Do humans contract more physical sicknesses and diseases than animals do?

The issue is more a matter of research focus than anything else. People care more about people than other organisms. Hence, more money is available for research and more money goes around in medical healthcare than in veterinary care. Research and drug development, in turn, focus on where the money is. The diseases of animals other than humans have simply not been investigated in such detail as in humans, because less effort has been done to document them as exhaustively as has been done for humans. Thus, when something is not in the literature, that doesn't mean it doesn't exist.


Generally speaking, bulk essential nutrients (e.g. amino acids, fatty acids) are used stoichiometrically to form macro cellular structures and are 'baked in' to the structures or compounds they are used to make. Once those structures are destined for degradation, sometimes the bulk essential nutrients can be recovered and reused in the synthesis of other structures or compounds, but catabolic elimination from the organism is always an option that yields useful energy.

Vitamins, on the other hand, are usually used catalytically. Vitamins are not 'baked into' the compounds they help make or process; vitamins transiently participate in the reactions required to make or regulate a compound or structure, but don't ultimately get 'used up' by that process.

Ultimately, vitamins don't have a bulk energetic value to a cell. For instance, once vitamin E (α-tocopherol) is oxidized, its only fate is to be excreted as waste. Fatty acids and amino acids, once destined for degradation, have their remaining chemical energy extracted prior to excretion of their downstream waste products.

It is philosophically interesting to remark on the diversity of bulk biomolecular building blocks that are still necessary for some organisms to obtain from their environment. Not all of them get called vitamins.


What is the biological advantage of bilaterity?

Bilateria, as a clade (all animals, excluding sponges, cnidaria, comb-jellies, and placozoans) is monophyletic, and as such, originated from a single species that was bilaterally symmetrical. Sometimes the explanation for a particular trait involves ancestry, and if an innovation is advantageous, it tends to spread. Along with this group came advances in the central nervous system, and digestive systems. It is advantageous to put senses up front, in the head, with the mouth. Having a tube-like digestive system, with a mouth at one end, a gut in the middle, and an anus at the other end, turned out to be efficient. Cnidaria (and other non-bilaterians) are not nearly as diverse as bilaterians, and most bilaterians are marine. So the bilateral advantage holds both in water, and on land.


PCR a plasmid with self-complimentary regions?

From experience, your present problem will not completely go away no matter what you do.  The idea for asymmetric PCR is not a bad idea. However, you will only get linear amplification of the desired product from the initial single primer, so you will not "see" any product even after 30-40 cycles.  This first single primer PCR might also cause downstream problems with amplification of undesired products made during the second PCR (junk products).

I agree with comment #1, but then neatly cut the "visible" "good" band out of the gel.  Suspend (crush) the agarose band in sterile TE buffer, and then use an aliquot of that as template for a secondary PCR (use equal primers - maybe 30 cycles).  This should provide more than enough "good" starting template.

Alternately, you could design a new forward primer that does not have a bad secondary location on your plasmid.


How to recognize a conserved motifs of the protein

It seems to me that you're asking about homology modelling. In that case, yes you need to compare your protein of interest to a protein (or proteins) of known structure. Homology modelling in a nutshell includes three (four?) steps: template identification/template alignment, modelling, quality assessment.

You start with finding a template for your modelling. This is usually done by sequence alignment, for instance BLASTing. Preferably you use multiple sequence alignment which more sensitively aligns conserved regions. You then want a template with as high sequence identity as possible (above 50 % usually produces models with about 1 Å RMSE [1] in main chain atoms. Avoid less than 30 % where modelling errors rapidly increase.)

There are then a number of different modelling strategies (wikipedia). But basically, they all aim to predict the structure of the conserved protein core as well as possible (which usually is what you're really interested in). Peripheral amino acids are more dynamic and more prone to evolution and are therefore more difficult to predict. Then, most importantly, you assess the quality of your model. This can be done by calculating violations of statistical potentials or physics based conformational energies (or using more advanced methods like multivariate regression methods). As in all modelling, this really is a most crucial step because prediction with a poor model is misleading and utterly useless.

If you don't find any template you could resort to the exciting field of De novo protein structure prediction, where the aim is to predict the structure from the amino acid sequence alone. I am not very familiar with their methods, but de novo prediction is hard (!). I don't remember any exact numbers but the number of conformations in a normal sized protein is astronomically large, which leads to great algorithmic and computational challenges. Additionally, without any reference sequence the model assumptions are greater than those of homology modelling. Although, I have heard that the field has been making great progress the last few years.

Edit:
It struck me that you might be asking about protein fold recognition as well. There exists a large number of different tools and methods for recognizing and locating protein domains using the amino acid sequence as input. Many of them are available as web servers. For instance phyre which uses the amino acid profile and predicted secondary structures to search structure libraries. Threading based methods like MUSTER. A number based on Hidden Markov Models (HMMs) also exist. For instance FISH which uses structure anchored HMMs.


Best method for measuring very young plant growth?

I am assuming you want to monitor these traits in controlled conditions because in wild type conditions it will be real challenge to monitor in details unless you have easily accessible way (like leave surface area and related visual traits). Remember these techniques will change according to your plant/seed and your study interest. Lot of things change during development. You need to look at characters which suits your study. You can try following,

Monitor real time oxygen consumption in controlled chamber ( Generally researcher do this by monitoring loss of oxygen in
current chamber by some non invasive method. However there are
other techniques like this which can be also implemented
depending on type of plant.)
There are some automated image acquisition techniques like this or this
Use of volatile organic compound (VOCs) traces
Change is fresh and dry weight during development
Root moisture sensors ( in microgravity environment ) like this
I don't know whether you can use this kind of sensors in any way but these are very useful in monitoring particular element in vivo

This is very big list. There many other components which you can monitor like protein content, lipids etc. However such techniques are most reliable but destructive and you can use if you have large amount of samples.   You can go through papers cited in above list. Take a look at their methods and materials. You will know how to do such measurements and what are advantages/disadvantages.


q-value is the corrected p-value to account for multiple testing (i.e. you are testing thousands of genes). Those with q-value <0.05 are significant experiment-wise. Cuffdiff uses Benjamini-Hochberg correction to compute FDR (i.e. q-value). The calculation does not depend on the number of replicates it's based on the distribution of p-values those, yes, are influenced by the number of replicates. The more replicates you have the better).


How exactly does mitotic recombination help repair damaged DNA?

Note: the technical term is homologous recombination (as DNA repair is actually its primary function), and this answer focusses on lesions affecting both strands at approximately the same level (as a lesion affecting only one strand at a particular location can easily be repaired by using the clean strand as a template), such as symmetrical double-strand breaks (where both strands of the double helix are severed at the same level; commonly caused by [and responsible for the main lethal effects of] overexposure to ionising radiation; used as the example type of damage for the purposes of this answer).

Short answer

The homologous DNA serves as a template for synthesis of new DNA to repair the damaged area.

Long answer (paraphrased from here)

If both strands of a chromosome are severed at or near the same location, special enzymes unwind the broken ends, and other enzymes then clip off a length of one of the strands from each end (the strand that gets clipped off is always the one with the exposed 5-prime end, in case you were wondering), leaving an exposed single-stranded flap on each side of the break.

At this point, other special proteins grab onto these flaps, and take them looking for an intact homologous piece of DNA (that's why it's called homologous recombination), which can be either a sister chromatid (which is guaranteed to be either identical or very nearly so, and is, thus, the preferred solution when possible) or a homologous chromosome (which is always available, except for haploid cells [such as human gametes], but is virtually guaranteed to be not-quite-identical, and, thus, is a less-optimal solution).

With the help of the aforementioned special proteins, one of the flaps then butts into the homologous double helix, base-pairs with the strand it's complementary to (forming a structure known as a Holliday junction [well, technically, seven-eighths of a Holliday junction, as one of the junction's four arms has only a single strand, rather than two]), and kicks the other strand out of formation.  The displaced strand forms a single-stranded loop hanging off to the side (known, unsurprisingly, as a displacement loop, or D-loop), while a DNA polymerase latches onto the bare 3-prime end of the invading strand and lengthens it, using the homologous DNA as a template.1

At this point, things can go in either one of two ways:

In the simpler pathway (the synthesis-dependent strand annealing, or SDSA, pathway), the polymerase simply continues to lengthen the invading strand until enough DNA has been added to the end to bridge the gap between the two broken ends and base-pair securely to the flap on the other end; at this point, the invading strand backs out, allowing the invaded DNA to reassume its double-helical dignity, and the newly-lengthened flap grabs onto the complementary flap on the other broken end.  More DNA polymerases fill the remaining gaps, and a ligase seals the helix back up.  The SDSA pathway is the major homologous-recombination pathway for cells not planning on undergoing meiosis.
In the more complicated double-strand-break repair (DSBR) pathway, the exposed flap on the other broken end also gets in on the action, base-pairing to the exposed D-loop and likewise being lengthened by a DNA polymerase.  When enough new DNA has been synthesised to completely fill the single-stranded gaps, the exposed ends are joined together by ligases, forming a structure with no exposed ends and two complete Holliday junctions.  To turn this back into a pair of separate bog-standard double helices, two of the four strands in each Holliday junction are cut by endonucleases, causing the two DNAs to separate.  (There are rules as to which two strands are cut; either both of the two strands that cross over in a given Holliday junction, or else both of the two strands that don't cross over in said junction, but never one crossing and one non-crossing strand [as this would merely create a new double-strand break at the location of the junction].)  Depending on how the Holliday junctions are severed, the portions of the two chrom[atid/osome]s distal to the original break may or may not be exchanged between the chrom[atid/osome]s; if both junctions are severed on their crossing strands, or both on their non-crossing strands, this distal DNA will not be exchanged, while, if one junction is cut on its crossing strands and the other on its non-crossing strands, said DNA will be exchanged.  Due to its possibilities for swapping bits of genetic material, this is the preferred pathway for cells that are planning on undergoing meiosis (although it also occurs to some degree even in somatic cells).

Here's an image to illustrate the process:

(Image by Emw at Wikimedia Commons.  Blame them for the typo in "Strand invasion", not me.)

1: This is why the 5-prime strand got pruned back, and not the 3-prime strand; all DNA polymerases known to science lengthen DNA strands in exclusively the 5-prime→3-prime direction, and can only add nucleotides to exposed 3-prime ends (exposed 5-prime ends need not apply).


Why does Penicillin only affect bacterial cell walls

Bacteria have a mesh-like structure surrounding their plasma membrane called a cell wall.  The cell wall is made up of peptidoglycan polymers that form a rigid crystalline structure that helps protect the osmotic pressure of the bacterial cytoplasm.

Penicillin and other β-lactams work by inhibiting the final step of peptidoglycan synthesis, which prevents transpeptidation (crosslinking) of the peptidoglycan molecules. This leads to the death of the bacterium by osmotic pressure due to the loss of the cell wall.

This drug doesn't affect human cells because they lack a cell wall surrounding their plasma membrane.


How exactly can dsRNA be introduced to a cell?

Besides viral infections there are different pathways for cells to take up dsRNA. Inside the cells these dsRNA are processed by Dicer which processes these RNAs into small interfering RNA, which play an important role in the regulation of gene activity.

These pathways have mostly been researched in Drosophila and C. elegans, I am indicating where evidence for them in humans is available. The different possibilities for the uptake are:

Uptake via transmembrane proteins: In C. elegans two different transmembrane proteins have been discovered which passively transport
dsRNA into the cells. They are called SID-1 and SID-2 (systemic RNA-interference defective protein), at least for
SID-1 a homologue exists in humans as well. These receptors are important for the uptake of systemic (produced by the own organism) dsRNA. See references 1-3 for
details.
Uptake via Endocytosis: In drosophila cells active transport happens through the scavenger receptors SR-CI and Eater. They bind
the dsRNA and are then internalized. Knockdown of these genes
inhibited the import of dsRNA and inhibited the endocytosis mediated
knockdown of genes. This process seems to be evolutionary conserved,
as knockdown of the orthologous genes in C. elegans led to similar
results. This mechanism seems to be more important for the uptake of environmental dsRNA. See references 4 and 5 for more details.
Uptake via Phagocytosis: At least for drosophila, there is evidence for a phagocytosis mediated uptake mechanism, which is
independent of endocytosis. See reference 6 for details.

References

SID-1 is a dsRNA-selective dsRNA-gated channel.
Uptake of extracellular double-stranded RNA by SID-2
RNA interference: a mammalian SID-1 homologue enhances siRNA uptake
and gene silencing efficacy in human cells.
The endocytic pathway mediates cell entry of dsRNA to induce RNAi
silencing.
Double-stranded RNA Is Internalized by Scavenger Receptor-mediated
Endocytosis in Drosophila S2 Cells
A phagocytic route for uptake of double-stranded RNA in RNAi


If I understand your question correctly, you are essentially distinguishing between the timescale on which the variation in the character of interest is generated, and the timescale on which selection prunes the population based upon that variation. The argument is then that "all the evolving happened gradually, long before the selection event" because that is when the variation was generated.

To me, this seems to be a misuse of the term "evolution", which is usually defined as a change in trait or allele frequencies in a population over time. Under that definition, much of the evolution does occur via the selection event. Before, you have a wide range of trait values; after, only a narrow selected set of trait values. In such a model, selection indeed is the major cause of allele frequency or trait value change.

In practice, both processes are usually acting in concert; variation is being produced by mutation and recombination and eliminated by selection at comparable rates so that the net amount of variation in the population is at an approximate steady state. This is essentially the model Darwin espouses, though note that Darwin does not have our modern understanding of heredity and therefore is not able to explain how variation is generated or preserved.

Additional note: When thinking about models of the kind that you describe, it is also key to understand that if you have a large number of loci affecting your trait (e.g. coat thickness), then the Gaussian distribution prior to strong selection will not include the extreme phenotypic values. If there are 20 diploid loci interacting additively to determine coat thickness and the mean individual has 20 thickness alleles and 20 thinness alleles, no individuals in a reasonably sized population will initially have all 40 thickness alleles, or even 39 or 38 etc. Selection for thickness will change the mean, and will also result in individuals outside of the initial range of variation. If the mean is 30, you may well get an individual with 38 or 39 or even all 40 thickness alleles. So once selection occurs, new more extreme phenotypes will suddenly appear. Nothing strange has happened in terms of rates of generating new variation; in fact this is just a consequence of reassorting the current alleles under the new allele frequencies.


No digested product bands, but markers are visible. What could be the reasons?

Usually there is no issue of mixing. One possible reason is degradation. But you say marker is faint (marker wont get degraded). Stain the gel with extra EtBr and see again. If you reused the gel then definitely stain it again because EtBr migrates towards the cathode.

It doesn't seem like degradation to me but to be cautious for the next time:

Use freshly autoclaved water. If you are not sure then filter using syringe and keep some 10ml for yourself
Ensure that the plasticware are also autoclaved properly.
Use endo - plasmid extraction kits, if available
Dissolve the plasmid in TE (only if conc is high and you need not put much in the reaction mix else EDTA interferes in the reactions. In that case use Tris-Cl pH-7.6 ).
If you have to digest a lot of DNA then set up small reactions in many tubes.
Do not incubate the reaction for a very long time (>6h).
Inactivate the enzyme by heating if you are not running the gel immediately.
Ensure that the gel running buffers are not too old.


Although your plastic bag tears are most likely due to light damage as @Chris mentioned above, there is a type of ant that chews its way through plastic, rubber and other manufactured polymers: Monomorium pharaonis, the Pharaoh ant.

It is capable of destroying many manufactured materials and is a great example of budding, a method by which new ant colonies form. They are very invasive and difficult to control.


Confluency or confluence, which term is correct to describe the % area covered by cells?

Searching Google Scholar for cell confluence returns 239000 hits, while searching for cell confluency returns 75000 hits.

A look at the context in which they are used supports my gut feel, which is that

1:  "confluence" should be used in contexts of "% confluence"

2:  "confluency" should be used in contexts where you describe high or low levels of confluency.


Yes the males of a group of bony fish Syngnathidae can bear offsprings or as you say produce offsprings. This group includes Seahorses and Pipefishes. In some species the male have either a brood pouch attached to the trunk or its tail while in others the egg is attached to the trunk or tail laid by the female.The fertilisation takes place in the pouch or in water before implantation.

Here are some pictures :

1.Male seahorse with brood pouch and a slender female without a brood pouch

2.Male seahorse giving birth to a baby seahorse

3.Male Syngnathus sp.(pipe fish) with the brood pouch

Inset image C shows eggs in pouch of pregnant male and Inset E shows Embryos in the pouch of pregnant male. (Images taken from researchgate.net and peaubleue.org)

Now coming to your question

  why are they considered male and not female?

Though the males here bear the baby but the baby results from fertilisation of a sperm produced by the male (the same seahorse that is destined to bear the baby) and an ovum produced by the female (the other seahorse without a brood pouch).
The sperm / male gamete producing individual is a male and a ovum/female gamete producing individual is a female. The provision of being able to bear a child does not change the sex.

Note: Seahorse is an oviviviparous organism i.e they are organisms in which the fertilised eggs develop inside the parent's body until they are ready to hatch.

P.S. Brood pouch is a cavity outside the body of these fishes in which the eggs develop and hatch.

Source: Wikipedia


Crows don't lay their eggs in sparrows' nests - they lay them in crows' nests. What you're describing, though, here is brood parasitism. This relieves the parasitic parent of the responsibility of rearing young, building nests, protecting the eggs, etc.

Brood parasitism is seen in a number of duck species, with females laying their eggs in the nests of others. One example is the goldeneye, Bucephala clangula. Interspecific brood-parasites include the most cuckoos and cowbirds, black-headed ducks, and indigobirds, whydahs, and honeyguides. About 1% of all known bird species are obligate brood parasites (never make nests, need a host).

Here is a picture of a reed warbler feeding a cuckoo which was a parasite, its egg having been laid in the warbler's nest.

Parasite nestlings suffer a relatively high mortality, either from rejection by the host (host bird will not feed the parasite) or rejection before fledgling (once nestling graduates to tree branch, the hosts stop feeding it). However, clearly since cowbirds and cuckoos are still alive and well, enough of them do survive.

Do they think they are of the host species? There was no literature I could find on this. While the parasite messes up the host parents and 'siblings' (when there are surviving 'siblings'), there is much less follow-up done on the behavior of the parasite once fledged. Common sense will therefore need to come into play.

If a cowbird thought it was an indigo bunting, it would not be able to reproduce, as it would try to attract a bunting mate and fail. Since the hosts continue to experience parasitism over many generations, and the population of parasites does not necessarily decline in a given area over several generations (in some areas, it is the host population that declines), I would have to say, yes, the bird 'knows' it's different (probably only on an instinctual - not cognitive - level); the parasite bird feels nothing about its bad behavior, and does not learn their own behavior from their host parents. Instinct takes over; they mate with their own kind, and continue to parasitize the host birds' nests.

Brood parasite
Host–parasite coevolution beyond the nestling stage? Mimicry of host fledglings by the specialist screaming cowbird
Brood parasitism by cowbirds: risks and effects on reproductive success and survival in indigo bunting
Brood parasite


Is it normal for corn to have multiple ears in one place?

This is an example of "bouquet ears", or, what Rob Nielsen coined in his 1999 paper2 as "MESS Syndrome" (Multiple Ears on Same Shank).

Although not a regular occurrence, MESS syndrome is not unusual. According to Nielson in an online article in 2014 [my emphasis included]:

  The fact that multiple ears sometimes develop from a single ear shank is not, in and of itself, physiologically unusual. Ear shank development essentially replicates the developmental pattern of the main stalk of the plant.

  The ear shank is comprised of nodes and internodes just like the main stalk (Fig. 7).
  Each node of an ear shank develops a leaf just like the main stalk, although we add the adjective "husk" to describe them.
  The ear shank terminates with a reproductive organ (the female ear), akin to the main stalk terminating with a reproductive organ (the male tassel).
  Secondary ear shoots can develop from individual nodes of the ear shank just like secondary ear shoots develop from individual nodes of the main stalk.

  Normally, hormonal apical dominance exhibited by the primary or apical ear on an ear shank (or simple competition for photosynthates) suppresses the initiation or development of secondary ears at lower shank nodes. However, under certain conditions or with certain genetic backgrounds, one or more secondary ear shoots not only initiate successfully, but also continue to develop to the point that their presence is clearly noticeable. While the appearance of one or more additional ear shoots with silks emerging from lower husk leaves may not be attractive, I do not believe there is any real detriment to the plant by their existence as long as the primary ear is "normal".

Bonnet (1966)1 described this phenomenon in the 1960s and reports of occurrences happen periodically. In 2006, Nielson3 coined the "bouquet" terminology to describe multiple reports of out-of-proportional growth of multiple ears from single shanks in numerous midwestern farms.

According to Nielson:

  The common factor in affected fields was some sort of damage to the development of the primary ear prior to or during silking that seemed to "set loose" the continued development of the secondary ears on the same ear shank.

An Ohio State University article suggests that the cause of this phenomenon is unknown, but Nielson is probably the expert:

  Some hybrids may be genetically prone to developing multiple ears on a single ear shank. A threshold genetic trait may be triggered by particular stress events that occur during primary ear formation. Dr. Bob Nielsen at Purdue University has proposed that more than one external “trigger” may enable the development of multiple ears to occur on these hybrids. He has observed that the “bouquet” effect is more prevalent and severe in late plantings where silk clipping by rootworm beetles prevented kernel set on the primary ear (i.e., possibly minimizing or negating apical dominance against secondary ears).

You can see an image of a buoquet from one of Nielson's studies below:

 Source: Purdue Dept of Agronomy; Credit: Bob Nielson (2014)

1  Bonnet, O.T. 1966. Inflorescences of Maize, Wheat, Rye, Barley, and Oats: Their Initiation and Development. Univ. of Illinois, College of Ag., Agricultural Expt. Sta. Bulletin 721.

2  Nielsen, R.L. 1999. What A MESS! (aka Multiple Ears on a Single Ear Shank). Corny News Network, Purdue Univ. http://www.kingcorn.org/news/articles.99/990823b.html

3  Nielsen, R.L. 2006. A Problem with “Bouquets”. Corny News Network, Purdue Univ.  http://www.kingcorn.org/news/articles.06/Bouquets-0912.html.


What species is this interestingly colored brown moth

It could be Pyralis farinalis, the meal moth. It is a cosmopolitan moth of the family Pyralidae. Its larvae are pests of certain stored foods, namely milled plant products. I don't think it's adults feed as they do not live long after mating.
Here is a link to its Wikipedia article:Pyralis farinalis


What is doubling of genetic material invented in flowering plants?

Yes, D. Attenborough probably refers to ploidy number

Ploidy number

Humans for example are 2N (except during the spermatozoid and ovule phase of human existence) meaning that they carry two copies of each autosome (=non-sexual chromosomes). Some species are 1N (haploid), some are 3N (triploid), etc… It would actually be more correct to talk about the time a species spend in each of its phase or talk about the number of cells in each of its phase because many species undergo change in chromosome number during their existence as it is the case for humans. Humans are 2N most of the time but they are 1N when they are ovules or spermatozoid. The correct word to describe the human lifecycle is diplontic. Some species are diplontic, some are haplodiplontic and some have phases when they have a greater number of chromosomes. Those species are said to be polyploid.

Ploidy number, chromosomes and chromatids

To make sure one don't mix up things... One chromosome is made of one or two chromatids (depending on the cellular phase). The chromatids of the same chromosome (called sister chromatids) are (almost completely) identical. A given "chromosome type" is either alone (1N) or accompagnied by one very similar chromosome (2N) or two other very similar chromsomes (3N), etc.. Considering the case of a 2N individual: If at a given locus (position in the chromosome) the two alleles (gene variant) are different than the individual is said to be heterozygote for this locus. The ploidy number describe "this number of chromosomes"! Now there may have different number of different "types of chromosomes". Humans for example have 23 different types of chromosomes and in its haploid phase has therefore 23 chromosomes (23 or 46 chromatids depending on the cellular phase) and has 46 chromosomes (46 or 92 chromatids depending on the cellular phase) in its diploid phase

Ploidy number in angiosperms and other plants and non-plants organisms

Yes, D. Attenborough (who I don't know and I haven't read anything of his work) probably means doubling, tripling, quadrupling, .. the number of N of chromosomes. And, yes indeed polyploidy (3N, 4N, 6N, 8N) is relatively often observed in flowering plants. There are many crop species that are polyploid. According to this article an important part of the speciation that occurred in plants is accompanied by a change in ploidy number but this is not only true for angiosperms.

Polyploidy is also found in many fungi species and some animal species as well. There are lots of terminologies linked with the discussion of chromosome number and reproductive system and many articles discuss these mechanisms and also the evolution of polyploidy. I found the work of Sally Otto to be of the greatest interest for example.

Notes

The words inventions are not really used in evolutionary biology but rather in popular books. Also, there are many non-angiosperm plants that have symbiotic relationship with animals. For examples: some angiosperms and the squirrels or birds. But it is true that angiosperm have particularly important symbiotic relationship with animals, in particular insects and this probably allowed an important diversification in both angiosperms and insects. As already said angiosperms are not the taxon of plants to include polyploid species. There are other characteristics that allow to tell an angiosperm apart from other plants. The number of aperture on pollen grain or the positions of the meristems (tissue where mitotic division of unspecialized cells occur allowing the growth of the plant) for examples.

You may be interested in reading this post on the effect on fitness of ploidy number


what are some examples of how evolution's limitations prevented species from climbing to the absolute highest peak on the fitness scale?

The "limitations" of evolution is somewhat subjective, I suppose, but a couple of the important ones include random mutations, lack of foresight, and environment. Evolution is a complex process by which mutations occur which either benefit an organism, making it more fit, harming the organism, leading (usually) to death, or to no noticeable change. Over time, these mutations bring about significant phenotypic changes. There's no goal, no purpose to it. In your example of plants, chlorophyll could certainly have evolved a structure that absorbed light in different wavelengths.

Another example is the difference between the vertebrate eye vs the octopus eye. For mammalian eyes, the optic nerve covers part of the retina. This is commonly known as the "Blind spot". For Cephalopods, on the other hand, the optic nerve is located behind the retina, so they have no bind spot.

Both of these examples are the result of random mutations coinciding with ideal (or non-ideal) environmental situations. The author of the post you cited is accurate to say that evolution is not an engineer, working towards a goal. The only goal of evolution is "What maintains life?" It's merely millennia of trial and error, and occasionally calamities occur, causing extinctions and loss of genetic potential.

I really think ANY characteristic of any species you care to name could be considered a result of evolution's limitations.


What product of cellular respiration creates an acid when in solution with water?

Cellular respiration itself, defined as the activity of the respiratory chain complexes I -- V (including ATP synthase), is not acidifying. On the contrary, free protons are captured during ATP synthesis, so cellular respiration acts to raise pH. But then ATP synthesis is always matched with ATP breakdown in reactions that utilize energy (muscle contraction, for example), and ATP breakdown liberates the captured protons again. So the complete cycle of ATP turnover is pH neutral. (For more information, see for examplle http://www.ncbi.nlm.nih.gov/pubmed/6298937)

The activity of the TCA cycle, on the other hand, produces CO$_2$ when oxidizing carbohydrates, and CO$_2$ dissolved in water is slightly acidic (pK$_a$ = 6.3) and so tends to lower pH. This is the main acidifying effect of oxidative metabolism. In animals, the CO$_2$ generated is of course released via the lungs, so the amount of CO$_2$ dissolved in body water is (more or less) constant, and therefore pH is stable.


Difference between protozoa, protists, protoctista?

These terms are all somewhat obsolete as taxonomic terms, but they may still be used to describe certain groups of organisms.

The term "protist" is used informally in two different ways.  One usage refers to the paraphyletic group consisting of all eukaryotes other than the animals, plants, and fungi.  The other usage is to refer to those eukaryotes that exist as independent cells or, if colonial, do not form colonies with differentiated tissues.

The term "protozoa" is used informally to refer to the "animal-like" protists, i.e. those that are non-photosynthetic and motile.

Wikipedia gives a good summary of how these terms were used historically.


Why do I always close my eyes when someone takes a photo of me using a flash?

What you are describing is called a "corneal reflex" and it is a measure to protect the eye from too bright light or foreign bodies.

It is a involuntary movement (i.e. not intentional, as you say), mediated by the cranial nerves, specifically the ophtalmic branch of the trigeminal and the temporal and zygomatic branches of the facial nerve.

I have to admit that I had a very hard time finding an exact complete explanation of the phenomenon, which makes me think (but I may be wrong) that it has not been widely researched. Although it is not difficult to imagine how the trigeminal nerve could be stimulated by a foreign body touching the cornea, it seems that several theories exist on how light can stimulate it.

The great part of the information that I could find at this regard are about a similar reflex, called the  the photic sneeze reflex or or ACHOO (Autosomal Cholinergic Helio-Ophtalmologic Outburst) syndrome. This occurs in ~1/4 of the population, and consists of sneezing when looking at the Sun.

In this case, several theories have been proposed, that essentially boil down to the fact that some other nerve (e.g. the optic nerve) stimulates the trigeminal after having being itself stimulated by bright light.

From: "General anaesthesia and the photosternutatory reflex" - Yarrow - Anaesthesia. 2003

  The physiology underlying the photosternutatory reflex remains unclear and several mechanisms have been proposed. The theory of optic-trigeminal summation holds that the optic and trigeminal nerves are intimately linked in the midbrain. Bright light stimulates the optic nerve, causing photophobia and pain via the ophthalmic branch of the trigeminal nerve. Conversely, nasal irritation can lead to blinking and lacrimation. It is suggested that intense stimulation of the optic nerve could cause sneezing if the maxillary branch of the trigeminal nerve was stimulated as well as the ophthalmic branch. The theory of parasympathetic generalisation invokes co-activation by one stimulus of neighbouring parasympathetic branches. Light falling on the retina stimulates pupillary constriction (via the third cranial nerve) and lacrimation
  (via the seventh). A stimulus of sufficient intensity could generate
  enough parasympathetic activity to cause nasal congestion and secretions, and
  stimulate sneezing by an effect on the maxillary branch of the trigeminal nerve.
  The theory of parasympathetic hypersensitivity suggests that individuals
  with photic sneezing may have a more active or sensitive parasympathetic system,
  leading to hypersensitive nasal mucosa.

Although what you describe does not involve sneezing I think we can assume the same, or a similar afferent pathway is activated also in that case.

Recent works also found an activation of visual regions of the cortex in response to this stimulus.

From the conclusions of:

When the Sun Prickles Your Nose: An EEG Study Identifying Neural Bases of Photic Sneezing - Langer et al. - PLoS One, 2010

  We propose that the photic sneeze phenomenon might be the consequence of higher sensitivity to visual stimuli in the visual cortex and of co-activation of somatosensory areas. The ‘photic sneeze reflex’ is therefore not a classical reflex that occurs only at a brainstem or spinal cord level but, in stark contrast to many theories, involves also specific cortical areas.


Are the processes on afferent neurons that go from the sensory receptor to the cell body considered axons or dendrites?

They are considered axons. Pseudounipolar cells have a bit of an odd morphology.

The reason you consider the entire length an axon is because it all grows from a single process from the soma which then branches. Terminology is just terminology, so "rules" are often made to be broken in biology: yes, an axon typically carries information away from the soma, but that's not the case here for neurons where the information sort of bypasses the soma.

Besides the developmental origin from a single process, the initiation site for an action potential is out in the distal end of the axon, rather than at an axon hillock connected to the soma, and if you had a section of axon on either side of the soma it wouldn't be apparent which end you were looking at.

Tandrup, T. (1995). Are the neurons in the dorsal root ganglion pseudounipolar? A comparison of the number of neurons and number of myelinated and unmyelinated fibres in the dorsal root. Journal of Comparative Neurology, 357(3), 341-347.


What type of distribution should binding affinities fit?

P-values reflect how well the data fits some background model. This background model should reflect some assumptions you make about the data. What assumptions do you think would be reasonable in this case? For example, do you assume high values are more likely to be incorrect?

Throwing away outliers like kmm suggested is probably not a good idea, because it means you will remove $K_i$ values which are very high or very low. It is not clear there is much biological justification for that, since we know some $K_i$s can be low and some can be high, but it doesn't tell us they are wrong.

The bottom line is that without making some assumption about what the values should look like, you can't identify what incorrect values look like.


How can the child and the mother have different blood types?

The blood of the fetus does not mix with the blood of the mother.  Instead, the placenta provides a system where the two separate blood streams flow past each other with thin separation allowing nutrients to flow between the two streams but the not the blood cells and other large components.


Is it possible that by mutation a human could see infrared or other 'colours'?

Yes.

Far-red vision (>700nm)

The ability for retinal-binding proteins to absorb far-red (between 700nm-850nm) light has been experimentally confirmed in this paper. While the authors did not attempt this in vivo in an animal model, they managed to use directed mutagenesis to induce a significant shift in the absorption peak of the chromophore of the retinal binding protein.

The authors show the shifts induced by these mutant proteins in the figure below. The mutants have significantly different absorption peaks, and assuming that the proteins do not lose their ability to transduce signals via optic nerves, they would allow vision in different wavelengths.

Ultraviolet vision (300-400nm)

It is known that humans lacking a lens (aphakia) are able to see ultraviolet light. As noted in the question, the lens blocks out long-wave UV, and its removal or absence results in ultraviolet vision (although with low sharpness due to the lack of a lens).

  However, aphakic patients report that the process has an unusual side effect: they can see ultraviolet light. It is not normally visible because the lens blocks it. Some artificial lenses are also transparent to UV with the same effect. The receptors in the eye for blue light can actually see ultraviolet better than blue. Military intelligence is said to have used this talent in the second world war, recruiting aphakic observers to watch the coastline for German U-boats signalling to agents on the shore with UV lamps.


Two-fold cost of sex and r/K selection theory

r/K selection has become more of an heuristic for characterizing a species' strategy of reproduction and less a matter of predicting what sort of species will emerge from a given environment as it had originally been proposed by MacArthur and Wilson in 1967. The paper you cite tries to determine whether rotifers become more r or more K selective in different environments.

The thought here on k-selection is not almost from the definitions of the term, which is why it isn't explained in the paper.

In R-selected strategies, many more offspring are produced, but less investment is made in each one.  Think about a cockaroach laying thousands of tiny eggs.  The hatchlings might be eaten by their own mother; they are so 'cheap' the insect who layed the eggs doesn't have any anxiety about their survival.  In extreme cases, most of these hatchlings will not reproduce, they may even be a bit of food for the ones which do reach maturity.

In k-selected strategies, very few offspring are produced.  In addition to the 'cost of sex' limitation, they are invested in so heavily that the female may stop being fertile for a while.  An example would be how female mammals which are lactating are not fertile or seasonal mating like many birds do; the females turn off reproduction so that they can focus on the success of one or two produced offspring.

k-selection is advantageous over R-selection when more of their investment pays off.  If one out of ten R-offspring survive and one out of four k-selected offspring survive, then for these competing rotifers, the k-selected strategy is advantageous.

The cost of sex is that its half as efficient as asexual reproduction because males don't really reproduce - they only provide genetic material for females.  You can argue r/K selection independently of this factor, but the article is suggesting that k-selection can be so advantageous as to also give sexual selection an advantage over asexual selection.  I think asexual reproduction could be k-selected as well, but that seems to be the point being made here.

The reason that k/R has toned down in importance in the past couple of decades is that it has been found that individual species can adapt to shift their k/R strategems.


I worked for a long time at a leading high-quality antibody company, so I'll try and share some of my experiences with you. The process of making a highly specific antibody (I'll focus on monoclonals) has three important parts - antigen design and immunization, cloning and subcloning, and screening/validation. Each part is crucial on its own, and the better one is performed, the higher your chances of success downstream become.

In order for an antibody to work, it needs to bind specifically to its target. I won't get into all the specifics here, as there is a good open literature on antigen design, but basically you need something that will promote a strong immune response in the host, give you a variety of clones to choose from, and be specific - it shouldn't bind other targets besides your protein of interest. There are lots of factors to consider, including antigenicity, solubility, ease of production (for immunizing and screening), steric considerations (does another protein or nucleic acid obscure the target site in vivo?), and others. Antigens can be roughly divided into two types - peptides (typically less than 20 or 30 amino acids) and proteins or protein fragments. You will most likely want to try several antigens to maximize your probability of success. After the antigen is synthesized and purified, you need to come up with an immunization schedule for priming and boosting the animal(s), then determine when and how to test them (screening), and at what time and how to harvest it for the monoclonal process.

The cloning process then comes next. Clones can be generated by a variety of methods, some widely available, such as the various hybridoma methods, and some proprietary to individual companies. My former company employed a mix of both, depending on the species of animal, using some really cool in-house tech that was constantly being improved and expanded upon. These processes are very dependent on the quality of materials being used and the expertise of the cloners. The input B cells (which make the antibodies) need to have been harvested, treated, and stored according to a set of precise steps to allow for the highest number of viable clones. Once the immortalized cells have been obtained (after fusion with the myeloma partner cells in the hybridoma process, for example) they are diluted to a pre-determined cell count and plated in 96-well plates and allowed to recover and grow for a time, during which they are secreting antibodies into the medium. This media is then tested quickly (before the cells overgrow the well), and positive wells are diluted out to (hopefully) single-cell suspensions and subcloned, or frozen down for later. The first testing is frequently by ELISA using the immunizing antigen, although depending on your application of interest it may be by high-throughput screening via flow cytometry, immunohistochemistry, or immunofluorescence. After the initial testing, subsequent steps of subcloning and re-testing can occur at a more measured pace, as the cells can be frozen indefinitely after generating sufficient quantities of antibodies in the supernatant.

This is where the quality of your screening program comes in. Your assays need to be well-designed, robust, well-documented and performed, and have appropriate positive and negative controls so that you can truly tell whether a certain clone is of interest, or performs better than an existing product. This means controlled conditions, standardized reagents and protocols, and a high degree of repeatability from assay to assay. Also, the appropriateness of your controls cannot be emphasized enough. Do you have a knockout or non-expressing sample for comparison, or a way of looking at baseline vs. induced or inhibited activity? For ChIP, unless you have a good control antibody and primer pair for your gene of interest, how will you know if the assay works? You may get a great result doing a straight immunoprecipitation-Western blot, but still not pull down DNA-bound protein. If your ChIP method doesn't produce clean DNA, you may never get binding. And if you don't have appropriate data analysis protocols in place with multiple replicate wells, you may waste time chasing noise instead of specific signal. Additionally, along with testing all your clones, you also need to titrate them to determine the optimal working concentration. I've seen a lot of antibodies that look like crap when you first test the supe, but diluted 100 or 1000X they are clean, specific, and still strong. Be patient, testing is a lot of work and requires a ton of repetition to confirm your results, but it'll be well worth it in the end.

Finally, after all this is done, you hopefully have a great clone that does what you want it to do, and better than anything else out there. You now need to decide what you're going to do with it, because if you're an academic lab and publish with it, the world will come knocking at your door. Don't slack off at the end and decide 100 ml of supernatant will be enough to last forever - save the clones and put them in a cell bank, or try to get a commercialization deal with a manufacturing company so you don't have to do all the work!

I hope this helps, please let me know if you have any additional questions or concerns.


It resembles Lantana Camara, from the family of Verbenaceae that is native to American tropics according to Wikipedia.

They come in variety of different colors, and the one you have photographed is the Pink Caprice.

Image Source: Cindy Dyer's Blog


What is the name of this moth found in Virginia USA?

Oh, found it. It is called a Euonymus Leaf Notcher Moth. It is an invasive species from Asia. It was first found in Maryland and Virginia in 2001.

http://www.insectid.ento.vt.edu/exotic-pests/euonymus/


How is sexual selection evolutionarily stable?

first off you are talking about runaway sexual selection, run away sexual selection works because attracting mates matters MORE than individual survival. An immortal survivally perfect creature that cannot mate is an evolutionary dead end and might as well not exist where its genes are concerned. A bright red neon sign on your back that draws  the attention of potential mates is an advantage as long as it attracts mates more often than it attracts predators. Coincidentally this is why so many sexual displays are things you can turn off, even a peacock can fold its tail fan down. These displays often exploit existing attention  factors, like eye shaped objects, bright contrasting colors, loud noises, ect, things organisms are already predisposed to pay attention to.  Of course once neon sign displays exist your second idea comes into play, once neon signs are in play a female is best served if her own male offspring and descendants also have neon signs, which makes attraction to the  neon signs (and thus the genes making them) an advantage.
For normal sexual selection both your ideas also come into play, likely more often. common attractive features are things like size, symmetry, health, or excess energy, direct signs of fitness.
Most of the time displays reaches a point of stability where the cost is balanced by the attractiveness, this is how most displays work.  But sometimes runaway selection can drive it past the point of no return, where the cost of reducing it is so high (lack of mates) the only winning strategy is to invest more and more, on and on until the cost is so high you never get a chance to mate.


Extra-mitochondrial conversion of Acyl Carnitine to Acyl CoA

The introduction to Ann N Y Acad Sci. (2004) 1033:17–29 lists the various carnitine acyltransferases and mentions CPT-1a, CPT-1b, CPT-1c (tissue specific) but states there is only a single CPT-2 in humans. It does not appear that there is any other variant, so extra-mitochondrial conversion of acyl carnitine to acyl CoA would require a post-translational variant of CPT-2, or CPT-1 working in the reverse direction.
The discussion of carnitine metabolism in Berg et al., Section 22, implies the reaction is near equilibrium. Hence, if the concentrations of substrate and product were appropriate it would be thermodynamically possible for CPT-1 to operate in the reverse direction.
Thermodynamically possible does not necessarily mean enzymically possible. I am not familiar with kinetic studies on CPT-1 and CPT-2, but imagine that CPT-1 has a higher affinity for acyl CoA and carnitine than for the product acyl carnitine, and that the reverse situation holds for CPT-2. I imagine that the ability of CPT-1 (or one particular isoform) to catalyse the reverse reaction in physiological circumstances would depend on its Km for acyl carnitine and the concentration of the latter. It might be worth seeing what kinetic analysis has been done.
The ‘appropriate’ situation for (2) might be if something were preventing utilization of acyl carnitine in the mitochondria of ‘target’ cells.
If you work in this area you will know better than me that there are various clinical conditions and sub-clinical conditions (e.g. obesity) that result in abnormal utilization of acyl carnitine. Could the abnormal instances you observe be for such individuals?


dNTP concentration for reverse transcription from RNA to cDNA

You will probably be fine. Lower dNTP levels might reduce the amount of product you obtained since it is usually the primers or the dNTPs that run out near the end of the reaction. The only other effect I am aware of is that the reaction might be slightly less specific as dNTPs sequester magnesium which is a big factor in determining the stringency of the reaction.

You say how many microliters you used but it would be more useful if you mentioned the concentrations of the dNTPs and the desired final concentration.


Im trying to find out what type of snail this is

I'm guessing it's an invasive apple snail, popular in fish tanks.

http://texasinvasives.org/animal_database/detail.php?symbol=15

https://www.youtube.com/watch?v=Pi2wcFPPJsI

Some people keep apple snails as pets, they are very interesting to keep for a while.

Your photo doesn't give enough info, location, sea or pond, clear image of shell, underside, soft body, to say for certain. apple snails have a wide variety of colors.


What benefits do sloths and manatees gain from algae growth on their fur/skin?

I don't know about manatees, but sloths have a symbiotic relationship with the moths living in their fur because the moths supplement the sloth's diet with additional nutrients via algae. Sloth moths grow and die in a sloth's fur, decomposing to provide nutrients for the algae. The sloth then eats the algae. What the moth gets out of this is that its larvae can feed on the sloth's poop, and when they grow up, they make a home in the sloth's fur again.

Here's an infograph summarizing the relationship: http://www.pbs.org/wnet/nature/sloth-named-velcro-sloth-moths-mutually-beneficial-relationship/11159/


Applying Constraint Programming to sequence alignment/analysis

First read how local and global alignment differ from each other. Then decide an objective function, i.e. how to measure the similarity between two sequences? Maybe use Hamming distance? Or Levenshtein distance? After this the optimization part probably comes out quite naturally.

Be sure to check the existing softwares. Easy things have been tried out already. (And by the way, for some reason biologists call n-grams as k-mers.)


Strictly speaking, all nucleated (eukaryotic) cells contain linear DNA. In addition to the nucleus, the mitochondria (which break down food molecules and create chemical energy) and chloroplasts (which facilitate photosynthesis) also have small stores of their own DNA and this DNA is circular. This adds weight to the hypothesis that these organelles were once prokaryotic cells that came to exist in symbiosis with early eukaryotes.

There is also cytoplasmic DNA free-floating in eukaryotic cells. These are also circular and normally contain short copies of chromosomal DNA sequences. Their function is not well understood.

In prokaryotes, some species of spirochaetes and bacteria have been found with linear chromosomes. In addition, prokayrotes contain extra-chromosomal DNA called plasmids. Bacteria are able to pass plasmids from one to another and express the genes on them: this is an important source of the spread of antibiotic resistance genes through bacterial populations. Plasmids are also normally circular, but linear structures also exist.

References:

Cohen, Sarit; Andreas Houben; Daniel Segal (2008). "Extrachromosomal circular DNA derived from tandemly repeated genomic sequences in plants". The Plant Journal 53 (6): 1027–1034.
Hinnebusch J; Tilly K (1993). "Linear plasmids and chromosomes in bacteria". Molecular Microbiology. 10(5):917-22
Finbarr Hayes (2003). "Chapter 1 - The Function and Organization of Plasmids".


Reasons why this protein is not suitable as an immunogen?

The article implies E proteins are quite different between the previous known strains - so a vaccine targeted against E protein may only affect a limited range of strains.

But when I do a BLAST search on CS079032.1 I find nearly all the protein sequences are identical (results below).


Can domestic breeding be considered evolution?

Yes, selective breeding results in evolution.

Definitions of evolution

I don't understand why you say that for 3 of the definitions you found, selective breeding would not be considered as evolution. To me, all of these definitions match with the idea that selective breeding results in evolution. If you think otherwise, can you please explain why?

There are a number of related definition out there, some of them being more clear and straight forward than others. The simplest definition is probably the classical population genetics definition which says

  Evolution is a change in allele frequency over time.

See wikipedia > allele. You might want to have a look at How to define evolution? too.

Under this definition, any event of death or birth in a population is evolution as it affects allele frequency. In the human species for example, that means an evolution happens about 254 times per second (computed from these numbers from ecology.com)!

Specific statements

All these statements are stupid and none-sense! The easiest is probably for you to just have a look at an intro course to evolutionary biology (such as Understanding Evolution by UC Berkeley for example) and you will be able to refute those statements yourself.

Let's go through these statements...

  There is no natural selection

First, evolution is much more than just natural selection. There is genetic drift, mutations, gene flow and plenty of interacting processes.

Second, it is silly to separate natural selection from artificial selection (aka. selective breeding). The only difference between these two is that in artificial selection someone is willingly affecting the environment of the individual to affect selection pressures. This is really it.

Note, btw, you never totally get rid of natural selection. Under selective breeding you may affect the environment but some things will remain the same. For example, a mutation causing the cell membranes to be extremely unstable will not be selected for whether under an artificial setting or a natural one.

  It doesn't direct towards 'fitness'

The claim is unclear. What is "it" and assuming it refers to a population, then what does it mean a population is directing toward "fitness"?

Fitness is a function of survival and fecundity. Each genotype is associated to a particular fitness in a specific environment. Ignoring stochastic processes such as genetic drift, the mean fitness of a population is increasing from one generation to the other by the amount of the additive genetic variance. This is true for (artificial or natural) selection.

The only thing to consider is that the environments under which this happen is different. Under selective breeding, the population evolves to a higher fitness for the specific environmental conditions set by the farmer (or who ever who selectively breed). It is possible (and quite common in fact) that genotypes associated with a high fitness under one environment has a low fitness under another environment.

  It does not lead to new species

In short, 1) it does lead to new species 2) the concept of species is often meaningless as poorly defined 3) evolution > speciation. In more details, below..

It does lead to new species. Different lineages of cabbage are considered different species. Cows and ox are different species. Pigs and boars are often considered different species. While wolves and dogs are considered same species, some lineages within this species (such as a Chihuahua and a Great Dane) are, I think, reproductively isolated. You might also want to have a look at the post Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
The question of whether selective breeding lead to speciation or not does not matter much on the question of whether it leads to evolution. Speciation is one outcome of evolution but is definitely not the same as evolution. Evolution does not need to lead to speciation. For example, evolution of the lactase gene in humans (see this post) did not lead to any speciation. It is still an evolutionary process.
The concept of species is mainly arbitrary. If you want to understand the concept of species, have a look at the post How could humans have interbred with Neanderthals if we're a different species?.

  It decreases, rather than increases, the size of the gene pool (is this actually true?)

The term "size of the gene pool" is very undefined. I suppose, it just means genetic diversity, aka. expected heterozygosity.

All act of selection, whether artificial or natural, decreases genetic diversity. This is correct. Mutations is the fundamental process increasing this genetic diversity and selection selects the variants associate with the highest fitness.

Because, the selection pressures imposed under selective breeding are often extreme, the decrease of genetic diversity via selection is often faster in selective breeding than in nature.

Note however, that if we split a lineage in two and select the two populations under different optimas, then the total genetic diversity will increased (the within-population genetic diversity will still decrease). As such, via selective breeding we created a gigantic diversity of dogs and a fantastic diversity of cabbage but each cabbage lineage (e.g. brussel sprouts) and each dog lineage (cocker spaniel) have very low genetic diversity.

What the claim is suggesting is that because selection is often stronger (and therefore change in allele frequencies is faster) under selective breeding than in natural environments, we should not consider artificial selection as resulting in evolution? How silly is that!


What bird is this seen trekking in Nepal during descent on Manaslu circuit?

You found an Alpine accentor (Prunella collaris). It's a bird of mountain areas in the Paleartic.

Here is a picture for comparison:

The only similar bird in the area is the Altai accentor (Prunella himalayana), but you can tell it apart because your bird does not have streaked flanks and the more uniform grey head (in your picture it is clearly visible the supercilium)


Is it possible to sequence only the 16S rRNA component? If so, how?

Basically, all 16S genes are highly conserved, i.e., they share much identical bases. This means one can bind the 16S gene piece (after DNA was cut) to a specific other piece of DNA, even if you don't know exactly the 16S gene bases. Everything else is discarded then. Now finally, using PCR the rest is amplified and sequenced. Sequencing 16S only is much less work, so that's how they did it years ago. Today, whole microbiomes are sequenced by professional labs.


What type of force holds my body rigid & doesn't make it collapse?

Adding on to what Martin said. If you imagine an atom to be the size of a football stadium, the nucleus would be the size of a fly on the fifty yard line. The vast majority of an atom is empty space.

In the 'classical' view, atoms are mostly empty space and the reason they feel solid is that if you try and push them, the electrons around your atoms bump into the electrons around the other atoms and because they're both negative they repel each other and push away. You feel this force as 'solid'. It's like pushing a really, really stiff spring or trying to force 2 magnets together, except it's electronic in origin.

In quantum physics, each particle has a wave function. Wave functions can only exist in certain forms, and when electrons are bound in an atom their waves spread up over a big volume (it's the only way mathematically to get a stable wave, ie an electron that exists. Since it exists, its wave function spreads out much further than the thing you classically think of as an electron).

Electrons have something called antisymmetric wave functions, which means they obey the Pauli exclusion principle:
http://en.wikipedia.org/wiki/Pauli_exclusion_principle

You can't have 2 electrons in the same state (and 'state' includes 'space'. You can have 2 oppositely spinning electrons, but no more in the same place). So atoms spread out because you can't squeeze the wave functions in. The rest of it is electrostatic repulsion just like in the classical model.

I'm sorry if that sounds a little complicated, but it's a combination of quantum physics (which doesn't really make sense, even though it works!) and electronic repulsion (from like-charges-repel).


Are stroma lamellum and grannum lamellum the same?

I will try to help. But, in the future, please post a picture of the confusing diagram to help us help you.

edit: now that I see your diagram, I'm not sure if this answer is helpful. Will re-consider and possibly edit this response. Thanks for including it!

Grana lamellae refer to the lamellae (membranes) in direct contact with photosynthetic stacks (grana), where the stroma lamellae are the ones that are connecting between individual stacks (see here). My understanding is that they are functionally and compositionally very similar, the only difference being the region of the lamellae in question (link to paper, sorry for JSTOR paywall). Check out the Wikipedia page for Chloroplasts for some more diagrams. Maybe one here will help this make more sense to you!


Jellyfish move by a form of jet propulsion and it moves in the direction that the head is facing. If it needs to change direction, it just needs to pivot and propel itself in the direction that it needs to move. Comb jellies (which are not really jellyfish) have cilia that beat continuously in the water for it to move forward. So water currents are not necessary. Here is an article with videos on how jellyfish move.


What is a "homologous pair" of chromosomes in cross joining or cross over?

The term sister chromatids refers to the pair of chromosomes which have been produced from a single parent chromatid by DNA replication, while a homologous pair refers to chromosomes which are more distantly related (e.g. those inherited from one's mother and father, which I guess is what you mean by 'male and female chromosome').

So the two options you give are identical, and neither are joined together by a centromere. The sister chromatids are joined by the centromere, while the homologous chromosomes exchange material during recombination (cross over).


Looking for the closest example of life forms similar to some mathematical patterns

For the second subquestion (papers or references of similar models), it could be useful for you to look at the books by J.D Murray for inspiration; Mathematical Biology, vol I & II. A pdf of volume 1 can be found here, and the second volume here. Even if they are a complete of years old (last edition from 2002 I think) they provide a really nice background to the field of Mathematical biology, and he has quite many examples on pattern formation of different kinds. I don’t remember if dynamics systems are included per se though.

However, several chapters include reaction diffusion systems and wave models, to model e.g. coat/fur patterns and wound healing. It is also packed with references, so you should be able to find lots of classic citations that might be useful.

Some chapters you might find interesting:

Reaction Diffusion, Chemotaxis and Non-local Mechanisms
Travelling Waves in Reaction Diffusion Systems with Weak Diffusion: Analytical Techniques and Results
Animal Coat Patterns and Other Practical Applications of Reaction Diffusion Mechanisms
Mechanical Theory for Generating Pattern and Form in Development
Bacterial Patterns and Chemotaxis

I've mostly looked at population modeling in his books, so I'm not very familier with these topics myself.


What is the name of this big plant with a purple trunk and green to purple berries?

The plant looks like Pokeweed (Phytolacca americana) to me, a common "weed" in the U.S.


The buffers are usually supplied with the electroporation instrument; at least Lonza provides buffers for different types of cells. Single cell electroporation techniques exist, but they have been mostly done on neurons.[1,2]

You can also try microinjection but it requires some practice. This study reports a transfection agent called VisuFect which can be used for zygotes as well.

I am not very sure about the success rate (AFAIK it is not that good) but I think it is anyway risky with organisms which do not produce a lot of embryos.


Exclusive microtubule minus-end labeling

γ-Tubulin is specifically localized to the minus end of microtubules. GFP labeled γ-Tubulin can be used to label the minus ends in-vivo and without the requirement of staining. Fan et al have developed a phage display antibody specific to α-Tubulin that can be used to visualize minus ends. See the figure below.

The image is an electron-micrograph but it is certainly possible to do a fluorescent microscopy after IHC staining.


Why can one swim longer underwater by blowing out air?

This is purely a psychological response, and it does not help in decreasing the speed of CO2 level rise. As CO2 level in your blood rises, you instinctively want to breath out the 'bad' air and breath in fresh one. The latter is impossible under water, but the former eases you psychologically a little; you have "started doing something" with your predicament of high CO2 level.

Most freediving courses (as well as my own experience - humble as it is) suggest not to have the last breath substantially larger than your normal one; this comes from people who train to achieve 6-7 minutes dives, so I would assume they meticulously tried various methods.

The key here is not to have a victory over physiology; the key is psychology. Most people fail at diving because they unnecessarily get into a positive feedback loop: they get excited, their brain and muscles become even more active, they produce more CO2, brain receives information about rising CO2 in blood, and it becomes excited even more, produces even more CO2, etc, etc, until a panicked diver surfaces or inhales water. Without such unnecessary excitation, each moderately healthy human would be easily physiologically capable of 3-4 minute dives.

My take is the amount of air you have in your lungs should be primarily the amount that eases your psyche the most and helps to stop needless stress.


What in the brain has gone awry during sleep paralysis?

Body paralysis occurs during REM sleep to keep your body from acting out your dreams.  You experience sleep paralysis when the mind awakens from REM sleep before the body paralysis has subsided.  I've had this happen before also, along with the "jolting" out of it you describe.  It usually happens when I'm very tired and trying to stay awake.  I try to stay calm but it's not easy as you know.  There is a good description at WebMD.


Is it better to maximize sleep, or align to ~1.5 hr cycles

Neither
Sleep cycles do not have a set length.

sleep for 7 hours every night and you won't interrupt a sleep cycle. 6 hours may be fine for a person but it is unlikely.

You feel tired when you interrupt a sleep cycle becasue many of the sleep inducing hormones are still present in your system.
http://apsychoserver.psych.arizona.edu/jjbareprints/psyc501a/readings/Carskadon%20Dement%202011.pdf

If you are sleeping different lengths every night (or say sleeping longer on the weekend) that will also make you feel tired. Normally your body adjusts the length of your sleep cycle to how long it predicts you will sleep for, if that is constantly changing however it cannot do this and you often wake up in the middle of a cycle making you feel tired. Sleep the same length of time for ~14 days and you will see your sleep cycle stabilize.

http://journals.sagepub.com/doi/abs/10.1177/1534650103259743

https://www.researchgate.net/profile/Martin_Moore-ede/publication/15765130_Human_Sleep_Its_Duration_and_Organization_Depend_on_its_Circadian_Phase/links/557881b308aeb6d8c01f1715.pdf

http://healthysleep.med.harvard.edu/healthy/science/what/sleep-patterns-rem-nrem


It depends on the altitude of the plane, species of ant, flight length, location in hold, and more, but generally yes, they should be able to survive. At such locations that a plane flies at, the temperatures range from 0 to -50 degrees Centigrade. At such extreme temperatures the ant's entire body system is brought to an almost complete stop, where their heart is barely beating, and nervous system barely functioning other than to tell the heart to beat, and other normal involuntary actions. This means they won't need to consume as much oxygen (because their slowed brain won't need as much) allowing them to survive with the minimal oxygen in the atmosphere.


Looks more like aglais io, the European peacock.  At any rate, oak and stinging nettle leaves are quite too dissimilar to make a crossover of comparatively specialized caterpillars likely.


Bioinformatics : Drawbacks of using ORA(Overlap Analysis)

It really depends on the specific methods you're using. If you're using a pathway-based methodology, I'd strongly recommend reading Khatri et al (2012) (1), which provides a good overview.

The main issue that's not touched on in that work is that pathway-based methods are highly dependent on the pathway definitions used, and the contents of the pathways are not always what you might expect in terms of their topology (a good example is KEGG's Neuroactive ligand-receptor interaction (2), which contains a huge number of events that look like 'single ligand binds to receptor', with no downstream events).


How does the age of a parent affect the chances of occurrence of certain genetically transmitted diseases?

In some studies, they have observed either positive or negative association between maternal or paternal age (the age of mother or father at the time of delivery) and earlier development of genetically predisposed diseases, such as diabetes type 1 and certain cancers, in offspring.

Diabetes type 1

Maternal age and diabetes in childhood (BMJ, 2010):

  ...the risk of childhood onset diabetes [type 1] increases with
  maternal age: 5% for each five years of age...the main explanations
  are that biological programming of the child is in some way affected
  by the age of the mother, or perhaps the father...

Cancer

Parental age and risk of sporadic and familial cancer in offspring: implications for germ cell mutagenesis (Epidemiology, 1999)

  We used the nationwide Swedish Family-Cancer Database to analyze the
  effect of parental age on cancer in offspring at ages 15-53
  years...Maternal age was associated with sporadic melanoma and
  leukemia, causing a 30% excess if mothers were more than 40 years vs.
  less than 20 years of age. A marginal effect of about 10% of both
  maternal and paternal age was observed for sporadic breast cancer.

  Paternal age increased the RR of sporadic nervous system cancer by about 15%. Accumulation of chromosomal aberrations and mutations
  during the maturation of germ cells may be a mechanism for these
  findings. In familial cancers of colon, melanoma, and thyroid, higher
  age showed an apparent protective effect, which was also noted for
  sporadic cervical cancer and melanoma.

Rheumatoid arthritis

Ages of onset suggestive of genetic anticipation in rheumatoid arthritis multicase sibships can be explained by observational bias (Rheumatology, 2007)

  There was no significant correlation between the age of RA onset and
  the maternal or paternal ages of conception.

Cardiovascular disease

In one study, they have found no significant association between maternal age and blood pressure in children. There seem to be no studies about the effect of maternal/paternal age on early-onset heart disease.

On the other hand, offsprings are at increased risk of developing a cardiovascular disease early if their parents had it early (PLoS One, 2016).

In another study, they have observed that maternal ages <25 and >45 have been associated with increased frailty index: a sum of 8 conditions (cancer, lung disease, mental health problems, diabetes, heart disease, stroke, blood pressure and arthritis)

Maternal Age and Offspring Adult Health: Evidence From the Health and Retirement Study (Demography, 2012)

  In summary, net of some obvious confounders, only maternal ages below
  25 and above 45 are associated with negative offspring health
  outcomes. (see Fig 1 and Table 2)

  The mechanisms thought to be responsible for the young maternal
  age–offspring health link are related to the physiological immaturity
  and sociodemographic disadvantage that often accompany young
  parenthood... On the other hand, the negative association between advanced
  maternal age and adult health is thought to be driven by the
  physiological reproductive aging of the mother.

In this study, they have not checked for the age of onset of diseases in offspring, though.


Is this experiment to check enzyme reaction rate according to substrate concentration correct?

I think there are a few important answers in your question

The concentration of enzyme is the same in each reaction chamber.  The volume of each chamber is 6ml, and you are using 1.5 ml of enzyme in a final volume of 6 ml, so the dilution factor (the same in all chambers) is 1 in 4. So if stock enzyme concentration is 4 micromolar (as an example), the concentration of enzyme is 1 micromolar in each reaction chamber.
The concentration of substrate varies in each reaction chamber.  You MUST take the dilution factor into account when calculating the final substrate concentration.  You do no tell me what the stock substrate concentration is, but if it is 1mM as an example, then in reaction chamber 1 you are taking 0.5 ml of a 1mM solution in a final volume of 6 ml, which is a 1 in 12 dilution.  The substrate concentration in the reaction chamber is therefore 1/12 mM (about 83.33 micromolar).  In a similar way, the concentration in the final reaction chamber (4.5 ml in a final volume of 6 ml, dilution factor of 1.33) is about 750 micromolar.
You are right, measuring the reaction velocity by taking a single time point after 3 minutes is dangerous!  You must of course measure the initial rate if you want to analyze results according to the Michalis-Menten equation. The assumption you are making is that the rate is linear over a period of 3.   minutes for all substrate concentrations.  If this is not so, you will need to redesign your experiment to take a number of time points and take the tangent to the curve. I think you must be interested in determining the Michaelis constant.
In the language of enzyme kinetics you are doing a discontinuous assay with a single time point after 3 minutes as a measure of the initial rate at a series of substrate concentrations.  A better approach if available is to use a continuous assay, for example by continuously monitoring the change of absorbance of NADH with time at 340nm.  But of course continuous assay not always available.
I am surprised that you use water to dilute. Where is the buffer? And how control pH in your chamber?  Maybe the enzyme and substrate stock solutions are made in buffer, is this the explanation?
You should also check that the velocity versus enzyme concentration is linear at all substrate concentrations.


How do the pharmacodynamics of the NSAIDs differ and are there "resistant" COX phenotypes?

This is a draft.

How do the pharmacodynamics of the NSAIDs differ - -?

Merck's manual ch. 36 to start little bit at an introductory level:

  The anti-inflammatory activity of the NSAIDs is mediated chiefly
  through inhibition of biosynthesis of prostaglandins (Figure 36–2).
  Various NSAIDs have additional possible mechanisms of action,
  including inhibition of chemotaxis, down-regulation of interleukin-1
  production, decreased production of free radicals and superoxide,
  and interference with calcium-mediated intracellular events.  Aspirin
  irreversibly acetylates and blocks platelet cyclooxygenase, while most
  non-COX-selective NSAIDs are reversible inhibitors.

and see the coming answer below.
These questions should be answered together.
To split them can be confusing.

Is there any difference in the degree to which these drugs manipulate/inhibit the enzymes (I assume their affinities for COX-1 and COX-2 are at least somewhat different)?

Please, see ch 1.03.3 in Comprehensive Natural Products II: Chemistry and Biology: 10 Volume Set:

and their conclusions about the structure

and please, see the whole chapter of the book, since its about the topic - and I think good one.

From Katzung et al.

  Selectivity for COX-1 versus COX-2 is variable and incomplete for
  the older NSAIDs, but many selective COX-2 inhibitors have been
  synthesized. The selective COX-2 inhibitors do not affect platelet
  function at their usual doses.

  On the other hand, selective COX-2 inhibitors may increase the
  incidence of edema and hypertension.

  To varying degrees, all newer NSAIDs are analgesic, anti-inflammatory, and antipyretic, and all (except the COX-2- selective
  agents and the nonacetylated salicylates) inhibit platelet
  aggregation. NSAIDs are all gastric irritants and can be associated
  with gastrointestinal ulcers and bleeds as well, although as a group
  the newer agents tend to cause less gas- trointestinal irritation than
  aspirin.

In short, there must be differences to which these drugs manipulate/inhibit the enzymes.
Please, see

Selinsky BS, Gupta K, Sharkey CT, Loll PJ. Structural analysis of
NSAID binding by prostaglandin H2 synthase: time-dependent and time
independent inhibitors elicit identical enzyme conformations. Biochemistry 40, 5172–5180 (2001).

Defining the COX Inhibitor Selectivity of NSAIDs: Implications for Understanding Toxicity. Expert Rev Clin Pharmacol. 2010;3(6):769-776. And see the chapter Expert Commentary which locates at the end of the publication there:

  Not withstanding the caveats on the merit of IC50 values, in vitro
  analyses of COX-1 and COX-2 selectivity of NSAIDs has driven the
  concept that inhibition of COX-1 explains the predominant reduction in
  synthesis of mucosal protective PGs and hence gastrointestinal
  toxicity of NSAIDs relative to COX-2 inhibition, which plays a role in
  ulcer healin

Merck's manual chapter 36

  The discovery of two cyclooxygenase isoforms (COX-1 and COX-2) led to
  the concept that the constitutive COX-1 isoform tends to be
  homeostatic in function, while COX-2 is induced during inflammation
  and tends to facilitate the inflammatory response. On this basis,
  highly selective COX-2 inhibitors have been developed and marketed on
  the assumption that such selective inhibitors would be safer than
  nonselective COX-1 inhibitors but without loss of efficacy.

Inflammatory processes are expressed by both COX-1 and COX-2 differently.
This means that a change in the cell membrane expresses lysosomal enzymes differently:

  The cell damage associated with inflammation acts on cell membranes to
  cause leukocytes to release lysosomal enzymes; arachidonic acid is
  then liberated from precursor compounds, and various eicosanoids are
  synthesized.

Also, the cyclooxygenase (COX) pathway of arachidonate metabolism produces prostaglandins, which have a variety of effects on blood vessels, on nerve endings, and on cells involved in inflammation. (See Merck, ch. 18)

I like the Figure 36.2 in Merck's manual.
To better answer your question, one could label the arrows there with relevant enzymes in each processes and compare those between COX-1 and COX-2 and relate to corresponding publications (only few existing!).

Adrenaline and other compounds activate the cyclooxygenase pathway, COX-1 pathway for instance, and the conversion of arachidonate to PGs and TXs. [2, p. 67]
The classic law of mass action allows to describe the reversible binding:

\begin{equation}
    [Protein] + [L] \rightleftharpoons^{k_{1}}_{k_{-1}} [Protein-L]
\end{equation}

where $L$ is ligand, Protein-L the protein-ligand complex, $k_1$ the rate constant of the forward reaction, while $K_{-1}$ the rate constant of the reverse reaction.
This fine regulation differs between COX-1 and COX-2 at enzymatic level regulated by cytokines.

COX-1 becomes only little activated in inflammation, in comparison to COX-2.
COX-2 is present in macrophages (chronic inflammation! - cytokines), fibroblasts, endothelial cells, synovial fluids, and chondriocytes.

[A]re there “resistant” COX phenotypes?

I have not heard about this that there would not be.
There are so many components in PGHSs which can develop resistances.

[A]re there any known phenotypes of COX-1 and COX-2 enzymes that are present in the general population that affect the ability of these drugs to act?

Please, see for the phenotypes of COX-1 here, while about COX-2 much less has been research, see here - no known phenotypes, see this.
Please, note also that COX has at least two isoforms: COX-1 (PGHS-1) and COX-2 (PGHS-2).

COX-1 phenotypes

176805, here

Is there any evidence as to whether the the NSAIDs collect in certain areas of the body in a compartmental fashion?

No.

Each disease has its own characteristics.
Gout, for instance, has swelling of syvovial joints and usage of NSAIDs with COX-2.
My professor of abdominal surgery answered to this question directly - impossible to answer generally which I agree with her. (17.10.2014)

I think the OP has in mind some antibiotics which concentrate in some parts of the body (such as 1st generation quinolones concentrating in the renal tubules and bladder, thus exerting local antibacterial effect).
There is no similar effect with NSAIDs.

Instead, NSAIDs have local and systemic effects, not because they are concentrating in some parts of the body, but because they have several mechanisms itself.
Please, see this thread about Effect of NSAIDS on stomach.

Are there differences in fat solubility, etc., between the different drugs?

Fat burner - of course, there are differences in fat solubility between different NSAIDs.
Please, see this publication Solubility of Nonsteroidal Anti-inflammatory Drugs (NSAIDs) in Aqueous Solutions of Non-ionic Surfactants.
I will update this part next week more.

Other sources

Basic and Clinical Pharmacology, 11th edition, 2009, Bertram Katzung.
My notes during Biochemistry classes in Tartu 2011-2013


Microchimerism, as defined by wiki, is the presence of a small number of cells in an organism that are genetically distinct, and originated from a separate organism. The example they give is an unborn child and the mother can 'swap' immune cells, and retain these for many years.

Your question about which parts of the genome are transferred is therefore not really valid, because the cells are transferred, rather than bits of genetic information. Therefore 'traits' are not transferred either, but distinct immune cell lineages can be transferred and persist - this can confer an immune advantage, so this 'trait' could be said to have transferred, but no genetic information has been swapped by the cells.

Although it does not say it on wiki, this presumably only applies to cells of the same species, but a different organism, otherwise infections would also count.

Update 20th July 2012

The New Scientist article you have linked to in the comments can be found online here.

It says that we may be more microchimeric than we imagined, because a recent study in Blood found that half of the mothers studied were positive for male T-cells (Dierselhuis, 2012). The authors note that it is remarkable that the immune cells from neither the parent or the offspring attack the other, and that this may explain the observation that siblings make better donors.

Another finding that mothers are found positive for cells from their own mothers, and even their own grandmothers, and that the cell numbers increase during pregnancy (due to clonal expansion of the inherited immune cells) reinforces the opinion that microchimerism is commonplace (Gammill, 2011).

So to reiterate, immune cells can be inherited from your mother, and she may also end up with leukocytes from her offspring, which can in turn be passed on. This is a very fascinating way in which the immune system seems even more complex and helpful.


Assuming that you are looking at data used to describe the differences for a new individual, as opposed to a human reference genome build:

A fastq file is the typical format of data from a sequencer.

It would require a text field of some sort as they can be quite large, even for single reads.  If you had a specific sequencer in mind with very short read you might use a fixed length field for the data column, but its probably not worth it.

After the data is processed, then the data is currently usually exchanged in the form of Variant Call Format files (a vcf file) which only documents differences versus a reference genome build.  This fits nicely into an SQL table with relatively small columns.


As jamesqf points out in comment, "the less we use it the longer it lasts" isn't always true even of machines. Sometimes if a machine isn't used, the moving parts start sticking together through rust or other decay processes, which does not happen when the machine is used and the moving parts move regularly against each other.

Another example that comes immediately to mind is a hybrid car, which needs to be driven regularly or the battery runs out. Granted this doesn't affect the car's longevity (I think?), but it is another example where use maintains functionality better than disuse does.

This is even more true when we actively maintain machines, fixing them as they break, replacing parts, oiling, etc.

The key point here is that decay is inevitable. It is a law of thermodynamics, and it doesn't care whether something is in use or not. Granted, things will sometimes decay faster if they're used, but not always, and they'll always decay either way. The only way to forestall decay is active maintenance. This isn't contradictory with decay being inevitable, because you can actively maintain something only for so long (it takes work and energy).

This is relevant to biological system because that is how our body works: it is constantly self-repairing and self-maintaining, for the length of the person's life. One reason we die is that it stops doing so as efficiently as one ages. But as long as we are living, these processes mean our bodies aren't a static object: they are a dynamic system that is constantly reacting to outside and inside stimuli. And that system, including the self-repair mechanisms, are set up such that they work best within a certain range of motion and activities. It so happens that range doesn't include "no motion or activities". Likely because we evolved as an active species, so being able to function efficiently when active is useful, and some of the things that make us able to function efficiently when active can cause some harm when we aren't. For example, we store fat in order to use it when food isn't available and as fuel for effort, but if too much of it accumulates it has effects on hormones and inflammation that our bodies don't deal with well. Another example is how our muscles waste away when we don't use them; this is useful for an active species that needs the muscles it uses and shouldn't waste energy and protein on those it doesn't, but an inactive species might be better off conserving its muscles through periods of inactivity, so that they would still be capable of moving well those rare times they do need or want to.

Having said that, look at high-level athletes getting injured, getting early arthritis, etc... It is possible to exercise more than the body's self-reparation abilities can handle, and that also leads to health problems down the road.


Detecting cancer or a genetic predisposition based on DNA sequencing

When sequencing a human's (i hope im stating this correctly) genome is
  there a difference between the genome before and after the patient is
  found to have developed some sort of cancer.

If you are asking if cancer cells have an altered genome as compared to the rest of the organism, yes, this usually is the case.

  What would be a method for determining whether or not a patient has
  cancer based only on a genomic-sequence.

If you scrape some cheek cells to do DNA sequencing, you will know what the sequence is in those cheek cells, and you can figure that most of the cells in the rest of the body have that same sequence.  But if some, say, brain cells have acquired genetic errors causing them to start going haywire, that won't magically change the DNA in your cheek cells.

A genetic predisposition could be identified...if scientists had determined one.  For instance, Angelina Jolie got a double mastectomy because both her family history and her genetics strongly indicated that she would get breast cancer otherwise.


How do you calculate or predict the charge of a protein at pH 7?

ExPASy to the rescue! Although I didn't comb through all the tools, this nifty website provides quite the myriad of bioinformatics resources which most certainly contains the tool to calculate what you want.

Bear in mind though, most tools will tell you the isoelectric point of your protein. However, bearing in mind the relationship between pI and pH (i.e. if pI < pH, then protein is - charged, and vice versa), you can easily figure out the charge of a protein at pH 7.

http://expasy.org/tools/

*Update

Here's the exact tool to calculate isoelectric points: http://web.expasy.org/compute_pi/


The speculations are right.

Topoisomerase I changes the linking number by changing the number of twists and Topoisomerase II changes the linking the number by changing the writhe of DNA.

Confirmed by a college professor.


I think the Global Biodiversity Information Facility (GBIF) may be what you are looking for https://www.gbif.org. It is not limited to plants and insects.


How is mRNA directed out of the nucleus to its ultimate cytoplasmic location?

There is a complex progress involving many proteins that directs RNAs to the nuclear pore complex and ensures that they are moved into the cytoplasm. Below is part of a diagram (edited) from a Nature review article on this topic, showing the transport of mRNA. It is available from the authors online.

Another general review with an illustrative poster is by SR Carmody and SR Wente, and can be found in the Journal of Cell Science.

As far as I am aware, interaction of mRNA with cytoplasmic ribosomes occurs by diffusion. Direction of the ribosomes to specific locations, such as the endoplasmic reticulum, can occur, but is generally through recognition of features of the nascent peptide after tranlation has started. The Wikipedia article on protein targeting provides an introduction to this area.


What inhibits linkage between actin and myosin filaments

I am not sure if you are referring to a mechanochemical cycle of "stepping" of a myosin molecule along an actin filament, or a cycle of contraction and relaxation of a muscle cell as a whole. These take place on completely different timescales and control the binding and unbinding of the two proteins in entirely different ways.
In the mechanochemical cycle, there are no proteins directly involved other than actin and myosin themselves, and the breaking and re-formation of contacts is controlled by the nucleotide occupying the ATPase site of myosin. ATP binding leads to a low affinity (weak interaction) state and ADP binding leads to a high affinity (strong interaction) state. ATP hydrolysis and nucleotide binding/unbinding "power" this cycle.
The cycles of contraction and relaxation of the cell occurs on a much longer timescale--each contraction involves many repetitions of the actin/myosin "stepping" cycle across many actin and myosin molecules, while relaxation involves slowing or stopping this cycle. This is where calcium and the troponin I/C complex come in--they are a "switch" that allows the stepping cycle to happen or not. So when the calcium is low and the troponin complex is bound, the actin/myosin interaction is continuously disengaged, whereas when calcium is high and the troponin complex releases, the cross-bridges form and release in a cyclical manner as ATP binds to myosin and is hydrolyzed.
As an analogy, think of a person walking across a room full of chairs. As the person is walking, his feet alternately make and break contact with the ground, and this is due to the coordinated movement of the legs. If the person sits down in a chair, then his legs stop propelling him entirely for a while and are still, and this is like when calcium is low in a muscle cell.