MSA Tools

compare the amino acid sequence of protein 1 with nine homologous proteins and make a multi-alignment of the sequences.

EBI have a portal for many MSA tools and there are also other MSA tools available elsewhere.
In research, it's good practice to use several alignment techniques and look at which generates sensible indels. Usually, this is the lowest number of indel events.
Clustal Omega is probably the most sophisticated MSA tool hosted on the EBI site, however, it is relatively new and isn't as established as T-coffee or MUSCLE.
Note that these tools are updated fairly regularly. This question and top answer about "cutting edge" MSA tools from 2014 refer to a paper from 2011 that attempts to benchmark MSA tools. As you can imagine the state-of-the-art tools change rapidly (for example, clustal-w2 was released, and now clustal omega since that benchmarking paper). For most researchers though, it's a personal preference, and different MSA tools are "better" for different situations (speed of computation, number of alignments, similarity of sequences, complexity of secondary structure, local vs global alignments etc.).
Consensus sequence

Determine a consensus sequence for the proteins based on the
multialignment.

This depends entirely on the information from your alignment.
A common way to make a consensus sequence is to just take the most abundant residue at each position in the MSA. I don't like this approach because it heightens the significance of abundant residues, and diminishes the appearance of less abundant residues. This distorts the biochemistry and can easily lead to sequences that would be impossible or useless in biology. I would always rather see a raw alignment.
Conservation amongst alignments

Find any specific parts of the proteins that are conserved, then explain why these parts are conserved.

Conservation usually implies function, and hopefully you'll have a homologue that has a categorised function. Perhaps in your case one could attribute this function to a conserved sequence in the other homologues.
One brilliant tool is called consurf.

You can upload your MSA file to it and it will colour code regions of conservation from purple to blue. A purple region implies an evolutionary selection to not change that region, implying that it is a "functional" region.
Consurf works better with more sequences, so perhaps it isn't appropriate for this project. Instead try loading the alignment in Jalview and show "sequence conservation".

Caution.
When performing an MSA remember that the algorithm assumes that the sequence is homologous and that assumption can produce errors. If it looks wrong, it probably is!


Is it possible to re-align of SAM/BAM files?

Looks like I solved it by using PICARD: extracting the aligned reads but without sorting, I used

java -jar picard.jar SamToFastq I=<file_alnMAP.bam> FASTQ=<filemap_1.fq> SECOND_END_FASTQ=<filemap_2.fq>
bwa mem -R <read_group> <ref2.fa> <filemap_1.fq> <filemap_1.fq>

From samtools flagstat the output looks fine.


Yeast can produce up to 16-17 v/v% ethanol without dying according to this article. Yeast is a primary industrial ethanol producer, it produces ethanol even under aerobic conditions, in contrast to bacteria that usually ferment sugar to ethanol under anaerobic conditions. Bacteria can also withstand up to several percent v/v concentration ethanol in their media. Check this paper for details. They produce ethanol because it is a natural byproduct of their cellular metabolism. Under anaerobic conditions sugar as the primary energy source cannot be oxidized and utilized as well as in aerobic conditions.

  Alcoholic fermentation converts one mole of sucrose into two moles of ethanol and two moles of carbon dioxide, producing two moles of ATP in the process.

from: http://en.wikipedia.org/wiki/Ethanol_fermentation

Anaerobic bacteria follow this path because fermentation of ethanol does not require oxygen. This byproduct is secreted from the cells. In natural environments ethanol either dilutes in the media bacteria live in or can be taken up by acetic acid bacteria and used as an energy source.


Are codons that map to the same amino acids interchangeable?

I think given that you're just getting started with genetics, you can say that the codons are interchangeable. This is generally true, though not technically correct. Here are a few reasons for why this is the case, though there's probably more:

Specific organisms use specific codons with different frequencies. This is usually related to the tRNA abundance in the cell. Using a codon for which there is relatively less tRNA available would be expected to lead to a decreased protein synthesis rate.
Using different codons can affect mRNA secondary structure, which could affect expression.
Some codons, especially stop codons, can influence translation contextually through a process called recoding. This can include frame-shifting, read-throughs, cleavage or, perhaps most famously, coding for the amino acid selenocysteine and much more. See here.
Different codons can also influence translation contextually through pausing. This affects the rate of protein synthesis as well as its folding. See here.
Changing codons can affect regulatory sequences such as miRNA binding sites. Though these are usually present in the UTRs, they can also occur in the CDS.


Bacteria or other microorganisms cannot really grow on anhydrous (totally dry) glucose because they need water.

However, they can remain there and cause contamination. Even if you haven't actually touched the glucose sample, there are many bacteria suspended in the air and they may settle down in your glucose packet. When you take the glucose out for weighing, then also bacteria that are in the air, on your gloves, on the paper that you use for weighing, can settle on the glucose sample. In fact any substance, for that matter (salts in PBS, water etc).

That's why before using solutions in cell culture, you have to sterilize them by autoclaving or filtering. Glucose solutions should not be autoclaved because the heat chars glucose. You should filter them using a 0.2 micron filter. All the materials that are to be used for cell culture purposes should be opened only inside the laminar hood.


Talcum powder was originally finely powdered talc, a rock, but talc is technically in the same mineral family as asbestos, it is completely harmless and not the same as the dangerous mineral used in insulation at all, (it is actually used as an additive in table salt). But some early talcum powder did contain actual asbestos, as does industrial talcum* today, this only made it more confusing. Manufacturers that used talc took a lot of flack during the asbestos scare (you tricked me into putting asbestos on my child), there were many lawsuits.  Corn starch is now used as a replacement for talcum powder in many many things labeled talcum powder, baby powder, or body powder.

The cornstarch is acting as a carrier/filler, so no its probably not the best thing because the fungus can metabolize it and it does not need to be there but the companies prefer using it to dealing with misinformed disgruntled buyers.

*talc and asbestos often occur in the same deposits.


Are chromosomal and plasmid DNA in the nucleoid?

"Nucleoid" (literally means nucleus-like), is a quite old term for "bacterial chromosome" (Better to write prokaryotic chromosome since in both type of prokaryotes i.e. Archaea (former archaebacteria) and bacteria (former eubacteria) the structure is similar).

Nucleoid structurally normally excludes the plasmid-DNA (the plasmid DNA is like additional or accessory). However sometimes a plasmid DNA could go through recombination with prokaryotic chromosome 's DNA (As seen in Hfr strain of Escherichia coli)

"Chromosome" in very brief means a structure made of DNA + Protein. In case of "bacterial-chromosome",  it contains both DNA and Protein; and if you take away the protein from bacterial chromosome; what you get, is the chromosomal DNA.

Reference:

Microbiology / Pelczar, Chan and Noel/ Edition-5;

Part 2: Bactria,

Chapter 5 (Morphology and fine structure of bacteria)

  "Because it is not discrete nucleus, this nebulous structure has been designated by such terms as the nucleoid , the chromatin body, the nuclear equivalent, even the bacterial chromosome"

General Microbiology / Hans G. Schlegel / Edition-7:

Chapter-2 ; The cell and its structure:

2.2 The prokaryotic cell (protocyte) -> 2.2.1: The bacterial 'nucleus'

  " Plasmids : In addition to chromosomal DNA, many bacteria contain extrachromosomal DNA in closed, circular, double stranded form. These autonomously replicating DNA elements are called plasmids. Linear plasmids have been found in some bacteria"


What determines the colors and patterns of a clam shell?

This post is pretty well written and seems to say that the evolutionary forces that produce shell color like this is not known.  There are suggestions that the color is camoflage or the result of metabolic byproducts or that the pigments serve to strengthen the shell.  Its hard to believe some of these theories given that some shells do fine without coloring (at least that humans can see).

Structurally, shells are living things.  [They consist of many layers of thin irregular calcium carbonate hexagonal plates that make the mineral portion of the shell. The plates are held together by a protein glue and renewed by cellular action][3].  Whatever their evolutionary motivations, the colors are biomolecules which are in the biomatrix binding the plates together. This is a reason that shells that are left out to dry in the sun can become bleached and brittle.

I wish I had some better references about the shell structure, but I'm remembering a lot of this from a one afternoon book report given in a class, not from any intensive study on my part.

This has influenced some ideas about things like tank armor, by the way.  At least there is funding for biomaterials research by agencies interested in tank armor.  Lamellar armor made of segmented plates can withstand tremendous impacts at a single point like a shell being dropped from a great height by a seabird or a shell hitting a tank. Plates just a few microns wide and a fraction of a micron deep shaped like irregular hexagons are hard to make if you aren't a mollusc so far though.


Is it essential to add cholesterol to agar or liquid culture for C. elegans?

C. elegans needs cholesterol, but can't make it. Since bacteria don't make cholesterol either, the food bacteria aren't a source. As explained in the linked paper,  lack of cholesterol affects normal development.


Where does meiosis II of oogenesis end exactly in tuba uterina - uterus?

The location is exactly tuba uterina infundibulum, source, since the processes results in the following things before LH peak:

  The correct placement of the uterine tube infundibulum upon the
  ovarian surface
  The rupture of the follicle wall and the flow of the
  follicle fluid with the oocyte into the infundibulum
  The inhibition of
  the maturation of further follicles


When you say, why don't we see more sexually reproducing species than asexual, I presume you are referring to bacteria, protists, archaea, some fungi, etc.

Most multicellular organisims do reproduce sexually, which makes sense since an organism would need to be multicellular to have cells specialized for gametes. As you stated, the advantage is that sexual reproduction offers an advantage by allowing more rapid generation of genetic diversity, allowing adaptation to changing environments.

However, look at the single-celled organisms that reproduce asexually. Asexual reproduction is beneficial in many circumstances in that it can create individuals rapidly and in large quantities. For example, yeast can duplicate every hour under the proper conditions. For yeast, that means survival by sheer numbers. For us, it means we can make bread in a few hours.

If you believe asexually reproducing organisms are at a disadvantage due to lack of genetic diversity, consider bacteria and antibiotic resistance. The rapid generation times allow mutations to be selected for in particular circumstances. Penicillin was introduced in 1941. Two years after this landmark event, strains of Penicillin-resistant S. aureus had already emerged. Now, perhaps 2% of Staph. aureus (SA) is susceptible to penicillin, and some SA are "superbugs" with multidrug resistance: good for Staph, bad for us.

Also, it is possible for single-celled organisms to "share" DNA through mechanisms sometimes likened to sexual reproduction; lateral gene transfer occurs through conjugation, transformation and transduction.

Thus, both asexually and sexually reproducing organisms are well-suited to their ecological niches.


Why did many species of Homo and their ancestors evolve in East Africa?

The question is based on a false opinion but I'll get back to that at the end.

Humans are still evolving

  Why did all species of Homo evolve in Africa first?

Humans are evolving all around the world. Evolution is not a thing that stops once we made the arbitrary decision of naming a lineage. When we first named humans, Homo sapiens sapiens, indeed the lineage was living in east Africa.

Humans is a lineage of Old World Great Ape

  One thing I find interesting about the theory of evolution is the idea that Homo Neanderthalis evolved in Africa

It would help if you could explain why you find that particularly interesting. It is possible that some falsy teleological view of evolution you may have might push you to make some unexpected conclusion from the idea that first Homo lineages lived in Africa (but might be wrong in your understanding of evolutionary processes). In any case, you can find an very introductory course to evolutionary biology here if you're interested.

If humans were a species of feline, it could have evolved elsewhere (it would look very different to what we currently call humans of course) but humans is a lineage of old world great ape. Old world great ape lived mainly in Africa. There is not much more to say about it.

  why Africa did Africa encourage evolution more than other areas of the world?

Africa is a continent. It is big! You can find pretty much any biome in the world in Africa (except toundra and taiga if I am not mistaken). Did the specific location where humans lived in Eastern Africa affect their evolution. Yes, the evolution of a population is always affected by its surrounding. For example, the presence of large game was probably a big selection pressure for cooperative hunting (but you can/could find large game everywhere).

It will be near impossible to answer in the general sense. A lot of things happened in human evolution. Even if you tackle down to a single trait, it will be hard to tell you what would have happened if the world would have been different because it was not. (WorldBuilding.SE welcomes questions like "if it was like that what would have happened?").

Origin of Homo lineages

There are a number of named Homo lineages, some of them have not lived in Africa. This include for example Homo floresiensis.


What is special about the N3 buffer for Qiagen minipreps?

The Qiagen manual for the Miniprep Kit states that buffer N3 contains guanidine hydrochloride and acetic acid. The MSDS for buffer N3 gives a bit more information:

Guanidinium hydrochloride 25-50%
Acetic acid 10-25%
pH 4.3

Buffer P3 uses 3M potassium acetate, the potassium is usually important in plasmid preparations as potassium SDS is used to precipitate the proteins in solution.

This information might be enough to create a buffer that should work with the silica-gel columns.

I also found a patent about a method for isolating nucleic acids that states that silica particles can bind nucleic acids in the presence of chaotropic salts, so the guianidinium hydrochloride is probably the important difference in the N3 buffer.

The patent for this method from Qiagen goes into even more detail, according to this the buffer composition  is:

N3: 4.2M guanidinium hydrochloride, 0.9M potassium acetate, pH 4.8


You have done the calculation correctly it is just the answer you have is in hours, try dividing by 24.

A  good method of checking answers is to use a trick which is horribly called "Dimensional Analysis". This basically means writing out your equations but use the units of each value rather than the value itself

so in this case you have T1/2 = Vd/Cl      (removing the unitless 0.693)

the units for this are then ? = (L/kg)/(L/hr/kg)

in this case the litres and the kilos cancel to 1/(1/hr) or just hours, comparing this with the correct answer which is in days should then be a little more obvious


Meaning of a negative value for non-fiber, non-sugar carbohydrate based on a nutrition label

The values on the nutrition label from the question (11 g total carbs, 9 g sugars, 3 g fiber) could be actually explained by rounding:

Total carbohydrates: 11.45 (rounded to 11)

Sugars: 8.55 g (rounded to 9 g)
Fiber: 2.55 g (rounded to 3 g)

...which would mean there are additional 0.35 grams of non-sugar, non-fiber carbohydrates...

...BUT...

...using such a label with only rounded values (and students not knowing the exact values), does not make it possible for students to calculate the amount of non-sugar, non-fiber carbohydrates.

So, another explanation is that there is an error in either total carbohydrates (11 g - too low) or in sugars (9 g - too high; more likely 6 g), according to NutritionData for 150 grams of raw onion:

Total carbohydrates: 14 g

Sugars: 6.4 g
Fiber: 2.6 g

In either case, it seems they have used a nutrition label that is inappropriate to ask a question about the amount of non-sugar, non-fiber carbohydrates in raw onion.


The optical density measurement is the quantity of living and non-living cells in a sample. The colony forming unit measures only the viable cells in a sample. An OD 600nm is equivalent to approximately 8 x 10^8 CFU/ml. However, this is only an approximation and cannot fully take into account the dead cells the OD may be reading, it also depends on the microorganism that is being researched. A standard curve can be calculated from data, but it is quite difficult to attain an exact result.
A very useful article on the correlation between the two measurements can be found here (from the Brazilian Journal of Microbiology).


Check these out. They provide the functionality that you want:

ApE
SnapGene viewer


Birds do groom, but not like mammals do. People tend to call their grooming behavior preening. Preening removes dirt and parasites, arranges the feathers nicely, and distributes oils over the feather (very important for waterfowl.)

To answer your question better, we need to look at the specific species. Lots of birds preen each other socially, so if you wanted to pet a bird (in a way it likes) it's good to know how the species behaves.

You mention crows and owls. Crows are social so they may preen each other; they're also sophisticated (cultural) so it's hard to generalize. A 'bird nerd' on YouTube shows convincing footage of such behavior. I think family groups of crows preen each other, but I don't have a source.

Owls tend to be solitary and would not understand preening behavior from a human. A social species of owl might preen; I don't know. Of course, if you just go ahead and pet your owl like a dog, it may appear to like it. It's hard to say if it does like it...it's easy to anthropomorphize a bird with binocular vision!


Can plants grow under extreme (>1%) carbon dioxide concentrations?

Yes they can, but their normal growth is somewhat impaired. A study by Bugbee and collaborators showed that while the yield of rice and wheat increases with CO2 up to about 0.1% CO2, yield decreases sharply as CO2 climbs from 0.1% to 0.25%. There is a smaller loss in yield as CO2 is further increased from 0.25% to 2%.

One interesting thing to note about the study is that the above results turn somewhat on how "yield" is defined. Bugbee defines yield in terms of the mass of the parts of the plant that people can actually eat. They make a note in the study that the vegetative growth of the plants (the green leafy parts humans can't eat) was not affected by the jump from optimal to super-optimal CO2 levels.


What does this equation about DNA replication mean?

The notation you are referring to is a way to express the elongation of a nucleotide strand (Fig. 1).

dNTP + dNMP(n) → dNMP(n+1) + PPi

means

Existing strand  +  deoxynucleotidetriphosphate  →  elongated-strand  +  pyrophospate.

Fig. 1. Elongation of DNA. Source: Concepts in Genetics.

This reaction holds for DNA replication as well as transcription.

Translation is all about protein synthesis from amino acid precursors. Each subsequent amino acid is coupled to the growing peptide by a peptide bond between the carboxyl of the growing peptide and the amino group of the new amino acid. A water molecule is eliminated during the reaction (Fig. 2).

Fig. 2. Peptide bond formation. Source: An Introduction to Molecular Biology

Hence translation can be written analogously to replication as:

amino acid + peptide(n) → peptide(n+1)

However, also in this polymerization reaction energy is needed and amino acids are activated while they are bound to the messenger RNA (mRNA) through the action of ATP. Moreover, during translation the ribosome (i.e., the protein synthesizing machinery) uses another source of energy to move across the RNA template, namely GTP. Hence, the net reaction can be written as:

amino acid + peptide(n) + ATP + GTP → peptide(n+1) + AMP + GDP + PPi + Pi

Note that this notation in itself is not a dogma as other ways are in use to denote DNA and RNA synthesis. According to Merriam-Webster a dogma is:

  A belief or set of beliefs that is accepted by the members of a group without being questioned or doubted.


There are many meanings of "factor" in Biology. In the context where you place it, namely bio-active substances, such as hormones and enzymes I would go for the definition given by the Medical Dictionary:

  factor [fak´ter] :
  an agent or element that contributes to the production of a result.

Within this definition, a transcription factor contributes to the transcription of DNA into mRNA, and nerve growth factor contributes to the growth and survival of neurons.


The U.S. Food and Drug Administration (FDA) has the following information regarding the risks of ultrasound imaging;

Ultrasound imaging has been used for over 20 years and has an excellent safety record. It is non-ionizing radiation, so it does not have the same risks as x-rays or other types of ionizing radiation.
Even though there are no known risks of ultrasound imaging, it can produce effects on the body. When ultrasound enters the body, it heats the tissues slightly. In some cases, it can also produce small pockets of gas in body fluids or tissues (cavitation). The long-term effects of tissue heating and cavitation are not known.
Because of the particular concern for fetal exposures, national and international organizations have advocated prudent use of ultrasound imaging. Furthermore, the use of diagnostic ultrasound for non-medical purposes such as fetal keepsake videos has been discouraged.

FDA > Radiation Emitting Products > Medical Imaging > Ultrasound Imaging
Further information

I had a bit of a look through PubMed and Scopus for any papers relating to ultrasound risk, but didn't find any.


Why fingers in human fists get folded in absence of neural stimuli?

I would assume that as a result of the lengths of the tendons and the arrangements of the various flexor + extensor muscles, the slightly folded positions (curved) fingers, hands, legs, etc. are the "default" positions, in which both antagonistic muscles are in their relaxed state (thus without neural stimulation)
The evolutionary benefit of the slightly curved fingers, hands, legs, etc. may have been more relevant in our primate ancestors than it is today


Is there any difference in terms of personal healthcare between complete DNA sequencing and SNPs genotyping?

This difference would have the greatest impact on treatment for cancer, in which a treatment protocol is based on genes deleted, amplified, altered in the tumor vs the reference genome for that patient.

In terms of health risks based on SNP genotypes, the data are far from complete. Sure, some level of risk can be assigned to a variant (SNP), say at certain markers within the FTO gene and risk of obesity. However, the complete list of risk alleles for this and numerous other complex traits is not fully described. Furthermore, the impact of environmental factors (EF), or lifestyle choices, on those genetic variants is only beginning to gain wider attention. For example, a risk allele may not show itself as risk until the EF, such as amount of physical activity or percent energy from dietary polyunsaturated fat, passes a certain threshold. Such gene-environment interactions are thought to contribute to the variance in traits (phenotypes), but to what degree is not known.

Added in edit 15 May 2012: Epistasis, or gene-gene interactions, also are important but far from being cataloged for humans. A situation could arise where one allele elevates risk for a certain condition, but compensatory alleles elsewhere in the genome decrease that risk. We don't know the full extent of epistasis in humans.

Thus, in terms of personal healthcare outside of something like cancer and monogenetic disorders, there may be little that is gained from genotyping or complete genome sequencing, little that is compared to other advice you already know. I carry risk alleles for certain conditions, but there is not really any advice one can give me that is specific for those alleles that I have, where that advice is different than or goes beyond general advice health care providers already have dispensed.


Is it possible to fuse DNA from two sperms into one sperm?

It would be theoretically possible to engineer such a cell, but something very similar can occur in nature, two sperm cells can fertilise a single egg cell, resulting in a fetus with DNA from both. See here


If animals aren't getting tooth decay because they don't eat processed foods, could similar work for humans?

I think your assumption is wrong : Our small mixed breed had to have all her teeth pulled in 2 operations a year apart. The caries were so bad it damaged her kidneys.  i have had other dogs with caries but not so severe .


Coefficient of relationship and path of coefficient

The expression $f = 2h-1,$ coefficient of inbreeding (COI) is a measure of homozygosity. Since in a randomly breeding herd (of cattle) we expect 50 per cent heterozygous and 50 per cent homozygous, the minimum for $2h-1 $ is 0. If the cattle's genome is purely homozygous (aa, AA) we have $2h-1 = 1.$ (h is total homozygosity--see Wright's paper, linked below.)

As we can see from this site, a basic calculation of relationship coefficient may not deal with f at all. For two descendants B, C, the quantities $f_B,f_C$ are an attempt to factor in existing relative homozygosity that the coefficient of relation (COR) would otherwise not capture. Likewise $f_A$ measures preexisting homozygosity in the common ancestor of B and C. If animal A is the product of siblings then the homozygosity could already be quite high and this would maybe have measurable effects on the vitality of a cross between B and C.

Now $f_A$ and $f_B$ vary between 0 and 1 so $s = (\frac{1+f_A}{1+f_B})^{1/2}$ varies between $(1/2)^{1/2}$ and $(2)^{1/2}.$ Note that the important thing here is relative homozygosity of an animal and its ancestor:

a. If the ancestor A and descendent B have the same known preexisting burden of heterozygosity we can disregard s (and f) entirely. Their COR will depend only on path distance.

b. The homozygosity of the ancestor A  tends to increase COR while that of B tends to decrease COR.

The expression $r_{BC }= \sum p_{AB }\cdot p_{AC}$ is somewhat confusing. On page 334 of one of Wright's earlier papers we can get a clear idea of the use of the coefficient.

He defines $p_{BA} = (1/2)^n (\frac{1+f_A}{1+f_B})^{1/2}.$ If the path from C to A is $p_{CA} = (1/2)^m (\frac{1+f_A}{1+f_C})^{1/2}$ then the total path BAC would be

$$ p_{AB,AC} = (1/2)^{n+m}(\frac{1+f_A}{1+f_B})^{1/2}(\frac{1+f_A}{1+f_C})^{1/2} $$

$$= (1/2)^{n+m}\frac{1+f_A}{[(1+f_B)(1+f_C)]^{1/2}}  $$

So the expression for the sum of such paths would be

$$r_{BC} = \sum_i p_{AB,AC} = \sum_i (1/2)^{k_i}\frac{1+f_{A_i}}{[(1+f_B)(1+f_C)]^{1/2}}   $$

in which $A_i$ is the ith ancestor through whom B and C are related. The total path length for a given term is $(n_i+m_i)$ which I abbreviated $k_i.$

So a less confusing expression for $r_{BC}$ might be:

$$r_{BC }= \sum_i p_{A_iB}p_{A_iC}. $$

Note that the sum is over all common ancestors back to some arbitrary generation.

A good example of this is Figure 11 at link 1 above.
It's really not ``dumbed down'' at all, it just leaves out the factor s, which for a carefully maintained herd may be close to 1 anyway.


What's the difference between releasing hormones and tropic hormones?

The releasing hormones could also be considered tropic hormones, and indeed they fit the definition as you noticed, but aren't usually named as such.

The special thing about the ones your textbook is specifically highlighting as releasing hormones is that they communicate from the hypothalamus to the pituitary through the hypophyseal portal system, vessels that travel directly from the hypothalamus to the anterior pituitary.

Therefore, they aren't really released into the broader circulation (they can get there, but they'd be in too low a concentration). They are easily identified in a list of hormone because they all share a naming convention where they are called "____-releasing hormone" and their primary function is to cause the pituitary to release whatever is in the "_____".

In terms of overall neuroendocrine function, the "releasing" hormones all cause release of tropic hormones, which in turn cause release of hormones that affect other tissues.

Therefore, the sequence is releasing -> tropic -> non-tropic. They could have been named something else, like "primary tropic" and "secondary tropic" but this terminology keeps them separate as "tropic hormones that cause release of other tropic hormones."


how does a dna probe work in DNA fingerprinting?

You should look up VNTR. Take a look at the wiki page and it will tell you that VNTRs are Variable Number Tandem Repeats, the length of which varies between individuals, making these irreplaceable in DNA fingerprinting and such.

The trick is, all individuals will have it, but the pattern will be different, so you probe such regions which are formed as a stretch of k-mers. And you already know that they will be complementary, because we all carry them.


Tool for nucleotide alignment with all nucleotide codes (e.g. R, Y, W, S, etc.)?

If you're looking for an exact match, you don't really need a complex aligner. Perl regular expressions are pretty powerful at string transformations or conditional matching of substrings. For example, to find all matches of AASYWSRA in a nucleotide sequence $seq, you can do:

@matches = $seq =~ m/AA[CG][CT][AT][CG][AG]A/g;

The [] brackets are known as Perl character classes, which allow different characters in a position.


The main difference between a rooster and a hen is that the former is male and the latter is female. Their appearance differs in several ways [1].

A rooster also known as a cockerel or cock, is a male gallinaceous bird. The term usually refers to a male chicken [2]. The hen or the chicken (Gallus gallus domesticus) is a domesticated fowl, a subspecies of the Red Junglefowl [3].

And yes, the chickens laying eggs could be the same as the chickens that we use for poultry meat.

References:

Anjus Chiedozie. Rooster Vs. Hen on eHow.com
Wikipedia. Rooster
Wikipedia. Chicken


Why can't you just take a vitamin? Why you need a healthy diet on top of that?

I think the piece of missing information here is the distinction between macronutrients and micronutrients. The info from Mayo clinic quoted in the another answer addresses some reasons why whole foods might be better than pills for obtaining micronutrients (i.e. vitamins and minerals).  While this may be true, most of it remains to be conclusively demonstrated (arguably). However, one clear reason “why….you need a healthy diet on top of that” is (unarguably) to obtain the fat, protein, and carbohydrates that your body uses to create energy. Unlike the minerals that act as cofactors, these macronutrients are the substrate. They are broken down to create the ATP that keeps everything running and they are built up to create the very structure of the body.

  The energy that is consumed in the form of food or drinks can either be stored in the body in the form of fat (the major energy store), glycogen (short-term energy/carbohydrate reserves), or protein. . . to be used by the body to fuel energy-requiring events. *

These are called macronutrients because they are required in gram quantities — hundreds or even thousands of times more massive than the requirements for most micronutrients. As such, they don’t fit in a pill. As tragic as it is, we must keep eating.

*Gibney, M. J., & Nutrition Society. (2009). Introduction to Human Nutrition. Chichester, West Sussex, U.K.: Wiley-Blackwell.


What is the leaf venation of a scuppernong vine leaf?

Using the link, it's netted veination, though it doesn't say if it's palmate or pinnate. So I relied on using my own judgement on looking at my scuppernong leaf and it looks decidedly palmate. It would be better if I had confirmation from some site or such, but as it has main veins and smaller veins sprouting from those main veins, I think it's palmate.

Additionally, for all other botany question confusion, I finally found this website which may be useful: http://rampages.us/fieldbotany/2014/05/23/grape-vine-3/


Chance of cancer as a function of smoking frequency

There is an approximately linear relationship between the total number of cigarettes a person smokes in their lifetime and the risk of getting lung cancer.

That is, each cigarette someone smokes increases their chance of getting cancer by about the same amount, whether it's their first cigarette or they've been smoking for 40 years.

Pack-years are a way of quantifying someone's total cigarette exposure; it's calculated by the number of packs someone smokes per day times the number of years they've smoked for. So someone who has smoked half a pack per day for 20 years would have a pack-year history of 0.5 * 20 = 10 pack-years.

The following graphs show the linear relationship between the odds of getting lung cancer (relative to non-smokers) versus pack-years smoked.

Source: Lubin and Caporaso (2006), "Cigarette Smoking and Lung Cancer: Modeling Total Exposure and Intensity"


This is a terrestrial isopod crustacean called a woodlouse (colloquially referred to as pill bugs, potato bugs, roly-pollies, sow bugs, etc.).

There are over 5000 species in the world with at least 64 in Russia (see Kuznetsova & Gongalsky 2012).

Habitat:

Woodlice are typically found in damp, dark places -- in the soil, under rocks/logs/debris, etc.

  Living in a terrestrial environment, woodlice breathe through trachea-like lungs in their paddle-shaped hind legs (pleopods), called pleopodal lungs. Woodlice need moisture because they rapidly lose water by excretion and through their cuticle, and so are usually found in damp, dark places

Description:

As with all Arthropoda, the woodlouse is a segmented animal with a rigid exoskeleton and jointed limbs.

However, this is not an insect! Insects have 3 pairs of legs while isopods have 7 pairs of legs.

The extended uropods on your specimen as well as the pereon-pleon junction, number of antenna flagella, etc. all are important for IDing to species. (E.g., see here).

Note: although many people associate these arthropods with the ability to roll up into a perfect ball, only woodlice in the genus Armadillidium and in the family Armadillidae can roll up into an almost perfect sphere as a defensive mechanism.

Diet:

Woodlice are generally detritivores, meaning they eat decaying organic matter.

Citations:

Kuznetsova, Daria M., and Konstantin B. Gongalsky. "Cartographic analysis of woodlice fauna of the former USSR." ZooKeys 176 (2012): 1.


Is the SRY gene the sole responsible of biological male sex?

To my knowledge, the SRY gene is the only gene that cause variance in sex determination in humans. Of course, many genes are then involved in sex determination cascade but none these genes have variance in humans. Because environmental variance has no impact on gene determination in humans (to my knowledge and despite a few highly criticized articles) and therefore, nothing else than the SRY gene explains the sex determination.

The genes that are involved in the cascade of sex determination are not necessarily on the sexual chromosomes. On the Y chromosome, there are some genes that are male beneficial (beneficial for the male function) but these genes are not involved in the sex determining system.

In all species, the sex is determined by the environment and/or the genes. The best way to look at it is by reaction norms. On the below picture, think of the x-axis as being the temperature. Then, if you ask the question "Does the temperature influence the probability to develop into one sex or another?" One should answer. "It depends on the range of temperature you're looking at!" If you look at only very high temperature (far right) or very low temperature (far left), only the genotype explains the sex determination. If you look at mid-range of temperature, then both the genotype and the environment determines the sex.

N. Perrin and L. Beukeboom are writing what is probably going to be a very good book that will obviously interest you. I think the book is going to be publish in 2014 only. Here is the amazon link to pre-command it.


A compound was proposed by error but then showed very good inhibitory properties. How to argue this in a manuscript?

Be honest (and possibly split the papers).

If the compound was identified as an error and you want to include in a paper describing the process of your simulation and the effectiveness of the predicted inhibitors, you'd have to do so as a sort of negative control for your calculations (unless there is some way to reproduce/rationalise why it showed up randomly). Since this is the only good inhibitor you have, you'd have to conclude that your calculation isn't much better than chance, or explain why it is better even though you found a better inhibitor by chance. If you have reason to argument that your calculations are good and make sense then exclude the 'random' inhibitor from that paper. You can the write an individual paper about a good inhibitor, the fact that you found it by chance isn't that important anymore.


Why does the stability of YAC increase with size?

This is a question which is not easy to answer, especially the 50.000bp number (which I haven't found anywhere in there literature). However, I found some evidence, partly derived from plant and mammal artificial chromosomes (references 1 and 2), partly from the original publication from Murray and colleagues (reference 3).

The problems with small chromosomes seems to be their passage through mitosis and meiosis, where smaller artificial chromosomes tend to get lost. They are also not controlled very well in their number.

Murray states that YACs of 55kB in size are relatively stable in the yeast cells are relatively stable, but have a lower stability than natural chromosomes. When you are interested in the deeper details, I recommend reading the article.

References:

Construction of mammalian artificial chromosomes: prospects for
defining an optimal centromere
Alteration of chromosome numbers by generation of minichromosomes –
Is there a lower limit of chromosome size for stable segregation?
Contruction of artificial chromosomes in yeast.


Are polyploidal organisms parasatized by selfish genes? And if not, why not?

In short, being haploid or polyploid should not protect you from Selfish Genetic Elements (SGES).

Almost all eukaryotes are polyploid. Plants are the oft-cited example. Wheat, I believe, is hexaploid for example. Polyploid bacteria are the exceptions typically (if we consider ploidy to be of the whole genome). However, even in truly haploid bacteria, the genome in any given cell is usually actively being replicated, so some of the genes are actually present more than once.

Regardless, replication and repair is an enormously well controlled and regulated process: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479556/

SGEs can take many forms depending on your definition and are ubiquitous in nature as far as we can tell. Plasmids which harbour addiction factors, insertion elements, transposons, prophages etc are all technically SGEs. See here for a review:
https://www.ncbi.nlm.nih.gov/pubmed/21227262

I can't find any literature on SGEs in polyploidy directly, but it is well documented that bacteria harbour a considerable amount of selfish DNA - it seems likely that this will be the same if not worse in polyploidy. Plasmid detection is a difficult computational and experimental process (http://bioinformatics.oxfordjournals.org/content/early/2016/11/18/bioinformatics.btw651.full) but one of the hallmarks of plasmid sequences are typically addiction factors (a gene that the host cell must maintain in order to survive - usually an anti-toxin to neutralise a toxin present on a different DNA molecule) as well as phage genes.

To address a couple of things specifically:

  As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time

This is somewhat true, there is always minor variation in a population (else evolution wouldnt work!). Sometimes you'll find this is also the case in a single cell - but less often. All cells we have found so far have DNA replication and repair mechanisms - https://en.wikipedia.org/wiki/DNA_repair. The frequency of mutation in the genome is not directly linked to the amount of selfish elements though, making your second point contentious:

  This seems like an ideal place for selfish copies to arise

I agree with the premise of polyploidy probably inviting more SGEs (thinking specifically of IS elements and transposons here really), but not because of mutation - rather, just because there are more DNA molecules and sites present for those elements to incorporate into.


What does (deaths / (resolved + deaths)) describe in an emerging epidemic?

The problems with the measure you've proposed have been addressed on MedicalSciences.SE:

https://medicalsciences.stackexchange.com/q/20970/8728

The short version is that this measure isn't very informative while there are unresolved cases, because it ignores what is known or expected about those unresolved cases, and it is not a standard measure.

In the long run (when almost all cases are either recovered or dead) it approaches the case fatality rate because the denominator of (resolved + deaths) becomes equal to the total number of cases. Until then, it doesn't tell you much at all.

You could track the case fatality rate over time based on time of initial diagnosis to look at effects of new treatments.


Disclaimer

It is not clear to me that requests for references are on-topic here. In general I would think not, as they are subjective and not about biology per se. I therefore solicit neither votes for, or acceptance of, this answer. I would have used the comment area to provide references, but there isn’t really enough space, so I decided to flesh it out into what follows.

Overall perspective of elongation in protein synthesis

The main concern of the question is the movement of mRNA during translation, so I shall focus on elongation (rather than initiation). Most of our detailed knowledge of the ribosome is based on static ‘views’ of the ribosome at different stages, although there is a paper (reviewed in Nature by Ehrenberg) in which the dynamics have been deduced from millions of time-resolved electron microscopy images. I doubt whether that is what the animation in the Wikipedia article is based, however.

After an introduction to the subject from Wikipedia, I strongly recommend graduating to a good text book. Text books have the advantage over Wikipedia that they are comprehensive, integrated, professionally illustrated and sent out by publishers for review. Berg et al. is probably as detailed as you will find in a general text, the 2002 edition is available online (as are others such as Alberts et al. and Lodish et al.) through NCBI Bookshelf.

Figure 29.24 of Berg et al. provides a static general view of elongation:

You need the associated text to understand this properly, but the step at which the mRNA is thought to move with respect to the ribosome is the penultimate one in the diagram: translocation.

Unfortunately you can’t just read through books on NCBI Bookshelf — you have to search for particular topics. But Chapter 29 of Berg et al. is what you need, and the links to the relevant sections are:

29 Introduction
29.3
29.4
29.5

How exactly does the mRNA move?

The details of the individual steps in protein synthesis are being deduced from examination of high-resolution structures of complexes at different stages. For the student who as able to go beyond the accounts in general textbooks, a review such as that published in 2009 by Schmeing and Ramakrishnan is perhaps the next port of call. But, chemical virgins beware, this is structural biology, and there is no simple answer that you can scribble on a table napkin!


Are there any types of cancer that cause neurons to divide?

I think that most mature cells do not divide in all tissues. If an organism needs to repair tissues, it uses tissue cell precursors -- stem cells.

In case of neurons, these are neuroblasts. Neuroblasts can divide and can repair brains under some circumstances (I don't know under which).

There is a cancer grown from neuroblasts, called neuroblastoma.

I think it is very improbable to have tumor from neurons, because division genes are turned off in mature cells. Can't state it is not occurring in practice.


You are trying to express the plasmid in C. elegans, so it should be a worm expression vector and promoter. Otherwise, it will be expressed in the host bacteria, but not in the worm, so you won't get the phenotype you're looking for.

One thing you can do is add a bacterial origin of replication to the vector (if one isn't already present) so the bacteria produce multiple copies of the plasmid after transformation. Otherwise, the amount of plasmid consumed by the worms will be rather low.


Copy number variation (CNV) has traditionally been detected in the wet lab via FISH, fluorescent in-situ hybridization. By combining targeted DNA oligos to fluorescent reporter proteins, a region with high CNV will "glow more brightly" than a region that doesn't have as many repeats.

More recently, with next-generation sequencing, a common approach is to align sequencing reads to the reference genome. If a particular region in the sequenced sample has a large CNV, then there should be disproportionately many reads (2x, 3x, etc) reads mapping to the CNV locus in the reference genome compared to the rest of the genome.

For example, if our sequenced sample has a 3-CNV for region B:

$$A-B-B-B-C$$

then aligning our sequenced reads to the reference genome, which is:

$$A-B-C$$

will yield 1x coverage at region A, 3x coverage at region B, and 1x coverage at region C.

There are, of course, more sophisticated approaches. For a good review, refer to
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059128


Do hermaphrodites have more nerve fibers in their puendal nerve?

Short answer
The genitals of true intersex individuals are not duplicated. Instead, their external genital features are hybrid structures. In turn, it's not a matter of duplicated neural innervations.

Background
Hermaphroditic phenotypes in humans are nowadays preferably described as  intersex phenotypes. In humans they come in different flavors, dependent on the underlying genetic causes, which are often caused by mosaics of X and Y chromosomes. Dependent on the exact genetic underpinnings, various types of intersex phenotypes occur, with different internal and external phenotypes of the reproductive tracts.

To proceed to the most extreme case, namely the true intersex individuals - these people display both male and female external genital tissues. However, this doesn't mean they have fully developed male as well as female genitals.

Now taking a step back to the normal male/female situation - you have to realize the clitoris and glans penis develop from the same tissue (Fig. 1). In true hermaphrodites, the external genitalia are not duplicated, instead they form a hybrid, where it becomes unclear what exactly is present: a small (glans) penis, or an outsized clitoris (Fig. 2).

So in all it is not a matter of duplication, but a hybridization of similar feats.

Fig. 1. Male and female genital development. source: University of the Cumberlands

Fig. 2. Intersex external reproductive organs. source: ImageSlideShare


If you're looking for an explanation of the parts of the waveform you recorded, here's an annotated version:

I hope that helps you map it back to the "standard" QRS you saw. The AV delay is the time between the depolarization of the atria and the ventricles.

I agree, the T-wave is too intense. I'm not familiar with a 3-lead ECG that connects to the wrists--I'm more familiar with chest ECGs. I'm guessing the large T-wave is an artifact of measuring through the wrists (hopefully it's not indicative of a health condition such as Hyperkalemia). It looks like your resting heart rate is around 52 BPM--that's healthy.

The signal itself comes from the heart muscles. It takes a number of milliseconds for the electrical impulse to travel from the sinoatrial (SA) node to the atrioventricular (AV) node, down the His bundle, and finally to the Purkinje fibers in the ventricles. It takes this long because the movement of charge is caused by ions in the cells physically moving. That change in charge is conducted (via normal electrical conduction, such as you see in a wire) through the tissue and muscle to the electrodes on the wrists--this conduction is effectively instantaneous (in this case, it's electrons "pushing" each other, not ions moving within cells as in the case of the heart's electrical system). ECGpedia has some good background on this.

The ECG system takes the voltage from your right wrist (call this VRA), and subtracts it from the voltage at your left wrist (call this VLA), so that Vlead I = VLA - VRA.

So, in summary, the signal you're seeing is produced by the heart's conduction system, not the muscles in your wrists. Muscle noise would manifest itself as noise or random spikes in the ECG.


Brain size vs intelligence

Of course brain size and intelligence are two very different things. Sure these two characteristics are correlated (assuming we manage to define intelligence in any intelligible way). The sperm whale has a brain that is 8 times larger than the human brain for example and the Brown thrasher (small bird) can learn thousands of songs while other birds can memorize the location of thousands of seeds. So really size is not the only thing that matters.

You might want to read about brain-to-body mass ratio and the encephalzation quotient.

Evolution toward smaller brain size

I am pretty sure such examples should exist but it might be hard to come up with good citation on the subject because

It is hard to tell other than through fossil record how big was the brain of a certain ancestor
It is quite a specific question

Someone might well come up with good answers. Of course, most examples of evolution toward smaller size (such as through insular isolation as pointed out by @user137) will result is reduction in brain size however, I am not sure these example would satisfy your needs/curiosity.

Evidence of metabolic cost of brains

In the meantime, I would like to point to a few among many evidences that brain comes at a fitness cost (that might be compensated by benefits of learning and other "brain abilities"). Those evidence mainly comes from experimental evolution in labs but some comes from comparative genomics as well. In short:

Brain consumes a lot of energy (Magistretti 2013). There are evidences in Drosophila (Mery and Kawecki 2003), birds (in this review I think: Nowcki et al. 2001) and guppy (Kotrshal et al. 2013) that evolution of learning abilities comes at an important metabolic cost. Johnston (1982), and more recently Snell-Rood et al. (2009) made reviews on the cost and benefits of learning abilities that you might want to have a look at.


What are the implications/predictions of the selfish gene theory?

The Selfish Gene theory "can be defined as the idea that the gene is the ultimate beneficiary of selection".   Argren, in Selfish genetic elements and the gene’s-eye view of evolution lays out the history of the theory and the arguments for and against it.

The theory is almost certainly correct; and it's almost certainly incomplete. The theory is testable.  It predicts, for example, that there will be genes whose sole function is to self-propagate.  Those genes can't confer much fitness disadvantage to their host or they will quickly be weeded out of the population; and they don't necessarily need to confer a fitness advantage. But to the extent that different individuals have different versions of the same genes, the versions that convey a fitness advantage are likely to win the evolutionary competition.

There are, of course parasitic genes like transposons which impose a cost by requiring the host to adapt to their presence.  As long as the host is able to adapt without losing too much fitness, the parasitic genes can ride along for free.

The Selfish Gene theory provides useful insights, but it is incomplete, because combinations of genes,  arrangements of genes, and even genetic diversity within a population can provide a fitness advantage or disadvantage. Even genes are subject to "group selection", where gene A can provide a disadvantage unless gene B is also present, in which case A and B together provide an advantage. This leads to selective pressure to link the two, e.g., by placing them close together on one chromosome, which is analogous to a cooperative relationship between the genes that provides a mutual fitness advantage.


Whether using quantitative models, or "animal models", I think this is a useful quote to keep in mind:

  A model is a lie that helps you see the truth.

  -- Howard Skipper

As for evidence that using mice models for human nutrition is justified -- I believe there has been a good deal of research that has provided useful insight on the influence of genetics on the susceptibility to diabetes in humans using mouse models, so ... yes?


"Toads", as commonly used, are not a monophyletic grouping - that is, all toads do not descend from a single common ancestor which only produced other toads. Instead, it's a polyphyletic grouping of those frog species which show common morphological characteristics related to a primarily terrestrial lifestyle. As a polyphyletic group, the parsimonious assumption is that various species of toads evolved from frogs on multiple occasions.

There's several possibilities for similar morphological features in the different toad lineages. The first is convergent evolution - similar selection pressure in the shared terrestrial environment selected for novel generation of similar features. Another is that the common ancestor of frogs and toads had morphological aspects that were a blend between frogs and toads, and depending on environment "toad-like" or "frog-like" features become more prominent or recessive - that is, "toad" genes are sitting dormant in the DNA of most frog species, waiting for the right environment to be expressed. In all likelihood the true explanation probably will be a combination of the two.

By the way, most toad species still depend on bodies of water, particularly for breeding. For example, the common toad (Bufo bufo) will go to a pond to lay its eggs, where the young toads will spend time as aquatic tadpoles before they metamorphosize into the adult form. So when thinking about toad evolution, it's probably incorrect to view it strictly as frogs compensating for losing access to water (though that might have happened for some species), but rather toads evolving to take advantage of the opportunities presented by a terrestrial habitat that's coexisting alongside watery environments.


Ploidy number vs number of alleles

You seem to be confounding number of alleles with ploidy numbers. You rightly figured the number of possible genotypes for a diploid individuals when there are 3 possible allelic states.  When you ask for a pentaploid, are you many alleles are you wiling to consider?

Pentaploids are very rare

If I am not mistaken, species with an odd ploidy number are very rare. Tetraploids and hexaploids, while still rare are much more common than pentaploids.

General case

It is indeed a simple math problem. Let's answer to the question in the most general case. If the ploidy number is $P$ and there are $S$ possible alleles, then the number of possible genotypes is

$${P+S-1 \choose S-1} = {P+S-1 \choose P}$$

, where ${\choose }$ refers to the binomial coefficient. For a pentaploid organism, with 3 possible alleles, there are therefore 21 possibilities.

More information

You can have a look at this webpage that offers much more info about the combinatorics of genotypes.


Competition with other individuals of the same species vs. adaptation pressure from predators

The correct answer is, "it depends."  The traits that will be under the strongest selective pressure will be those related to survival in the face of the most common causes of death for that species. If food is abundant but so are predators, then clearly predator evasion will be of supreme importance. If food is scarce, then perhaps metabolism-related traits will be under strong selective pressure. But it's important to remember that just because one selective pressure is stronger doesn't mean that the rest disappear. Thus, the individual's survival is dependent upon really a composite fitness that depends on a countless array of selective pressures, some of which may be larger components than others. The competition between individuals of the same species is really a complex interplay of fitness effects, then.

As for the maxim about outrunning a cheetah, what it's illustrating is that the gazelles are not competing with the cheetah for survival. They're competing with each other. If you want, you could expand it to say "...just the other gazelles and the rest of the herbivores in the environment". If a herd of gazelles and a herd of some slower animal are nearby and a cheetah attacks, one of the individuals from the slower species will probably get caught and all the gazelles will get away. The point is that the gazelles and the cheetahs fill very different niches in the environment, so they don't really compete for the same resources (as a matter of fact, one is the primary resource of the other).

When it comes to determining survival, one talks about fitness only within the context of the population (or, if you want, between species directly competing for the same niche). The less fit members of the population do not survive. Thus, the less fit ones that fail to evade the predator are simply doing a worse job evading the predator than the other members of the population. But it's not only the relative fitness that is important. Imagine that a new predator migrates into the environment, for which none of the prey has any evasive adaptation. Even though there may be a relative fitness between them regarding evading this predator, if even the best individual is not good enough to evade it, they would all have an absolute fitness that is too low to ensure survival. Then the saying breaks down, since none of the gazelles can out-run each other with respect to evading this new predator.

Of course, this idiom falls apart when you start talking about asocial species, since there aren't any other individuals around to out-run.


Could I use spiders to catch unwanted insects?

What you describe is called biological pest control. Lacewings and earwigs are more common, but there are ways to use spiders.

http://unossc1.undp.org/GSSDAcademy/SIE/Docs/Vol4/Rearing_spiders.pdf

http://www.annualreviews.org/doi/abs/10.1146/annurev.en.29.010184.001503?journalCode=ento


Would exposure to a strong magnetic field have deleterious effect on the human?

First thing comes to my mind is the Hall effect. Any directional ion or electron flow will experience a force (depending on the orientation with respect to the magnetic field). So if the magnet is very strong, I think some of the ion channels for action potential generation and propagation would malfunction. (11 mT stopped action potentials for a while but recovered in mouse as reported here.)

However, according to these papers static magnetic fields has little biological effect, and it seems to be reversible. But, this reports genotoxicity in 4.5T (in vitro), and developmental disorders in 1.5T (in vivo, mouse). Contradictory reports indicate we do not know the full answer yet as usual.


What is a concentration

A concentration of cells is the number of cells per unit of volume.

You are free to choose the units you like

It is very much up to you to chose the units you want as long as they express a concentration. There is no right or wrong.

You can express your graph in cells per liter or in 100,000 cells per $\mu$l or in billions of cells per ml, all would be correct. Of course, some are more intuitive than others. I would advice you to avoid expressing in cell per square meter or in billions of cells be nanoliter because the numbers will be very small and very large respectively and will not convey much intuition.

A good intuitive unit

I don't know what kind of concentration you have in you data but a priori, I would recommend expressing your concentration in cells/ml is quite intuitive.


Photoreceptors and light with mixed frequencies

Yes, current color models assume a linear response in the spectrum.

Given a light with mixed spectrum $\Phi(\lambda)$, the response of a cone with spectral sensitivity $\Psi_i(\lambda)$ is a (nonlinear) function of the L2 inner product:

This is how CIE XYZ color space is defined.

Reference:

M. D. Fairchild. Color Appearance Models, 3rd edition. 2013 (p.63)
https://en.wikipedia.org/wiki/CIE_1931_color_space


Body does not act against sperms because the testes are isolated immunologically by the blood testis barrier.

In mumps due to this barrier becoming ineffective due to inflammation, orchiditis (inflammation of testis) may occur and this may render the person infertile in some cases.

Such antigens which are not exposed to body's immune system are called cryptic antigens.

One more example of cryptic antigen is the antigens of the cornea.

For more information see here.

For more you can search for blood testis barrier.

For the second question, immune reaction will occur if the injected cell contains cryptic antigens. If there are no cryptic antigens then there will be no reaction.

For cryptic antigens see here.


Overall, bioluminescence has arisen over forty times in evolutionary history.[25]

There are bioluminescent funghi and bacteria.

Phosphorus is the 2nd most important nutrient for plants, so perhaps it's too expensive to use for bioluminescence, most plants don't live in phosphorus rich environments.

Bioluminescence also uses quite a lot of nitrogen, and most plants can't fix nitrogen.

there are 71 species of glowing funghi, perhaps to distribute spores, so plants with spores could have had the same strategy.

If two species of plants used light for night time insects, it can confuse the insects if they are plant specific, light is more confusing than scents.

A tree can potentially produce a lot of light, and it would turn into a forest lamp-post attracting lots of insects. It could be ecologically hazardous. perhaps a carnivorous plant could benefit from it.

It seems like plants and algea easily could have evolved bioluminscence easily, if bacteria and protists have, and that it wasn't profitable to the plants.

A crowdfunded project to make some failed because it was too difficult to put 6 animal genes into the plant.

land animals use light as an indicator of fitness, and plants don't need to indicate their individual fitness to others, and most bioluminescent animals have the option to switch things on and off very effectively, which difficult for trees.


What are the different, high-level programs along which a eukaryotic animal cell can follow?

To see the width of your question, have a look at what the Gene Ontology considers a cellular process:

http://www.ebi.ac.uk/QuickGO/GTerm?id=GO:0009987#term=children

I don't think you can agree on what's high-level, so it's better to see them all, I think. Also, for completeness, there is a list with cell types which is admirably maintained:

http://en.wikipedia.org/wiki/List_of_distinct_cell_types_in_the_adult_human_body


In mitochondria, what is the mechanism by which electrons are transferred between different cytochromes?

All of the members of the Electron Transport System (ETS) are organized in "complexes", clusters of enzymes and other proteins. These complexes are in proximity to one another such that electrons can be passed between them. The different cytochromes, and other electron handlers, have different affinities (attractions) for electrons. Those at the beginning of the ETS have less affinity for electrons than those at the end. The reason the electrons move through the ETS is due to that greater attraction of electrons by the subsequent complexes in the pathway. These complexes are positioned with respect to one another so that no "short circuits" occur; the electrons skip no steps down the ETS. Finally, the "low energy" electron from the last complex is mopped up by that great electron-hog oxygen.

The energy lost by the electron as it passes between carriers is not directly harvested to pump protons. The importance of this "loss of energy" is that it makes the transfer of the electrons a spontaneous process insuring their passage down the ETS. Typical entry into the ETS involves NADH donating a hydrogen ion to the matrix and a pair of electrons to NADH dehydrogenase. The electrons are eventually transferred to the mobile coenzyme Q. This now attracts a pair of hydrogen ions from the mitochondrial matrix which then induces the operation of a proton pump. This pumps hydrogen ions into the inner-membrane space creating the electrochemical gradient.

So, in general the arrival of electrons, with the attendant hydrogen ions, changes the conformation (shape) of pumps which translocate the protons to build up the gradient. The electrons are ultimately passed on to oxygen, forming water with the help of some spare hydrogen ions. This removal of the electrons allows the ETS members to be receptive to another load of electrons from the NADH.

Reference 2nd paragraph: http://www.physiologymodels.info/metabolism/ETSOXPHOS/ets.htm
This is a good site to read more and view some diagrams, especially focus on the second panel, "Complex I".

Reference 1st paragraph: Molecular Biology of the Cell; Alperts, Watson, et.al.


Nepeta cataria(Catnip, Catmint, Catnep) is a plant belongs to the family Lamiaceae.It is a  herb that has been recognized for its medicinal properties for many centuries. Over time it has been used in remedies to cure internal cancer, smallpox and scarlet fever.Also it was believed that a dense growth bordering fields helped to protect crops because of its ability to repel rats.

Major Active Constituents of catnip includes a and ß nepetalactone  citronella , a and ß citral , limonene , geraniol , thymol , and carvacrol  epideoxyloganic acid and 7-deoxyloganic acid

  Nepeta cataria has a carminative, anti-spasmodic, astringent and anti-flatulent effect on the gastrointestinal system, particularly on the stomach . It is also a diaphoretic and antipyretic in times of fever . Nepeta cataria is similarly recognized as a tonic, mild nervine, and sedative, with a slightly emmenagogue action . With respects to cats, Nepeta cataria produces an aphrodisiac effect.

http://scu.edu.au/scps/index.php/125/

A research paper published in 1994 states that,

  Catnip was  the most promising candidate lures tested. The 'catnip-response' is
  inherited as an autosomal dominant (Todd 1962). In trials, behavioural observations showed
  that 50% of the subjects (including all four domestic cats and 8 of 20 feral cats) showed the full catnip response (B. K. Clapperton, unpublished data). This includes sniffing, licking, rubbing and head-over rolling (Tucker and Tucker 1988). Nine of the remaining 12 feral cats approached and sniffed at the catnip samples. This suggests that, although not all cats are genetically determined to respond to catnip , these odours may act as more general attractants.

http://www.southwestnrm.org.au/sites/default/files/uploads/ihub/clapperton-bk-et-al-1994-development-and-testing-attractants-feral-cats-felis-catus.pdf

  When cats inhales nepetalactone it stimulates the olfactory bulb, the part of the brain that processes odors. The olfactory bulb then interacts with the amygdala, the brain region associated with emotion and decision-making, and hypothalamus, which controls a variety of bodily functions. From the hypothalamus, nepetalactone stimulates a sexual response in cats that are genetically predisposed to sensitivity to catnip. (About 20 to 30 percent of cats don't seem to react to the plant.)this is why mostly adult cats shows significant addiction to catnip.

http://www.compoundchem.com/2014/06/08/catnip/

  The catnip stimulates an Innate Releasing Mechanism(IRM) in domestic cats that elicits a predictably playful behaviour pattern apparently independent of experience and learning(Ewer,1973 and Leyhausen,1975) ,trans-nepetalactone is reported to produce behavioral respondse in cats.It has been verified by Todd in 1963 that capnip is mediated by Olfactory and not gustatory stimuli.Catnip sensitivity has been related to a dominant autosomal geneand to the estrous cycle by Todd.The reports shows catnip elicits behavioral respondses in domestic and wild cats, but these responses are not shown by female sex.In addition, it has been suggested that catnip mimics a pheromone found in cat urine, however evidence supporting this theory is scant.(Todd 1962)

http://link.springer.com/article/10.1007%2FBF00987747#page-1


Infant tissues, organs, body parts or reflexes in an adult organism

"Remnant" is the closest term I can think of; "residual" is also used. You can find both used to describe the foramen ovale for example, which typically closes at birth (and has served its purpose at that point), but remains patent in a substantial proportion of adults, sometimes causing symptoms.
However, these terms are of course not specific for the circumstance you describe; I don't know of any that is.


Quick answer: use tblastn.

As a general rule, when comparing two datasets using BLAST, it is recommended to use the larger of the two sets as the database and the smaller as queries. The main difference is one of computational time. Blast is optimized for large databases.

You are also likely to get different hits. Blast's e-value is calculated based on the size of the database, among other parameters. Roughly, the e-value answers the question: "How many high scoring sequence pairs with X% of sequence identity and Y length would I expect to find in a database of size X by chance?". Your e-values could be artificially high if you use the protein sequences as a database. I am not sure about this, but there may also be differences in the way gap penalties are dealt with by tblastn and blastx.

That said, I would first try doing this using a tool specifically designed for the task. BLAST has no model for dealing with splicing and it is a pain to build gene models from BLAST results. To align protein sequences against genomic DNA I would use either exonerate (with the p2g model) or genewise. Both programs incorporate splicing models and will give you a decent prediction of the gene structure of your target genes. The following are extracts from each program's man page:

GENEWISE:

  Genewise2 compares a protein sequence to a genomic DNA sequence,
  allowing for introns and frameshifting errors.

EXONERATE:

  exonerate is a general tool for sequence comparison.

  GAPPED ALIGNMENT OPTIONS

  -m | --model

  protein2genome

  This  model  allows  alignment of a protein sequence to genomic DNA.   This is similar to
                       the protein2dna model, with the addition of modelling of introns and intron phases.  This
                       model is simliar to those used by genewise.

In general, genewise gives slightly better results but is much slower and cannot deal with multi fasta files. It is best when you know that your query protein will align against a specific nucleotide sequence.

Exonerate is fast but uses some heuristics that can give slightly worse results in some cases. Personally, I use exonerate to get my hits and then, if necessary, refine the gene model using genewise. In most cases, exonerate should be enough though.

EXAMPLES:

exonerate -m p2g -q proteins.fasta -t scaffolds.fasta > output.txt

genewise -pretty -pep -gff single_prot.fasta single_scaff.fasta > output.txt


What is the name of this species which I found in an Epipremnum (Money Plant)?

The caterpillar in question is a kind of hawk moth caterpillar, most easily noticed by the pair of "eyes" on the thorax. From my experience with hawk moth caterpillars though, they generally have multiple sets of eyes, and so, this one was somewhat difficult for me to ID (not to mention a location has yet to be provided).

Looking at the OP, other defining features include: unique pattern on thorax; repeating triangular pattern on dorsal; a single tail; stripe along each side of the abdomen; overall coloration.

That being said, I believe this caterpillar is of the genus Eupanacra, and is most likely of the species E. elegantulus.

Such well defined patterns on the OP suggests full maturity. Consider the following instar sequence, and notice how the emergent patterns converge to the OPs.

images source

After undergoing pupation, the caterpillar will transform into the following:

And then, here's a distribution map.

source


Why does depolarisation by high intracellular K+ trigger calcium channels opening?

Ca2+ is very often the trigger to release neurotransmitter or, in this case, hormones. Ca2+ entry in the cell is important to activate the fusion of secretory vesicles with the membrane in pancreatic beta cells as shown in Fig. 1 (Thurmond, 2000). The function of Ca2+ entry is not so much related to its depolarizing actions.

Fig. 1. Ca2+-mediated insulin secretion. Glucose-stimulates insulin secretion by increasing the ATP/ADP ratio, which inhibits the ATP-sensitive KATP-channels, leading to membrane depolarization and opening of voltage-dependent calcium channels (VDCC), with a resultant major increase in cytosolic calcium, which, in turn, triggers exocytosis. SNARE proteins play a critical role in insulin granule secretion. The linking of the plasma membrane proteins syntaxin and SNAP-25 to vesicle protein VAMP-2/synaptobrevin-2 cause the docking of the vesicle, bringing insulin granules in close contact with the plasma membrane and calcium channels, after opening of calcium channels, the readily releasable pool (RRP) insulin granules located nearby are exposed to high level of Ca2+, resulting in RRP granule exocytosis. Source: Ren et al. (2007)

Ca2+ entry in the cell is potentially toxic and closely regulated. For example, internal stores are actively involved in the release and re-uptake of Ca2+ (Pian-Smith et al., 1988). Although Ca2+ influx will depolarize the cell further, it will not contribute substantially to the membrane potential compared to the effects of K+ and Na+.

References
- Pian-Smith et al., Endocrinology (1988); 123(4):1984-91
- Ren et al.,  J Transl Med (2007)
- Thurmond, Landes Bioscience (2000)


The most essential thing for a cell to survive is a membrane. Without a membrane there is no boundary between cell and its surroundings. A selectively permeable membrane is needed for cells (from single celled organisms to elephants and giraffes and whales) to survive. Cells will die quickly on removal of cell membrane.

The RBCs are good example of cells without mitochondria or ribosomes which survive for 120 days.

Please read the article on Erythropoiesis for detailed information on how RBCs form and how they have proteins in their surface.

In short, the RBCs acquire the surface proteins during their formation period in the bone marrow. Inside the bone marrow the premature RBCs have nucleus, ribosomes, mitochondria, etc... and produce all the required structural and functional proteins. On maturing they loose the nucleus and cell organelles and contain only hemoglobin in their cytoplasm.


E. Coli growth inhibited in Powdered Honey

If I understood correctly you want to grow E. coli in the presence of honey, right?

This migth be the problem as honey inhibits bacterial grow. See here. Therefore, it also doesn't matter which medium you are using.


Due to the long legs and the shape of the abdomen, this is probably a crane fly, a dipteran from the Family Tipulidae.

Just for comparisson, here is Holorusia hespera:

Crane flies can be very large. I still remember the first crane fly I saw, in New Zealand: it seemed like a humongous mosquito (mosquitoes are dipterans from a different family, called Culicidae), it was quite impressive. Have a look at the size of this crane fly:

Despite their scary size, do not fear them. Unlike mosquitoes, crane flies are completely harmless: adults have a short life span, only days (just enough to reproduce), and in most species of crane flies adults don't eat at all.

Regarding the exact species of your specimen: the number of species in Europe is huge and, together with the fact that your photo is not the best one, it will be very difficult narrowing this down to Species, or even to Genus. Therefore, a better photo is necessary.


IPTG and lac operator with e coli for foreign gene question

The lac operon contains genes which are important for the metabolization of lactose as an energy source - normally glucose is used for this purpose. Usually the operon is tighly regulated and as long as there is another source of energy it is kept in an inhibited state.

The presence of lactose removes the lac repressor from the lac operon and allows the expression of the genes and thus allowing the metabolization of lactose. The mechanism can be turned on and off depending on the presence of lactose.

IPTG is a substance which mimicks the presence of allolactose (a metabolite of lactose) and it can activate transcription from the lac operon. As IPTG (in contrast to allolactose) cannot be hydrolyzed by β-galactosidase, it's concentration in the cell stays the same. Using the lac operon and IPTG enables you to switch on the expression of the gene on your plasmid and to start the overexpression.


Why do cucurbits produce so much fluid when their stems are cut?

Looking through some papers it is not clear to me that botanists actually know why this should be the case, and I am sure that you are more qualified than me to comment on this Richard! However, there's some discussion of this in Zhang et al. (2012).

These authors argue that the "exudate from curcubits is copious" because of physiological adaptations due to their growth habit - i.e. they are vines and as such often require the structural support of other plants. Vines compensate for a lack of a supporting stem structure by having xylem vessels that are wider than comparable freestanding species  and "high hydraulic conductivity" (which is a measure of how readily water will flow through pores - in the case of curcubits - very readily). Similarly, sieve tubes and sieve pores are very wide compared to species in other families. Since these sieve tubes have such a large cross-section, they do not readily self-seal.

The Origin and Composition of Cucurbit Phloem Exudate
C Zhang, X Yu, BG Ayre, R. Turgeon - Plant Physiology, 2012 - Am Soc Plant Biol. 158, 3

See also:

Why vines have narrow stems: Histological trends in Bauhinia (Fabaceae), Ewers, F., Fisher, J, Oecologia, 1991, 88, 2


What is the effect of extra-cellular potassium concentration on heart rate and conduction velocity?

Pathological potassium concentration promotes arrhythmia.
Increased extracellular potassium inactivates $Na^+$ channels and opens $K^+$ channels, causing the cells to become refractory [1]:

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

Decreased extracellular potassium leads to hyperpolarization [2]:

Lower potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.
In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential less likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the $I_{Kr}$ potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.

References:

Wikipedia contributors, "Hyperkalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hyperkalemia&oldid=612096441 (accessed July 12, 2014).
Wikipedia contributors, "Hypokalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hypokalemia&oldid=612818488 (accessed July 12, 2014).


Is it true that the human brain has not evolved in 100 000 years?

tl;dr
Here are the two claims you make

human brain has not evolved in 100 000 years

Wrong!

there are no genes for intelligence.

Wrong!
The claim there are no genes for intelligence. is unclear though (see below) but if rephrased in the most intuitive correct way, then the claim is wrong!
Are there genes for intelligence?

[..] there are no genes for intelligence.

The claim there are no genes for intelligence is unclear. Does that mean there is no genetic variance in the human population for intelligence? To understand why the claim "gene for something" makes no sense, please have a look at this post
Make sure to read this post..... Done? Now you understand why the concept of heritability is key. So let's rephrase the question so that it makes sense and can be answered
Is Intelligence heritable?
Well, the issue here is to define the term 'intelligence' in a way that is non-arbitrary and yet match our intuition of what we like to call intelligent. A number of studies have investigated the heritability of intelligence, often using different definitions / metrics for intelligence.
All these studies agree on one point. Yes, intelligence is heritable! How heritable it is varies a lot from one study to another (because those studies vary in the population studied and in the definition of intelligence). See the wikipedia article on Heritability of IQ for more layman information.
Has the human brain evolved in the past 100 000 years?
First you need to understand how evolution is defined. Here is a commonly used definition

Evolution is a change of allele frequency through time in a population

Have a look at the post What is meant by individuals do not evolve, populations do? to understand what this definition mean.
Well... first. Everything evolve. You can't stop evolution from happening on any phenotypic trait or on any genomic region. So, of course it evolves. But let's not stop there.
There is still one issue with this question. The saying brain characteristics rather vague. But I'll deal with it as I can.
Is the brain still evolving - phenotypic evidence
Spoting changes in brain structure through time is not easy, as brains don't preserve well. Over such a short period of time (100,000 years) it will be even harder to detect much difference on gross metrics we can use such as cranial cavity.
We can compare the volumes of cranial cavity. Neanderthals interbred with humans (see this loosely related post) with Homo sapiens and Nanderthals had a cranial cavity that is bigger than Homo sapiens, so this gene flow would very likely affect H. sapiens cranial cavity.
Is the brain still evolving - genetic evidence
Consider for example Evans et al. 2005 showing that the allele coding for micro-encephaly at the gene MCPH1 is currently increasing in frequency in the human population.
This article from NewScientist also reports the findings of Evans et al. 2005 in layman terms.
Is the brain still evolving - current selection pressures
You should have a look at the post Is intelligence declining due to the lack of selection pressure? and eventually on the wikipedia article for the Flynn Effect.


Are there any theories using thermodynamics/statistical mechanics or information theory principles to modelling in ecology?

John Harte's work on applying the mathematical theory of maximum entropy to ecology is certainly one of the better known examples of the application of this area of mathematics to science, in part because he literally wrote the textbook: Maximum Entropy and Ecology: A Theory of Abundance, Distribution, and Energetics (Oxford Series in Ecology and Evolution)

To be clear, maximum entropy (also known as MaxEnt in some of the literature, though most/all researchers use the longer form in publications) is a mathematical tool stemming from the fields of probability theory, statistics, and information theory.  Its use is classically most often seen in thermodynamics, statistical thermodynamics, physics, and information theory, primarily because these were the areas in which E.T. Jaynes was working when he posited the idea. Wikipedia has links to his two seminal papers.But because of it's mathematical form, it can be applied in a multitude of areas, typically where one can utilize probabilistic methods.

If you're looking for additional areas of application, simply google the phrase "applied maximum entropy" and you'll find a wealth of areas including: econometrics, natural language processing, nuclear medicine, queuing systems, mass spectrometry, image processing, machine learning, and many others.

For ecology related work, a cross search on maximum entropy and "genetics", "evolution", "species", and similar words will provide a wealth of papers like "A maximum entropy approach to species distribution modeling".

Given the generic nature of your question, I might suggest that you'll find E.T. Jaynes' paper "On the Rationale of Maximum-Entropy Methods" (IEEE, 1982) useful.

Those generally interested in the broader applications of information theoretic methods to biology will likely appreciate some of the work that came out of last year's NIMBioS Workshop on Information and Entropy in Biological Systems (which Harte both attended and presented at), the BIRS Workshop Biological and Bio-Inspired Information Theory, and the 2014 CECAM Entropy in Biomolecular Systems. The NIMBios Workshop was organized by John Baez, a physicist, who has worked with MaxEnt methods and explored them on his blog "Azimuth".

Those with a more sophisticated mathematical background (including measure theory, functional analysis, etc.) may appreciate Henryk Gzyl's text The Method of Maximum Entropy (World Scientific: Series on Advances in Mathematics for Applied Sciences, Vol 29, 1995).

-- Additional thoughts after the question was edited --

First for those who don't have the background, I highly recommend reading the two seminal papers on information theory and statistical mechanics by ET Jaynes and the standard text on information theory Elements of Information Theory by Thomas M. Cover and Joy A. Thomas.

In addition to the information theoretic related areas, you might want to take a look at the discipline of complexity theory, which has primarily grown out of the Santa Fe Institute over the past several decades and which includes information theory as part of its disciplines. If you're unfamiliar with the broader topic, Melanie Mitchell has an excellent overview with her book Complexity: A Guided Tour. Also related to complexity is the area of cellular automata which one could view as a very base model of more complex ecological systems. Here, perhaps Stephen Wolfram's A New Kind of Science or Cellular Automata and Complexity will be enlightening. The broader theories coming out of these primarily mathematical areas may be useful to you.

In particular, given the types of models in ecosystems, I might suggest taking a look at some of the mathematical modeling going on at the intersection of complexity and economics. For a relatively simple introduction to this area, one could look at the relatively introductory text Complexity and the Economy by W. Brian Arthur which is very interesting. The economy is essentially a very specific type of ecology dealing with human beings, assets, and the monetary system.

Another area which I've seen a lot of literature over the last few years is applicable to the ideas of resiliency and complexity in cities, for assisting in designing more robust city planning. This really isn't that far from the naturally evolving systems being looked at in ecology settings.

For those looking for researchers in the area of complexity, I have a list of many who are on twitter in a variety of sub-areas. In addition to individuals, it also includes a number of institutes and related organizations as well.

I'd also suggest, that for the broadest theoretical setting, one could actually start with the topic known as "Big History" which takes the broadest approach of looking at history and the evolution of the cosmos over 13.7 billion years since the big bang. This conceptualization includes ideas like evolution, complexity, and emergence on the biggest scales, a set of theories that could be similarly applied to ecologies both large and small. For this viewpoint, I would suggest two works by David Christian including Maps of Time: An Introduction to Big History and Big History: The Big Bang, Life on Earth, and the Rise of Humanity.

In essence, with many of these topics and viewpoints, one is treating individual animals or even entire species as elementary particles and then using the mathematical models of statistical thermodynamics to tease out specific types of data or trends. As layers of overlapping "particles" interact with each other, they cause emergent types properties, and then these resultant emergent properties combine to create further layers of emergent properties, none of which might have been necessarily deduced from the initial conditions. Within Big History, these types of emergence go from the big bang and basic particles in the early universe to the ultimate evolution of humankind by way of a variety of stages.


What do HG and NA mean in Geuvadis project RNAseq sample labels?

If you google HG00105, among the first hits is geo accession GSM649517 with the title HG00105/NA12878.

Channel1:

Characteristics gender: Male
cell line: lymphoblast cell line HG00105
ethnicity: British from England and Scotland, UK (1000 Genomes codes: GBR)

Channel2:

gender: female
cell line: lymphoblast cell line NA12878
ethnicity: Northwest European American from Utah (HapMap code: CEU)

So no, they are not coding for the ethnic background but are part of the unique identifier of the sample.


Here is a head and a neck:

Anatomy is fairly straightforward. regarding individual long bones, "heads" are curved ends of bones distal to a narrowing called a neck of a bone. Take the radius:

See how the radial head (curved) is just distal to a narrowing (neck)?

The ulnar head, though, is at the opposite end, because the proximal end isn't rounded, but the distal end is.

Metacarpal heads are distal (see blue area):

The humeral head is probably most obvious:

So, the head of a long bone is not determined by the position (it can be proximal or distal) but by the contiguous shapes.


Resources for interesting facts about biology

Whether you find the content interesting or not I can't say, but you might want to check out the BioNumbers database. It has a category for "Amazing bionumbers" and a "BioNumber of the Month" section.


The concept of fitness is very general. An adequate definition of fitness is hard to specify in the same way that a definition of "species" is hard to give. To be useful, scientific or technical definition of such broad concepets will often need to be so narrow that more than one is needed. A uselessly broad definition of fitness might be:

"Fitness is modeled as a utility function, where higher fitness is indicated by a higher score"

Here every important detail about whatever's fitness is being tested, how that fitness is measured, and the environment in which that fitness is determined are simply wadded up together and transformed into a different question that is no easier to answer.

The hypothetical problems you raise with various definitions are not (in essence) problems with the definitions, but problems with the definitions not being applicable to the domain in which such problems matter. You have to define your criteria for success, and then these constraints can be translated into a "fitness" function that allows the desired predictions.

Some issues that might matter are:

Are predictions about populations, or individuals.
Are predictions about dynamic fitness (snapshot at some time) or long-run steady state fitness.
Are predictions about quantitative values (like heights) or discrete values (like sex).
How do you want to present error in your predictions - p value, sensitivity/specificity, confidence interval, etc.

I'm sure this is not the kind of answer you were looking for, but I think part of your question revolves around a confusion that there is "one" technical definition for fitness. Part of the process of learning is comparing different presentations of the same concept, and realizing where they are different. A full walk over all the different ways one could evaluate and apply fitness would be a book, not a short answer. Perhaps some other people can provide good links to more detailed information.

I just found a blog posting, by Dr. John S. Wilkins, which says some of the same things. His perspective comes with a good pedigree; his PhD work was on trying to define "species" and he has authored a couple of books on the subject.


Is it possible to completely puncture a human hand and have no blood come out?

Yes, it is possible.
The needle should be passed through Fistula, which is an abnormal or surgically made entry between an empty or tubular organ and the body surface, or between two empty or tubular organs.
According to Magic Secrets Explained >>

This provides us with a reasonable explanation for Blaine's needle
trick. He has a fistula through his arm. He created this fistula to
himself, by repeatedly causing small damage to his arm in the same
direction, probably by actually stabbing a needle into it.
He basically drilled a tube of scar tissue through his arm just so he could perform this one trick.

In order to further cement their logic, they attached another video of a man who had a fistula through his body which empowered him to have swords cut through his body without hurting him.
Fistulas are also incorporated in dialysis, and infact referred to as dialyses’ lifeline. An article by Big D and Me expands more on this plus explains how it also threatens lives.


What happens if there is a blood incompatibility during pregnancy?

Little harm comes from ABO incompatibility (that would have been a major problem with reproduction.) Rh incompatibility is more dangerous, though.

If a fetus is Rh+ and the mother is Rh-, when there is mixing of maternal-fetal blood (at birth, but sometimes before that), the mother will form antibodies to the blood cell surface antigen. It doesn't usually affect the first baby (not sufficient antibodies), but if a subsequent baby is Rh+, there can be major consequences, which are multiplied with repeated exposure. Those maternal antibodies - which cross the placenta - can attack the fetal red blood cells and cause destruction of many of them (called hemolytic anemia) which, if severe enough, can be fatal to the fetus. It was a not-uncommon cause of fetal demise before Rhogam (Rh immune globulin) injections.

The immune globulin shots are given to women who are Rh- with Rh+ mates at a period before birth (before blood mixing), and immediately after birth if the child is Rh+. The antibodies bind with Rh+ antigens and "mask" the antigen from the mother's immune detection, so to speak, preventing the mother from making antibodies that can be used against subsequent pregnancies.

The major risk is to the fetal blood cells, not the placenta. The placenta isn't attacked. But with anemia, the fetus struggles, for example, without enough blood, the fetus can go into congestive heart failure and die.

It's also possible to form anti-Rh antibodies from blood transfusions. If an Rh- female has had a blood transfusion prior to her first pregnancy, maternal antibody levels will be drawn earlier during the pregnancy.

What Is Rh Incompatibility?