of such network structures, or even if such exists. Our knowledge of the brain at this fine level is still limited I think, the more global attempt to map 'the connectome' generally consider things at a higher resolution.


Do we posses technology to rebuild sequenced DNA?

Yes, in fact synthesizing short stretches of DNA and RNA is available through several commercial services. However this limited to tiny DNA fragments (say 120 base pairs or so). Longer sequences require custom laboratory work.


Upon activation plasma B cells upregulate death receptors as part of being activated. Presence of the antigen overcomes the death signal, thus the cell survives. When antigen is lost, the death signals overcome the survival signals as there is no antigen, so the B cell dies via apoptosis.

Memory B cells don't do this. They survive and continue to produce antibodies for years, although this slowly wanes. Antibodies have to be produced as antibody mediated immune mechanisms are extremely important for memory and the reason why a subsequent infection is cleared so rapidly. Furthermore for the example of HPV, antibodies induced by the vaccine prevent the virus even infecting cells (so called neutralising antibodies).


Short answer
Yes they can, but with less efficiency.

Background
Efficiency of sticking to a glass surface decreases about 20-fold when the gecko's feet are wet (Stark et al., 2012). On dry glass, Gekko gecko holds on with about 18 N, which is about 18 times their own body weight. Hence, the gecko attachment system is over-designed (Knight, 2012). Wetted toe pads reduce the adhesive force significantly down to 0.9 N. A wetted glass surface does not significantly affect the grip of Gekko gecko, except after the gecko takes multiple steps. Hence, geckos can cling to wet surfaces, but only when their feet are not getting too wet.

Note that gecko attachment is not based on suction, such as the suction cups seen in octopus. Instead, geckos cling to surfaces with Van der Waals forces. Van-der-Waals-based adhesive systems take advantage of weak intermolecular forces between two surfaces. Upside is that these forces are not surface specific, allowing geckos to climb trees, rocks, walls and even glass windows.

Geckos achieve their strong attractive force to the substrate by utilizing small hair-like structures on their toes called setae, which are made primarily of keratin (Fig. 1). Setae contain flexible spatulae which make intimate contact with rough and even dirty surfaces.

Fig. 1. Left panel: Close-up of the underside of a gecko's foot as it walks on vertical glass. Source: Wikipedia. Right panel: Images of (A) dry and (B) wet setae using the same digit of an individual tokay gecko (Gekko gecko). The image in A was taken prior to exposure to water and the image in B was taken after 30 min of soaking in water. Source: (Stark et al., 2012).

The drawback of using Van-der-Waals forces for grip is that the Van-der-Waals forces only exist across surfaces very close together, and an intimate contact between the spatulae and the substrate is required for van der Waals forces to be effective in the gecko adhesive system (Stark et al., 2012). Wetting of the feet decreases the Van der Waals interaction with the surface.

References
- Knight, J Exp Biol 215, i
- Stark et al., J Exp Biol; 215: 3080-6


Why is there more variation in proteins than genes?

There are several concepts to understand:

Alternative splicing

From one gene, several proteins can be constructed depending on which introns are spliced.

Tissue-specific genetic expression

Genes are differentially expressed (and differentially spliced) depending on the tissue.

Post-transcriptional modifications

Those are modifications that are made directly on the proteins (in opposition with alternative splicing which are modifications made on the RNA)

Structure of the proteins

Proteins may fold (to what we call primary, secondary, tertiary and quaternary structures) differently in different environment.

Therefore there is variance in proteome between cells although there is no variance in genome between cells (except mutations and red blood cells). Moreover, one gene sequence can give rise to many different proteins due to the processes of alternative splicing and PMT.


Does contracting Rubella give one some kind of immunity to Measles and vice versa?

Short answer: No, there is no cross immunity between these two diseases. Having the same symptoms doesn't mean that diseases are related.

Both have in common that they are caused by viruses, but similarities end here. Rubella is caused by the rubella virus, which is the only member of the genus Rubivirus and belongs to the family of Togaviridae and are encapsulated positive strand RNA viruses.

Measles on the other hand are caused by the measles virus, which belong to the genus Morbillivirus within the family Paramyxoviridae and are negative stranded enveloped RNA viruses.

Historically speaking, the measles vaccine was available first in 1963, with mumps following in 1967 and rubella in 1969. All three are attenuated live vaccines which have been combined into a single vaccine in 1971. The sequence of this developments also shows that there is no cross immunity. You wouldn't develop another vaccine, when the disease is already covered by another. Drug development is a very expensive business.


Definitions and examples of some math-releated ecology branches

Although work in those areas is definitely all related, there are some kind of general differences in how those labels tend to be used, and I'll take a stab at defining them:

Mathematical ecology - this is typically the creation of theoretical models composed purely from math (i.e. not stochastic computer models). Examples include a lot of classics from ecological theory, such as Lotka-Volterra models of predation and competition, but there are also people who still do this kind of research, such as Peter Chesson in his research on the storage effect.

Numerical ecology - this is not a term that I've heard used very frequently, but I think it tends to cluster pretty closely with mathematical ecology, perhaps with more of an emphasis on also including and analyzing empirical data. I hear it used more to refer to techniques than actual ongoing areas of research.

Statistical ecology - I think this term gets used more loosely because obviously statistics are important to most ecology research. It can either refer to research that makes heavy use of advanced statistics because the questions that its getting at are hard to untangle from other effects, or research that uses a statistical model to make its point (note that statistical models are generally different from the mathematical models mentioned above in that their goal is generally to determine how likely something is to happen rather than to untangle some fundamental principle of ecology). A lot of studies on neutral vs. niche-based community assembly would probably fall into the category of statistical ecology. Here is one of many examples.

Ecoinformatics - maybe this is just because I study ecoinformatics, but I tend to think that this is the most distinct of the fields that you mentioned, although it certainly still has a great deal of overlap with the others, especially since it's a pretty diverse subfield. In general, ecoinformatics focuses on making use of large datasets in ecology. This involves both research on developing methods for doing this (for example, I study ways to efficiently collect information from ecological wireless sensor networks. Another good example is the development of GIS tools) and research that uses these methods (e.g. a study that uses GIS to synthesize sensor data and observations of a given organism to determine what that organism's range will be as climate change progresses, or that otherwise seeks to pull ecological concepts out of the data).

Computational ecology - I left this until last, because I think it's the vaguest of the labels you listed. It definitely includes ecoinformatics, but it probably also includes a lot of statistical ecology (and perhaps numerical and mathematical ecology too). I think that the main reason that it's a useful label is that it can catch areas of research that don't really fit in to the other labels. For instance, I once saw a study on quantifying niche space using support vector machines. It was really interesting, and maybe it could be classified as ecoinformatics or statistical ecology, but it didn't really quite fit into either of those. So I guess I tend to see computational ecology as a catch-all term.

These are just the impressions that I have gotten - if others chime in too we can probably build a better consensus definition of these labels.


Why are there so few multicellular anaerobes?

I did a bit of reading myself, and it seems as if Loricifera are the only multicellular obligate anaerobes.

I see your point with niches for anaerobic organisms in deep water. Many organisms near the hydro-thermal vents use anaerobic cellular respiration.
From my understanding of Loricifera, it seems as if they would utilize chemosynthesis as their method of obtaining energy.

  Loriciferans are found exclusively in marine habitats, and live in the spaces between sand grains or in the mud at the bottom of the deep sea. The nanaloricids prefer sand with low levels of detritus (material derived from the decomposition of once-living organisms) or clean shell gravel, whereas the pliciloricids are often found in such deep-sea sediments as the white abyssal Globigerina ooze and the red deep-sea clay from the hadal zone (below 20,000 ft; 6,100 m).

--From Encyclopedia website: Loricifera (Girdle Wearers).

Lociferans live in a rather oxygen-less environment.

So you're right about niches in the deep sea.

But typically the deep sea has extremely high levels of pressure that few multicellular organisms are built to handle.

Additionally, I was able to find a few other obligate anaerobic Eukaryotes, but those were Protozoa, so thereby not unicellular.

About it fundamentally being difficult to be exclusively anaerobic while multicellular, with multiple cells, there is more upkeep and more energy is required to run the "system". Aerobic processes tend to be a lot more efficient, producing more ATP for usage.

Only 1 ATP (from my understanding) is produced from this, whereas with aerobic respiration:

Aerobic ATP sum

Much more ATP is produced from aerobic processes.

In the end, the majority of obligatorily aerobic organisms are unicellular, or are extremely small.

  Their sizes range from 100 µm to ca. 1 mm.

So... that's why multicellular organisms are typically carry out aerobic cellular respiration.

Also, about the fungi you mentioned, it goes through Horizontal gene transfer, which unicellular organisms typically use:

  Horizontal gene transfer (HGT) or lateral gene transfer (LGT) is the movement of genetic material between unicellular and/or multicellular organisms other than by the ("vertical") transmission of DNA from parent to offspring. HGT is an important factor in the evolution of many organisms....
  Most thinking in genetics has focused upon vertical transfer, but horizontal gene transfer is important, and among single-celled organisms is perhaps the dominant form of genetic transfer.

--From Horizontal Gene Transfer Wikipedia page

So yes, it seems as if the fungi that you mentioned and other similar types of fungi would be strictly unicellular, such as yeast (thought yeast is a facultative anaerobe).


What is the difference between neurotransmitters acting as neurotransmitters and hormones?

This figure from Campbell (2011), chapter 45, is very didactic and may clarify this nomenclature for you.

The processes of interest here are a, d and e:

The definition of hormone (in animals) is quite simple: a signaling molecule released in the bloodstream. That's the process a in the figure.

On the other hand, a neurotransmitter is released in the synapse, acting locally. That's the process d in the figure.

However, some nerve cells release their signaling molecule in the bloodstream (process e in the figure). Unlike the synaptic signaling, this molecule can act on a target cell at great distance.

So, despite the fact that we're talking about the very same molecule (norepinephrine in your example), in that last process this molecule is technically speaking a hormone, not a neurotransmitter anymore.

Source: Reece, J., Reece, J. and Campbell, N. (2011). Campbell biology. Boston: Pearson Learning Solutions.


Why have certain plants evolved to contain psychoactive compounds?

The evolutionary history of different plants expressing psychoactive compounds can vary, and in many cases it's difficult if not impossible to pinpoint a particular origin. However, we can make some general observations:

Homology across wide ranges of species

Despite the differences between, say, a human versus a locust, animals share a lot of their physiology. Mammals and insects tend to use different neurotransmitters for different purposes, for example, but the actual neurotransmitters and their receptors are often homologous. A plant could therefore develop a compound that acts as a neurotoxin in certain insects, but also has some psychoactive effects in a human. Nicotine is an example of a psychoactive compound that has insecticidal effects: not only does nicotine protect a tobacco plant, but humans have even used nicotine as an insecticide. Plants could of course also develop toxins to protect them from other mammals, and those would be even more likely to have effects in humans.

There is even homology across kingdoms, such that plants could make compounds to prevent growth of competing plants, act as antibiotics/antifungals, etc, and all have a possibility to act on some homologous proteins that humans have.

Artificial selection

Once humans are aware of a plant's psychoactive or other medicinal properties, that plant can be cultivated and selected for desirable properties. In the case of a compound like THC, there is good evidence that this has occurred recently. In the case of plants that produce opiate compounds, many have been cultivated by humans for thousands of years, so they are a lot more prevalent than they would be if humans had not chosen to do so.

Selection bias

Maybe I should have opened with this one, because I think it's very very important to be aware of. I'm not talking about selection in evolutionary terms here, but in terms of cognitive biases. Selection bias happens when you focus on certain outcomes and not others. There are innumerable compounds produced by plants that can potentially have some biological activity in humans: thousands and thousands. Some do have psychoactive effects, others have effects on other body systems, and many have little effect at all besides dietary contributions. You notice all of the plants that do produce something "interesting" but ignore those that are benign or simply toxic.


Are resonances the reason receptors work?

Photoreceptors themselves dont act as oscilators, a single receptor is either 'on' or 'off' - it does not respond differently to different wavelenghts. Humans have Trichromatic vision, which means that we have 3 different kinds of photo-receptors that respond differently to light of a given wavelength at a given intensity. By combining multiple signals from these 3 different receptor types the brain can translate this to different colors (its actually kind of similar to how RGB color works).

Therefore I would say that even photo-receptors don't work like oscilators, only their specific ligands switch between the 11-cis & trans state, but this is more of a statistical and physico-chemical process (which does involve resonance between the energy of the photons and the electrons in the cis bond)


Heritability of trait stronger from one sex over another?

It has been shown in Drosophila that cross-sex heritability is low for lifespan, where within-sex heritability was three times greater than cross-sex heritability. This means that, sons more closely resemble their fathers and daughters more closely resemble their mothers. This could be considered one such example, if you consider the trait to be a sex-specific thing, i.e. that fathers have a greater influence on lifespan in sons than mothers do.

In humans (and numerous other species, e.g. Indian Meal Moth), it has been shown that several traits have small cross-sex genetic correlations, suggesting that (in such traits) the parent of the same sex is a better predictor of a child's trait value.

It is common (in quantitative genetics circles) to consider homologous traits in two sexes as separate traits (e.g. male lifespan and female lifespan are separate traits), and analyse them in a multivariate framework such as a G-matrix. They often have some genetic covariance between the sexes because of pleiotropy and linkage disequilibrium (though covariance by LD is generally more transient: see books on quantitative genetics by Lynch & Walsh, Falconer & Mackay, or Roff, for more reading).


Will the "frog in boiling water not jumping out" work on warm blooded animals

This answer belongs on Skeptics. Sorry to disappoint, but the "boiled frog" phenomenon is an "old folk warning". This essentially negates your original question altogether. Neither a cold-blooded animal (such as a frog) or warm-blooded animal will boil to death under the conditions implied by the warning (i.e. escape is permitted and water is heated very gradually).

1897 research by German scientist E. W. Scripture, upon which the fable may have first been based, has been deemed flawed by scientists:

  From Scripture's research: “. . . a live frog can actually be boiled without a
  movement if the water is heated slowly enough; in one experiment, the
  temperature was raised at the rate of 0.002 degrees Celsius per
  second, and the frog was found dead at the end of 2.5 hours without
  having moved."

  According to Dr. Karl S. Kruszelnicki (Australian scientist): "[T]he numbers just don’t seem right. If the water comes to a boil,
  that means a final temperature of 100 degrees Celsius. In that case,
  the frog would have to have been put into the water at 82 degrees
  Celsius. Surely, the frog would have died immediately."

  According to Dr. Victor H. Hutchinson (Herpetologist and Zoology Professor at University of Oklahoma):
  "The legend is entirely incorrect! The 'critical thermal maxima' of many species of frogs have been
  determined by several investigators. In this procedure, the water in
  which a frog is submerged is heated gradually at about 2 degrees
  Fahrenheit per minute.  As the temperature of the water is gradually
  increased, the frog will eventually become more and more active in
  attempts to escape the heated water.  If the container size and
  opening allow the frog to jump out, it will do so."

Whit Gibbons (University of Georgia) says that there is an important message behind the false legend:

  So where does that leave us with the boiling frog as a metaphor for
  the human response to economic change or environmental degradation?
  Well, it's not true that you can induce a frog to willingly remain in
  boiling water by starting it off in cold water. But that does not
  diminish the truth of the message that the accumulation of
  imperceptible changes can have a significant effect on the economy and
  the environment. We need to be aware of what changes are occurring and
  to respond to them in a timely fashion. The metaphor lies in the
  frog's ability to escape from the container: if there's no way out,
  then the frog's fate is a foregone conclusion.


Why is it thought that protein folding is determined solely by amino acid sequence?

This question is, in my opinion, based on an incorrect premise but nevertheless throws up a number of points about protein folding and protein structure that can be addressed, albeit briefly.

The False Premise

  “it is a generally accepted idea that protein folding is completely determined
  by the sequence of amino acids”

(My emphasis.)

No…

What is thought to determine protein folding?

The basic principle thought to be the main determinant in protein folding is thermodynamic. If possible†:

  “A protein will fold so that the whole system of which it is a component is
  in the state with the lowest Gibbs Free Energy”

Thus, the protein itself is a major contributor — but not the sole contributor.

There is no argument that amino acid sequence (and composition) will be an important determinant of the contribution of the protein to the thermodynamically most favourable state, as the chemistry of the amino acid residues determine how it can interact chemically with its environment (albeit with weak interactions) and how it may interact with itself to produce a conformation which may have an appropriate effect on the entropy of the whole system.

So this is viewpoint is based primarily on chemical thermodynamic assumptions, rather than special ideas of molecular biology. An elementary exposition of this idea can be found in Berg et al. Section 1.3.4.

How can the environment affect protein folding?

One major influence is whether the protein is in an aqueous (hydrophilic) environment, like the cell cytoplasm, or a non-aqueous (hydrophobic) environment, like the cell membrane. In the former environment a protein will fold so as to expose its hydrophilic residues to the environment, in the latter its hydrophobic residues (discussed, in this paper, for example). Or it may be unable to fold at all in the wrong environment.

Another influence on the folding of a polypeptide chain may be the presence of another polypeptide chain with which it can interact, as in the case of the alpha and beta subunits of haemoglobin (see the classic paper by Perutz (1970))

Small molecules can influence the structure of a protein such as in the case of 2,3-diphosphoglycerate (2,3-BPG) on haemoglobin mentioned below.

When a protein is synthesized in an environment unconducive to correct folding it may require a chaperone protein to transport it to an appropriate environment.

And if the final structure of a protein requires covalent linkages, e.g.  between the SH groups of cysteine residues, an enzyme is need to oxidize them.

What evidence do we have for this?

We have evidence that some proteins that have been unfolded by putting them in environment that is thermodynamically unfavourable to their native (end enzymatically active) structure can refold when the environment is slowly returned to one that is favourable. This is the famous Anfinsen experiment with ribonuclease (described in this book section). Important as this experiment was in supporting the thermodynamic idea and showing that the contribution of the protein was inherent in its own composition,  it does not prove that this is what happens in vivo, nor that the structure formed is the one with the lowest thermodynamic free energy.

The importance of individual amino acids in the sequence is attested by examples such as the mutation of a single amino acid in beta-globin in sickle-cell anaemia (glutamic acid to valine). Under certain circumstances this allows the haemoglobin molecules to polymerize into long fibres because of the interaction of the hydrophobic valine residues with residues in  another subunit rather than with water.

Different states of folding are possible in a single protein

This addresses the section of the question regarding a possible:

  …example of a protein with two different functional foldings

There are many so-called allosteric proteins that are regulated by interaction with small molecules (their environment) which cause a shift from one conformation to another. The example par excellence is haemoglobin, which is in an equilibrium between two states that are influence by the binding of oxygen, hydrogen ions (i.e. the acidity of the blood) and 2,3-BPG.

Another type of example is the shift that can occur between the secondary structures producing amyloid proteins.

†Can we be sure that a protein always adopts the structure of the lowest energy?

No.

The manner in which a random coil is a highly complex field, but, in brief, one can imagine that the path to the structure of lowest energy is blocked in some way (an energy barrier that would have to be overcome, perhaps) so that the structure adopted is, instead, the lowest attainable in practice.

[A rugged energy landscape with hills, traps and energy barriers and some narrow throughway paths to native — from Dill & Chan, 1997]


How do I find the sequence of the phage BxB1 gene?

http://phagesdb.org/phages/Bxb1/ here you can click "Locally BLAST this genome" it will give you the sequence in FASTA format and then you can click BLAST if you want additional information about the sequence, alignment, etc


Do plant-plant interactions inhibit growth?

The phenomenon you are asking about is allelopathy.
Remarkably, it has its own journal - Allelopathy Journal (ISSN:
0971-4693) published since 2009 and currently at volume 30, issue 1.
Here are the titles of the papers from the most recent issue:

In-vitro assessment of allelopathic effects of wheat on potato.
Allelopathic effects of sunflower on seed germination and seedling growth of Trianthema portulacastrum.
Effects of simulated acid rain on the allelopathic potential of invasive weed Wedelia trilobata.
Allelopathic effects of Brachiaria ruziziensis and aconitic acid on Ipomoea triloba weed.
Effects of Butia capitata pyrenes extracts on the germination of lettuce seeds.
Effects of root exudates from crop plants on the growth of Fusarium oxysporum f.sp. niveum.

So, if you have specific questions, this might be the place to look.


Will climate change affect flower population?

Its really hard to say for any given field of flowers and its hard to separate temperature from so many other factors that are accompanying climate change.

For example, rainfall is changing as well as CO₂ levels.  The pH of the rain may change because CO₂ becomes a mild acid when its absorbed into water.  The speed at which the seasonal temperatures vary and how cold is the minimum temperature and how hot is the hottest day will cause parasites and infections which kill plants to appear.

To be sure the heat is important, but the timing maybe just as important.  The temperature is causing earlier blooms and later growing seasons.

Each different species is responding differently, but odds are that nearly any given field of flowers is going to feel it.  The temperature is important, but its sometimes hard to guess if its the specific culprit in changes.


Following the link you provided confirms that the C. elegans expression vector will express your insert of choice in the transgenic animals' pharyngeal muscle cells (driven by the myo-3 promoter).

From examining the two images of the plasmid's restriction map on the page you linked to, I infer that a SacI x XbaI double digest should excise the mCherry insert, and be suitable for sub-cloning your fragment of choice.

However you will need to confirm this for yourself. In general, I think it extremely unlikely that you would find an individual on Biology SE who could provide such precise information as "what enzyme sites should I use for my sub cloning experiment."

A general approach would be to

Research to find out if you can obtain a fasta file containing the complete DNA sequence of the starting plasmid.
Search GenBank to see if there is a record containing annotations for the starting plasmid sequence--that will tell you the start points and end points of each functional region.
If the plasmid is not in a sequence database try using the sequence in a BLAST search of a Non-redundant sequence database. In this example you would have retrieved high scoring hits on the unc-54 gene, the myo-3 gene, the mCherry gene, the beta-lactamase gene from pMB9/pBR322/pUC, and the E. coli lacZ gene (among others).
You should also consult the original publication (if there is one) because it may contain additional useful information, including how to contact the authors--who may have sequence files, useful maps, etc.
With the sequence in hand you will be able to create your own restriction map using a suitable software program (there are many commercial ones), e.g. the EMBOSS suite of open source bioinformatics software.

In your case most of this work was done for you because the AddGene site had two annotated restriction maps that showed almost all of the information you needed.  N.B. One map had the locations of the useful restriction enzyme sites, and the other map had the annotations showing the extent and locations of the worm fragments and the reporter gene. It was only by integrating the information from both maps that I was able to suggest one possible solution to your query.


will an earthworm survive after covering its skin with a wet cloth

This is one of those speculative questions where you don't have a definite answer unless you specifically experiment and find out for yourself.

It is a known fact that earthworms breathe through diffusion. It has a thin cuticle over its body and requires moist skin which is achieved by a slimy mucous (reference). It is interesting to note that earthworms are also capable of going into a state of hibernation called estivation (in American english) (reference) which helps them maintain a low metabolic state.

Since you are planning to cover it with a cloth, the material of the cloth also matters. It has to be a material with low breathability. For eg: the survivability of the worm would depend on if you were using a wool or a silk cloth to cover it. Here is an article on the breathability of different fabrics (reference).

In conclusion, I would take a guess that it should survive if the material let air pass through and would go into a state of estivation on low availability of oxygen but maybe not die. After all, they are said to be able to survive even in water  if it contains enough available oxygen. (reference).


Can someone help me with this Pedigree Analysis?

With the currently given information both autosomal and X-linked recessive is possible:

(WARNING extremely sloppy Paint editing ahead)

This is a possible scenario for an autosomal recessive trait:

And this is one for a X-linked trait:

Ideally you would extend the chart until you encounter a scenario where an affected female has healthy male offspring (which indicates an autosomal trait).


How do I efficiently grow bioluminescent algae?

I have no experience with that particular species but dinoflagellates are often slow growing, very tricky to get to high densities and hard to maintain for a long time without proper experience and lab conditions.

If you still want to have a go I would recommend the following. Growth conditions are rather similar for most dinoflagellates: use a rotary shaker (gentle rotation) in a 12:12 day night regime, don't dilute to hard when subculturing and use standard F2 medium (see link for recipe). If you cannot get hold of seawater you can use saltwater aquarium salts such as Instant Ocean.

Most hate temperature changes so best to keep them at 18-21C


constitution of read and gene region (IGV)

You have asked quite a few questions here. I will try to answer a subset of them.

To answer your question, I started by going to the UCSC genome browser, and selected the BLAT from the tools dropdown menu. Then passing your primer sequences as queries, we can clearly see where they map to the reference genome.

Looking at the figure above, I can guess that your data comes from a targeted sequencing experiment (exome, or gene panel, etc); where you have primers around each exon of EGFR on two strands, on 5' end of exon sequence on each strand (think about DNA polymerase acting in PCR to amplify the number of DNA molecules before sequencing).

Regarding the adapter, I am not sure which read you are referring to. Can you clarify please?

About percentage of mapped vs unmapped reads, you can use bamtools.

Example Usage:

/user/me/src/bamtools/bin/bamtools-2.3.0 stats -insert -in my-sequence-file.bam

Example output:

Total reads:       103277668

Mapped reads:      90088436     (87.2293%)

Forward strand:    58136735     (56.2917%)

Reverse strand:    45140933     (43.7083%)

Failed QC:         6529806      (6.32257%)

Duplicates:        0    (0%)

Paired-end reads:  103277668    (100%)

'Proper-pairs':    87439672     (84.6646%)

Both pairs mapped: 87910438     (85.1205%)

Read 1:            51638834

Read 2:            51638834

Singletons:        2177998      (2.10888%)

Average insert size (absolute value): 6317.39

Median insert size (absolute value): 301


Probability of carrying an autosomal recessive trait given both parents are carriers

Monty Hall does not apply here because there is no decision point past where information is given: the information is already known that the mother is normal phenotype, and the probability for each child of the mother's parents is independent; in the Monty Hall problem, it is known that exactly 1 of the doors contains the prize. Because this sum is known (that only 1 door has the prize), if you know the contents of one door it changes the probability of the others. That is, the occurrence of the prize/goat is sampled without replacement: the thing behind each door is dependent on what is behind the other doors.

2/3 is the correct probability for the normal phenotype mother to be a carrier. Therefore the probability for a child to be homozygous recessive is (2/3) * (1/2) * (1/2) = 1/6.


Mutation-immunity in Luria-Delbruck experiment

No. Surprisingly, there is an adaptive immune system in prokaryotes. This is still widely unknown. The newest review is

S. Al-Attar, E. R. Westra et al: Clustered regularly interspaced short palindromic repeats (CRISPRs): the hallmark of an ingenious antiviral defense mechanism in prokaryotes. In: Biological chemistry. 392, 4, April 2011, 277–289. doi:10.1515/BC.2011.042. PMID 21294681. (Review).

Cited from abstract:

  Many prokaryotes contain the recently discovered defense system
  against mobile genetic elements. This defense system contains a unique
  type of repetitive DNA stretches, termed Clustered Regularly
  Interspaced Short Palindromic Repeats (CRISPRs). CRISPRs consist of
  identical repeated DNA sequences (repeats), interspaced by highly
  variable sequences referred to as spacers. The spacers originate from
  either phages or plasmids and comprise the prokaryotes' 'immunological
  memory'. CRISPR-associated (cas) genes encode conserved proteins that
  together with CRISPRs make-up the CRISPR/Cas system, responsible for
  defending the prokaryotic cell against invaders.

and

  An application of the CRISPR/Cas system is the immunization of
  industry-relevant prokaryotes (or eukaryotes) against mobile-genetic
  invasion. In addition, the high variability of the CRISPR spacer
  content can be exploited for phylogenetic and evolutionary studies.
  Despite impressive progress during the last couple of years, the
  elucidation of several fundamental details will be a major challenge
  in future research.


Glybera doesn't target all cells, and doesn't target fat processing cells. Glybera is adeno-associated virus 1, which normally infects skeletal muscles. Glybera is delivered by intramuscular injection, so the virus easily infects the muscle tissue. The infected muscle cells produce a variant of lipoprotein lipase that has better activity than normal LPL and secrete it into the bloodstream. Once in the blood LPL can interact with chylomicrons and make them smaller.

Here is a paper about viral gene therapy for LPL deficiency, specifically about glybera, but I don't think it's open access.


Any difference between inverted microscope objective vs normal microscope objective?

Apart from the way it works and certain structural differences (reference), the decision of which kind of lens you need to use is left to your own personal choice based on your needs. You can find a list of the different lenses being offered by Olympus in this link.


During the process of plasmid isolation, how can we be sure that only plasmid DNA has been isolated and there is no chromosomal DNA?

It comes down to the size of genomic DNA (relatively huge) compared to that of plasmid DNA (rather small).

Cell lysis for plasmid extraction involves an alkaline buffer that includes sodium hydroxide and SDS. Both plasmid and genomic DNA denature in this condition. When the alkaline reaction is neutralized with potassium acetate, the fairly short plasmid DNA can quickly re-anneal, while the much longer and more complex genomic DNA tends to become tangled up with itself, which prevents sister strands from properly aligning and often results in protein-DNA binding interactions.

DNA bound to protein will then get pulled down during centrifugation, while soluble plasmid DNA remains in solution.

Qiagen and BiteSize Bio both offer some more description of the process:
https://www.qiagen.com/us/resources/technologies/plasmid-resource-center/key%20steps%20in%20the%20plasmid%20purification%20protocols/

http://bitesizebio.com/1660/plasmid-v-genomic-dna-extractionthe-difference/


What is the definition of Mitotic Index?

According to cancer.gov, it's the ratio of number of dividing cells to the number of cells not undergoing mitosis. This is equivalent to the number of dividing cells over the total number of cells.

Note that most papers, such as this one, report the mitotic index as a value from 0-100 (I.E. a percentage)


Proof of mechanisms and causal relationships in biology

You are missing a much simpler and more common method. film birds in flight, then demonstrate mathematically that the wings as used are providing the lift that is enabling flight. That is direct evidence for your hypothesis. You can further test it by clipping the wings or putting the birds in a vacuum, or a hundred other strange experiments. You may want to look into biomechanics, the types of studies you are looking for are far more common. How a limb works is not really a statistical question but more of a dynamics one.

Statistics is a secondary way of testing, used when more direct methods are not possible or terribly impractical. to use your last example yes that would be a perfectly valid way to determine a proteins function, there are limitations reasons we don't usually determine protein functions this way, not just becasue often we discover the function before isolating the protein), but even when it is you also want to test it in other ways that is true of anything in science.  This one reason science prefers multiple lines of evidence since one line can compensate for the flaws in a different line.

"Proof by explanation" has specific connotations in biology that may not be what you are really asking about*. Often it refers to unverifiable narrative explanation which is not acceptable in science. Also you never prove anything in science, (even more so with statistics) we shy away from the term proof because it brings to mind absolute proof which cannot exist. In science you can demonstrate something or show it is the most likely known explanation but you do not "prove" it. Research is not one off events but cumulative and constructive, the more lines of evidence the firmer a concepts standing.

What I thinks you are really asking is something much more fundamental to how science works and what empiricism and verification is. You may have better luck with this on a philosophy of science discussion, than a specific field of science since you seem more confused about how science operates. science has both experimental and descriptive research each with its own value.


Do chromosomes line up as pairs in mitosis or meiosis?

You are correct.  The books explanation is mistaken, and badly written ("the pairs line up as individuals"???)

https://en.wikipedia.org/wiki/Homologous_chromosome

  In metaphase I of meiosis I, the pairs of homologous chromosomes, also
  known as bivalents or tetrads, line up in a random order along the
  metaphase plate.

https://www.khanacademy.org/science/biology/cellular-molecular-biology/meiosis/a/phases-of-meiosis

  So, during metaphase I, homologue pairs—not individual
  chromosomes—line up at the metaphase plate for separation.


is this true to select 100 volume higher concentration of a drug test?

Typically when working with compounds I come from two directions:

Does the drug appear in the literature and what concentration do they use?

I think a quick literature search is a wonderful thing because like many problems, often times someone else has asked your question (what's the right concentration?), and done the necessary legwork to find you a starting point. I don't think we can avoid this next part though, especially if your drug has never been used in your system/organism/etc.

Titrate your compound

For almost anything out there, even if the manufacturer has a number in mind you should always titrate for your own application. Things aren't simply going to work for you as they did for another investigator, in part, because you're never asking the same question as another investigator. A good literature search can help strengthen your finding, however.

In finding the working concentration for your compound you aren't going to be doing the optimizing. It doesn't make sense to find the best concentration when you don't know what concentration works to begin with. As a rule of thumb I try to make the range of titers broad enough that I can see where undesirable or no-effect is, so for example with a drug I'd try 100µM, 10µM, 1µM, 100nm, 10nM, 1nM, 0.1nM.

If you can pick out a good working concentration there, you can optimize by using a tighter criteria. For example, I find that 10nM works the best; now I know 100nM and 1nM are my respective maximum and minimum. May I'd try 40nM, 20nM, 10nM, 5nM, 2.5nM.

It's important to reduce technical variability by using the same starting materials such as cell number for each condition to get the best titer.


don't use the perfect square model. You will keep getting Pi but it's not a real life formulae only used for theory. Try to use a Cartesian graph but three dimensions to take into account curve flexibility. Integral calculus is similar too or better.