How do I name a binding antibody? “Binding antibody to”, “binding antibody against”, or “anti-[antigen] binding antibody”?

The adjective “binding” is not used to qualify “antibody” in English scientific usage because linguistically it is thought to belong with the antigen the antibody binds.

Generally it is omitted if the prefix “anti” is used, e.g.

  anti-cetuximab antibody

(e.g. “two or more anti-hapten antibodies” here)

However if you wish to refer to the particular small portion of the antigen that is recognized (the epitope), you might write, e.g.

  tyrosine-binding antibody

(e.g. “Hapten‐binding antibodies…” here)

As far as the use of prepositions is concerned, “to” is used with binding, although it is optional. However generally with the antigen, e g.

  cetuximab binds to the antibody

(e.g. “Antigen binds to the antibody on the B-cell membrane.” here)

But

  the antibody binds cetuximab

(e.g. “An additional VNAR, Help6, which binds Hepatitis B precore protein” here.)

Completely illogical, I know, and this distinction is not universal.

However, “against” is used in relation to preparing or raising antibodies, e.g.

  We raised an antibody against cetuximab…

(See the legend to Fig 1. in this paper.)

So in general one would write:

  Assay of anti-cetuximab antibodies in serum

Addendum: Binding antibodies v. Neutralizing antibodies

The revised question makes it clear that the authors are referring to “binding antibodies” as a specific contrast to “neutralizing antibodies”. This expression was not known to me (I am not an immunologist), and, although the poster documents it, its use would appear to be limited, perhaps because the topic is or was controversial.

The question remains, how to express this idea in a clear and unambiguous manner, with the specific problem that the poster is a translator, not an editor. I would still try to avoid the use of the word “binding” in the expression. I have two suggestions:

I believe that an alternative expression would be “non-neutralizing antibody” (the paper just quoted does not hyphenate this term, but others do, and I would). If this belief is correct, one could write:

  Assay of non-neutralizing anti-cetuximab antibodies in serum

Alternatively one could use the abbreviation, “BAb”, from the paper cited by the poster, although this would have to be defined somewhere.

  Assay of anti-cetuximab BAbs in serum


How to biologically interpret path weight summation in weighted and directed gene regulation network?

There's quite a bit of use of graph theoretic approaches in gene regulation, so I'd suggest you start there and Stand on the Shoulders of Giants rather than reinventing gravity:

https://scholar.google.com/scholar?hl=en&q=graph+theoretic+gene+regulation

Although this isn't my area of expertise, I think the thing most obvious to me as a biologist and statistician is:

Sums are misleading in non-linear systems

Biology is very non-linear. You can probably get closer to linear in the graph you are describing if the weights reflect log-transformed ratios: this transformation makes a multiplicative system linear. But even after this transformation, you are making substantial assumptions. The only way to verify those assumptions would be with either a more complex model of the underlying system (since the graph you describe is quite abstracted) or the old-fashioned way: by experiment.


What is the difference between the usages of bis-tris methane and bis-tris propane?

They have different acid dissociation equilibria and so buffer at different pH.

                    pKa1    pKa2
Bis-Tris methane    6.5     -
Bis-Tris propane    6.8     9

[source]

The two titratable secondary amines of Bis-Tris propane make it usable over a wider pH range.


Has autogamy been observed in any animals?

Yes, there are some animals which are known to self-fertilize (although generally not exclusively).  For instance, among invertebrates some nematodes are known to use self fertilization, as discussed in this paper about its evolution.  Among vertebrates, it seems to be very rare, apparently known only only in a single genus of fish.


why are malarial parasites specific for anopheles

The host/parasite relationship is normally very specific: because there are a lot of molecules that have to bind each other for the parasite to complete its cycle, a parasite is not capable of invading any given organism; the same way, a host is not invaded by any given parasite.

That being said, you have to keep in mind that mosquitoes are also hosts (despite of, in the case of malaria, having less symptoms when compared to the human host). In fact, regarding malaria, some parasitology books classify the mosquitoes as the "definitive hosts", while humans are "intermediate hosts" (because the sexual reproduction of Plasmodium happens in the mosquito, not in the human being). So, there are a lot of molecules that have to be present for the parasite finding its way through the mosquito's organism. A plasmodium cannot survive inside a Lutzomyia mosquito, the same way a Leishmania cannot survive inside a Anopheles mosquito. There is specificity.

Actually, not all Anopheles are the same (just as not all human beings are the same). They have differences regarding the susceptibility to the parasite:

  Some Anopheles species are poor vectors of malaria, as the parasites do not develop well (or at all) within them. There is also variation within species. In the laboratory, it has been possible to select for strains of An. gambiae that are refractory to infection by malaria parasites. These refractory strains have an immune response that encapsulates and kills the parasites after they have invaded the mosquito's stomach wall.

(source: https://www.cdc.gov/malaria/about/biology/mosquitoes/)

Please note that other mosquito species are not resistant to the plasmodium, because we call "resistant" a host that's capable to fight the parasite. The other species are not even hosts!


Adult Bugs in Low Humidity House Heated With Wood?

The pictures are not entirely clear, but I’m relatively certain that it is a wood wasp of the genus Xiphydria (family Xiphydriidae). Traits that point to this is e.g. 2 pair of wings (i.e. a wasp and not a fly), narrow slender antenna, elongated body, the shape of the head sitting on a relatively long “neck”, often with light/white markings on the top and or the back of the head (which can be seen on picture 2) and often white markings along the side of the abdomen (which your insect has) The second picture also shows the relatively robust ovipositor (used to inject eggs into wood).

They also lay eggs into dead wood (usually deciduous wood) and are not uncommon to find in houses, hatched from fire wood.

The species is very hard to determine though, but X. mellipes could be one bet. This species also seem to be found in Canada, see zoology.ubc.ca/entomology. It is also similar to Xiphydria camelus which is common here in Sweden, but I’m sure if it is also found in Canada.

(Xiphydria mellipes from wikimedia commons

Pictures of some species can be seen at bugguide.net).

These insects are not dangerous to find inside, and they only attack dead wood in standing or fallen trees, not construction wood. They are not uncommon to find indoors (along with longhorn beetles and other wood insects) if you bring in mixed fire wood, especially if the wood wasn’t processed and dried quickly after felling. An interesting feature of these insects is that many (all?) inoculate the wood with particular fungi spores, and the fungi later function as the food for the larvae.


In order to keep the hair from decomposing, my first assumption is you'd need it in an environment that inhibits decomposers, e.g. dry. We can see in the mummification process that hair may be preserved for hundreds of years. Hair is also composed largely of keratin, however, and in my own search of the literature: (1) we need microbial (bacteria, fungi) keratinases to decompose the keratin in hair [source], and (2) this process is slow. There's a really old article here, from the abstract:

  Keratin, prepared from horn meal, was added to moist field and garden soil and allowed to decompose in the laboratory. The keratin was found to undergo a decomposition resulting in a slow, but steady accumulation of ammonia and nitrate. 35–40 per cent, of its nitrogen was transformed into nitrate after 120 days.

More recent numbers to shed light on a rate of degradation for keratin are either obscure, or untested. This is more so for hair specifically as I couldn't find much more.


Which one is better to use for water stress experiment GWAS or RNASeq?

bambara groundnut does not have a reference genome

This is your biggest problem if you want to do any sequencing based analysis. Neither GWAS nor RNAseq data analysis are possible without a reference genome (or at least transcriptome).
Depending on the availability, quality & similarity of reference genomes from related species it may however be possible to construct a reference transcriptome for your species from RNA sequencing data you get from RNAseq experiments. I'm whether it's feasible (or indeed possible) to try the same with genome sequencing data, since with only 10 individuals/strains you may only be able to get huge linkage groups for GWAS analysis.

Either way I'd highly recommend you to talk with someone (i.e. from your institute) who has experience in doing RNAseq or GWAS on plants, when planning this. (The experience with platns important, mammalian/model system genomes are much better studied and generally have less genome duplications, so analysis of plant data comes with its own set of baggage)

  Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?

If you want to use RNAseq to find genes that are differentially expressed between states of water stress and no water stressin the same plant/species you will need to compare samples taken from corresponding conditions. This is only possible with RNAseq data.
Another approach could be to do some other experiments to determine which plants show a phenotype when exposed to water stress, and then look for correlations of this phenotype with (sequence) isoforms variants [GWAS like approach, possible with RNAseq or genomic sequencng data] or with expression levels of certain genes [again only possible with RNAseq data]. In thsi approach you need to be aware that your sequencing data either represents the ground state of all plants (no stress) or a potentially stressed state and missing one of these may mean that you can't find genes that change expression levels based on stress.

  It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?

First, while most analysis tools will always give you some values for up- or downregulation, that does definitely not mean that these values are always meaningful. Only proper statistical testing can tell you which up/downregulation is somewhat reliable (it still wont tell you if its biologically meaningful) and depending on the quality of your data and the actual biological differences you may not be able to find anything.
Secondly, if you care about the timepoint of expression for specfic genes, you will need to some time series experiments. (Doing that for the whole RNAseq/GWAS would be very expensive, so ideally you first identify some candidate genes and then study their specific expression profiles with easier methods).

  when is the appropriate time to take my samples, i was considering taking at 50% flowering stage.

If you are not an  expert on the species you#re working with, I'd again highly recomment you to speak with someone who is.


Can Serous inflammation on pleura pulmonalis cause dry cough and runny nouse?

If serous inflammation produces a large amount of serous fluid this leads to lung compression and limitation of respiratory movement. This, as you said produces dry cough by means of reflex arch.

However lung compression leads to alveolar collapse or atelectasis through pleural effusion. After atelectasis, pneumonia can develop quickly as a complication.

And nasal congestion is a symptom of pneumonia. Also if pneumonia develops, the cough, initially dry and reflex, will turn to cough with mucus expectoration.

Cough stimulates nasal congestion when it brings up mucus from the lungs and extends the alveolar inflammation up to the nose by taking and concentrating all the bacteria in the upper airway (pharynx and larynx bacteria gets in the nasal sinuses) - and in case of bacterial pneumonia mucus also contains the etiologic agent of that pneumonia (so not only from the upper airway).


I can't yet comment, so here's a (sort of) answer:

I've only ever heard the "2/3 of cellular expenditure" rule applied to neurons, and frankly, it wouldn't make much sense in any cell other than a neuron.  The Guyton and Hall Textbook of Medical Physiology says, "For some cells, such as electrically active nerve cells, 60 to 70 percent of the cells' energy requirement may be devoted to pumping Na+ out of the cell and K+ into the cell."  A cardiac muscle cell, for example, would probably use more of its energy for contraction than pumping ions.

In a neuron, the bulk of energy expenditures are for electrical signalling done via allowing sodium and potassium ions to temporarily run DOWN their respective gradients.  As such, the "purpose" of a neuron is to pump ions across a membrane and then let them run back when needed.  Since a neuron doesn't really DO much else, it makes sense that the bulk of the energy produced will go towards pumping ions.  A practical example is the use of barbiturate comas to reduce metabolic activity in the brain.  Flat-lining the EEG drops metabolic requirements by ~50% (Source: Medscape).

Please keep in mind that this answer is specific to neurons...other cells perform other functions, and those other functions will take up significant fractions of energy produced.  Further, other cells probably aren't devoting large fractions of their energy towards signalling, and so the fraction of energy devoted to pumping ions will be markedly less.  They'll still be pumping ions to maintain a gradient to perform tasks like membrane transport and osmotic control, but those tasks are ancillary to the "purpose" of those cells.  I can't find any solid numbers for Na/K ATPase energy expenditures in non-neuronal tissue at the moment, but if I do, I'll update appropriately.

UPDATE:
With regards to the question itself, which I apparently forgot to answer:

Can a cell function without an appropriate membrane potential? Can co-transport run without a membrane potential?


Most water moves up through the xylem by capillary action. Imagine dipping a pipette into a small pool of water; the water would rush up into the pipette. Or, imagine dipping the edge of a paper towel in water. The water "runs" up the paper towel. This is capillary action.

As water evaporates out of the leaves and such in higher regions of the plant, a capillary force pulls up more water. If for instance, you were to dry the top of your saturated paper towel, more water would be pulled up from the pool below to wet that top section.

As for a molecular explanation, Wikipedia has a good explanation of Cohesion-tension theory.


Can Bacteria Repair Dephosphorylated Plasmids?

As per WYSIWYG's suggestion, I tried the digest and dephosphorylation again with SalI and ran a gel. The gel showed that SalI was less than ideal at cutting this plasmid.

As you can see, the most intense band is the bottom band, which is most likely supercoiled DNA, with the linear DNA I want appearing in the middle, and open circle DNA coming in third. I very carefully cut the middle band out and did a gel extraction. When I ligated this the control plate had 1 colony. Unfortunately, the experimental plates had between 2 and 6 colonies each. I am running minipreps on those now, will just have to see what I get.

This explains why the previous attempts produced so many colonies on the control plates, most of the DNA was uncut, so no amount of dephosphorylation would help it.

One thing that does bother me, is that my gel extractions seem like they have had really poor yields. I typically start a digest with 4 ug of plasmid. After phenol:chloroform extraction and isopropanol precipitation, I'll usually recover 2 - 3 or more ug of DNA. After gel extraction, I'm lucky to get 300 ng of DNA. To make things weirder, the liquid that comes off the spin column in the final elution step will gel up, like a low density agarose gel. The only explanation I can come up with is that residual agarose in the spin column is somehow forcing its way through the membrane and into the elution buffer. The goo clogs pipette tips and makes life difficult.


Each chromosome location which has been identified as being a SNP is a location at which more than one nucleotide occurs at appreciable frequencies in the general population.  This means that there are two or more bases which can occur there, so a person's test must show which bases actually occur there in that person's genome.  Since a person has both a paternal and a maternal chromosome of a chromosomal type (a pair of homologous chromosomes), the person has two instances of the SNP location and so two nucleotides to be detected and reported.  Hence your dataset has two nucleotides for each SNP location for each patient.

Just from the reported base or the SNP name you can't tell which is more frequent in the population.  If you need to know that, you must consult SNP frequency data from some other database. (The SNP names in your example, e.g. "exm355" are not familiar; usually SNPs have names like "rs1234567".)


Yes, this is a cattle egret displaying its breeding plumage.

The cattle egret (Bubulcus ibis) is a cosmopolitan species of heron (family Ardeidae) found in the tropics, subtropics and warm temperate zones.

Specifically, this is the eastern subspecies, B. ibis coromandus.

 B. ibis coromandus [source: Wikimedia Commons]

 B. ibis ibis © Larry Thompson, 2007-2015

The cattle egret is the only member of the monotypic genus Bubulcus, although some authorities regard two of its subspecies as full species, the western cattle egret and the eastern cattle egret.

The eastern subspecies B. ibis coromandus, described by Pieter Boddaert in 1783, breeds in Asia and Australasia, and the western subspecies (B. ibis ibis) occupies the rest of the species range, including the Americas.
The eastern subspecies (B. ibis coromandus) differs from the nominate subspecies in breeding plumage in that the buff color on its head extends to the cheeks and throat, and the plumes are more golden in color.

B. ibis usually feeds in seasonally inundated grasslands, pastures, farmlands, wetlands and rice paddies. Their name comes from their tendency to often accompany cattle or other large mammals in these areas, where they catch insects attracted to and small vertebrates disturbed by these animals.

Originally native to parts of Asia, Africa and Europe, B. ibis has undergone a rapid expansion in its distribution and successfully colonized much of the rest of the world in the last century.

 [Source: Discover Life]

Major Source: Wikipedia


Chemistry of the phosphodiester bond in RNA

Generally hydrogen is not shown in DNA structure. I have made a simple diagram to show where all hydrogens go:

There are 3 hydrogens in phosphoric acid, each of them leaves as:

1 H joins with 3' -OH of previous nucleotide to form H2O during DNA replication.
1 OH joins with H of next nucleotide to form H2O during DNA replication.
1 H is released as H+ (remember it was phosphoric acid), hence giving rise to the acidic character of DNA (remember it is DeoxyriboNucleic Acid).

I think you should first study DNA replication (if you haven't, yet) to get more thorough knowledge about the topic.


The potato developed this pattern because it's (probably) natural to cultivar you're growing or due to cross-pollination.
Purple pigment is anthocyanin. It's perfectly normal and considered as more healthy (as those varieties of potatoes contain more antioxidants and vitamin C) and even 'gourmet'.


Coordinates of amino acids in a protein sequence

If what you are after are the structural co-ordinates of particular  amino acids crystalized individually (i.e. considered as small molecules independently of any role in proteins), then you should find them along with other small molecules in the Cambridge Structural Database.


What is the relationship between independent assortment and cross over?

During meiosis, the independent assortment will be made first and then cross over will be made.

No, independent assortment occurs after crossing over. Crossing over occurs in prophase I while independent assortment occurs in metaphase I and anaphase I.

  I am so confused, what is the difference between this two process?

During prophase I, a process called synapsis occurs. That is, homologous chromosomes (one from your mother and one from your father) come together and bind together, forming a tetrad. This binding is due to crossing over, which is when the genetic material on the maternal chromosome and the paternal chromosome exchange places. The maternal chromosome gives some of its genes to the paternal chromosome, and the paternal chromosome gives some of its genes to the maternal chromosome. Crossing over increases genetic variety by creating a new chromosome with a new combination of genes.

During metaphase I, the tetrads line up at the equator of the cell. During anaphase one, the tetrads are broken apart and each homologous chromosome that made each tetrad up is pulled toward one end of the cell. Look at the image below, where the blue represents paternal chromosomes and the red represents maternal chromosomes.

Independent assortment describes the phenomenon where the paternal and maternal chromosomes can be lined up randomly at the equator. There are many combinations. For example,

Both red chromosomes could face the top pole and both blue
chromosomes could face the bottom pole.
Both blue chromosomes could face the top pole and both red could face the bottom.
One red on the left and one blue on the right could face the top, as shown in the picture.
One blue on the left and one red on the right could face the top.

This random alignment at the equator makes it so that during anaphase, random proportions of maternal and paternal chromosomes get assorted into each of the resulting daughter cells. Some cells could get more maternal chromosomes and the other would get more paternal chromosomes, and vice versa. On the other hand, they could get similar amounts. Independent assortment increases genetic variation by allowing daughter cells to each randomly receive a different proportion of paternal and maternal chromosomes.

In conclusion, crossing over and independent assortment (sometimes called random assortment) are different independent processes that both lead to an increase in genetic diversity.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. “Meiosis and Sexual Life Cycles." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 252-266. Print.
https://www.quia.com/files/quia/users/dschnepp/Meiosis/Metaphase-I


Simpler answer (although I like Remi.b's):

Probably.

If you want to know for sure go to a doctor and have them look at your Epiphyseal Plates in your long bones (Femur, Tibula, Fibula). If they've fused, you won't grow anymore. If they're still distinct then you'll continue to grow until they fuse.

For males that can happen as late as early-20's. However, depending on genetics, you might not gain that much height.

Here's a graph you might be interested in:

You're at the tail-end of probably your last growth spurt. You have probably 2-3 years' worth of growing left, but don't expect miracles. You've got maybe another 1-2cm.


Were Telomeres the Master Key to Abiogenesis

No, they weren't. Interesting hypothesis though!

However, that hypothesis is missing a very important piece of information: prokaryotes don't typically have telomeres.

Because their DNA is typically circular, rather than linear, telomeres aren't necessary, and there is no shortening problem.

See the Wikipedia page on telomeres for more information. There are various theories on the origins of telomerases and telomere evolution, check out Google Scholar.


Book Recommendations: GRE Subject Test In Biochemistry, Cell And Molecular Biology

You can also try Lehninger Principles of Biochemistry...It covers all the topic except the part about cell motility...& possibly, the 1-A-g ( I'm not too sure about it)...but the book is for pretty advanced levels...& I would not recommend it as a last minute reference book..but for thorough study it's great....& of course it's my personal opinion...so before you consider any book, I would rather advice you download a pdf copy of the same, to get a 1st hand experience...hope this helps & good luck for your exam...


ATP Hydrolysis to AMP in the Urea Cycle. What is the Free Energy Change?

The answer, I reckon, is that as stated it isn't.
However,the hydrolysis of ATP to AMP and PPi yields considerable more free energy than does the hydrolysis of ATP into ADP and Pi.
That is, the free energy change for the hydrolysis of  ATP into AMP and PPi is considerably more negative that that for the hydrolysis of ATP into ADP and Pi and for the hydrolysis of ADP into AMP and Pi.
If we consider the the free energy change for the reaction ATP  = AMP + 2 Pi  (where, say, the pyrophosphate (PPi) produced by  argininosuccinate synthetase is broken down by a  pyrophosphatase), then  it is the equivalent to  the  hydrolysis of 2 ATP to ADP and Pi and (more or less) to  the hydrolysis of 2 ADP to AMP and Pi.
When dealing with ATP hydrolysis, we must take the 'chemical environment' of the phosphate group into account, not only in determining whether the bond is 'high energy' (in the Lipmann sense) or 'low energy', but also when considering the amount of free energy released by hydrolysis of a  'high energy' linkage: not all pyrophosphate linkages yield the same free energy on hydrolysis.

Cleavage of the 'inner' pyrophosphate linkage in ATP (to give AMP and PPi) 'releases' considerably more free energy than cleavage of this linkage in ADP (to give ADP and Pi).
Cleavage of the 'inner' pyrophosphate linkage in ATP  (to give AMP and PPi) releases considerable more free energy than the cleavage of the 'outer' pyrophosphate linkage (to give ADP and Pi).

If  one 'unit' of free energy is considered to be about 32 kJ mol-1 then:

The hydrolysis of ATP to ADP and ADP roughly releases 1 unit
The hydrolysis of ADP to Pi and AMP roughly releases 1 unit
The hydrolysis of ATP to AMP and PPi roughly releases about 1.4 units
The hydrolysis of PPi to 2 Pi roughly releases about  0.6 units
Hydrolysis of ATP to AMP and 2 Pi roughly releases 2 units.
Hydrolysis of AMP to adenosine and Pi roughly releases 0.4
units.

The question posed by the OP may now be answered as follows.
Hydrolysis the inner pyrophosphate linkage of ATP (to give AMP) rather than the outer linkage (to give ADP) provides a 'thermodynamic pull' of 0.4 'free energy units' to the  argininosuccinate synthase reaction.  If the  PPi is hydrolyzed by a pyrophosphatase an extra 0.6 'free energy units' are obtained and the free energy change for the combined reaction (that of argininosuccinate synthase and the pyrophosphatase) is equivalent to 2 'free energy units' (about -70 kJ mol-1).

As pointed out by Frey, & Arabshahi (1995), hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ATP, rather than the $\beta$,$\gamma$ linkage, is a common strategy in biosynthetic reactions.  To quote the final line of this paper: Cleavage of the $\beta$,$\gamma$-phosphoanhydride bridge in ATP takes place in metabolic reactions in which a smaller driving force is required.
A Small Piece of History
It was not always accepted that the hydolysis of ATP to AMP and PPi proceeded with a more negative free energy than for the hydrolysis of ATP to ADP and Pi.  To quote from  Standard Free Energy Change for the Hydrolysis of the $\alpha, \beta$-Phosphoanhydride Bridge in ATP , by Frey & Arabshahi (1995).

It  appears to be common knowledge in biochemistry  that the standard free energy change $\Delta G^{'o}$ for the hydrolysis of ATP to AMP and PPi is -7.7   to  -8.4 kcal  mol-1 [-32 to -35 kJ mol-1].  Most textbooks of biochemistry  list  values  in  this  range (Zubay, 1993; Lehninger et al.,  1992; Garrett & Grisham, 1994; Voet & Voet, 1990; Matthews & Van  Holde, 1990). Moreover, many  textbooks  also  list  the standard free energy  for  the hydrolysis of  PPi as  $\Delta G^{'o}$ = - 7.9 to  8.0 kcal  mol-1.  [-33 to -33.5 kJ mol-1]. However,  the  true  value for pyrophosphate  hydrolysis is significantly less negative (Flodgaard & Fleron, 1974). Therefore, the standard free energy change for the hydrolysis of ATP to AMP and PPi must be more negative  than 8 kcal  mol-1 [ 33.5 kJ mol-1]  as is explained in this paper

This reminder should not have been necessary.  The correct value for the free energy change in the hydrolysis of ATP to AMP and PPi is given by Schuegraf et al (1960)  , a paper co-authored by Sarah Ratner
The hydrolysis of UDP-Glucose
$\Delta G^{'o}$ for the hydrolysis of UDP-glucose to UMP and  glucose-1-phosphate is about - 43 kJ mol-1 (- 10.3 mol-1) [Frey, & Arabshahi, 1995], also considerably more negative that that for the hydrolysis of ATP into ADP and Pi
Specifics

The standard free energy of hydrolysis ($\Delta G^{'o}$) of the $\alpha$,$\beta$-phosphoanhydride of ATP to give AMP and PPi is about - 45 to -50 kJ mol-1

The standard free energy of hydrolysis of the $\alpha$,$\beta$-phosphoanhydride of ADP to give ADP and Pi is about -30 to -34 kJ/mol

The standard free energy of hydrolysis of the $\beta$,$\gamma$-phosphoanhydride of ATP to give ADP and Pi is about -32 to -36 kJ/mol.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

The standard free energy of hydrolysis ($\Delta G^{'o}$) of PPi to 2 Pi is about 20 kJ mol-1

The standard free energy of hydrolysis ATP to AMP an 2Pi about -70 kJ mol-1.

(For a diagram illustrating the  nomenclature of the $\alpha$, $\beta$ and $\gamma$ phosphates of ATP, see here).
Notes

Following Alberty (2000), all equations are written as 'biochemical equations' where everything is balanced except hydrogen ions.

$\Delta G^{o'}$ for the following reaction is about -50 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= AMP +PP_i $$

[1 ]  Frey, & Arabshahi (1995) give a value of -45.6 kJ mol-1 (-10.9 kcal mol-1).
[2] Dixon et al  (2000) give a value of  -48.5 kJ mol-1 (-11.6 kcal mol-1).
[3] Schuegraf et al (1960)  give a value of  -43 kJ mol-1 (-10.3 kcal mol-1).
[4 ] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -50.2 kJ mol-1 (-12.0 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -36 kJ mol-1 (-12 kcal mol-1)

$$ ATP + H_2O= ADP +P_i    $$

[1] Frey, & Arabshahi (1995) give a value of -32.6 kJ mol-1 (-7.8 kcal mol-1).
[2] Rosing & Slater, 1972 give a value of -31.5 kJ mol-1 (-7.53 kcal mol-1).
[3] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1 ) of -36.6 kJ mol-1 (-8.8 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -34 kJ mol-1 (-8.1 kcal mol-1)

$$ ADP + H_2O= AMP +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -34.04 kJ mol-1 (-8.13 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -71, kJ mol-1 (-16.9 kcal mol-1)

$$ ATP + 2 H_2O = AMP + P_i  + P_i$$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -70.68 kJ mol-1 (-16.9 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -13.7 kJ mol-1 (-3.3 kcal mol-1)
$$ AMP+ H_2O  =  Adenosine  +P_i $$

[1] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -13.74 kJ mol-1 (-3.28 kcal mol-1)

$\Delta G^{o'}$ for the following reaction is about -20.5 kJ mol-1 (-4.9 kcal mol-1)

$$ PP_i + H_2O= P_i +P_i $$

[1] Frey, & Arabshahi (1995) give a value of -19.24 kJ mol-1 (-4.6 kcal mol-1).
[2] Calculation from the tables supplied by Alberty (2000) gives a value (25oC, pH 7, ionic strength of 0.1) of -20.5kJ mol-1 (-4.9 kcal mol-1)


Why is the human body hair not uniformly colored?

The hairs you mention are also called "androgenic hairs", meaning their growth and pigmentation is influenced by androgens. These include pubic hair, the hairs on the breast and shoulders (almost exclusively for men) and the beard.

It seems, that these hair bulbs have different sensibilities (number and expression of androgen receptors) so they react differently to androgen levels. This includes balding, pigmentation, growth and so on.

These articles should be a good starting point, if you want to dive deeper into the topic:

Androgen actions on the human hair follicle: perspectives.
Mechanism of action of androgen in human hair follicle.


The video you linked to, and from which you got the still shot. is real.  There are  hundreds of such videos now that Underwater Remotely Operated Vehicles (ROV) are more commonplace.

...could the output from the ROV thrusters rip it apart(?)

A working class ROV needed for deep ocean floor exploration can be the size of an SUV. There's no reason to believe its thrusters can't generate the shear forces needed to (sadly) tear a delicate jelly apart.

...I couldn't find out if it's CGI or if it's an actual jellyfish.

Although not a jellyfish, it is similar in being delicate; it's a ctenophore or comb jelly. The refraction/bioluminescence pattern is common in ctenophores.

And what dazzling colors these creatures display! The cilia of the ctenophores refract light in iridescent waves. Certain species are even capable of producing light, like fireflies of the sea!

For more information and videos, this short Youtube video might help. Or for a written explanation, this article, Introduction to Ctenophora  (https://ucmp.berkeley.edu/cnidaria/ctenophora.html) is good.


Does DNA react in all of the ways most other acids do?

It may seem counterintuitive that deoxyribonucleic acid has nitrogenous bases. Nonetheless, nucleic acids (thus including RNA) were called that way because the phosphate backbone (linked by phosphodiester groups) is a derivative of phosphoric acid.
Phosphoric acid

Image Source
Phosphodiester group

Image Source
Note that the only difference between these two groups is that in the case of the phosphodiester, two O-H bonds are replaced by O-C bonds. This make the last remaining hydrogen atom quite acidic (can quickly be identified by how the conjugate base exhibits resonance). In fact, it is so acidic that at physiological pH, the phosphodiester group is deprotonated, giving that nucleotide a negative charge. This property does have a profound effect on DNA's structure and "behavior" in a cell, and is often exploited in genetics, such as in gel electrophoresis.
An interesting fact is that this acidity of the phosphodiester group actually competes with the basicity of the nitrogenous bases. However, since most often DNA is double-stranded, individuals bases will hydrogen-bond with its partner to make base pairs, which stabilizes and thus reduces this basicity.
TLDR: Although different acids of different molecular composition can act in very different ways, the overall acid-base chemistry is seen in nucleic acids.


Where are doxycycline's anti-inflammatory properties derived from?

Doxycyline inhibits iNOS and TNF-alpha expression.   It also influences secretion of IL-1beta, IL-8, and TNF-alpha, as well as other inflammatory cytokines.

[These are results collected from multiple systems.]

For appropriate references, see: Leite et al (2011). Anti-inflammatory properties of Doxycycline and Minocycline in experimental models: an in vivo and in vitro comparative study. Inflammopharmocology.

As for the chemistry of how doxycycline accomplishes these things, I'm afraid I don't know the answer, but hopefully, this gives you a place to start.


Why do we have the tibia and fibula (a 2nd bone) in the lower leg?

It does function in the rotation and stabilization of the foot, but that is not why we have it, even species in which it serves no function still have it. A bone does not necessarily have to have a purpose in an organism, instead it can have on in its ancestors.

We have this arrangement becasue we inherited the basic limb bone arrangement from our fishy ancestors. Basically all tetrapods share the same pattern of bones in their limbs, one bone, two bones, many small bones, followed by several groups of long thing bones. this goes for front and hind limbs.

tetrapod evolution


Trimming = removing RNA sequences from one end.

Splicing = removing introns and joining exons back together.


Yes is the simple answer. A nerve will go up to a specific part of the brain which the brain knows corresponds to a certain region of the body. It isn't perfect though e.g. pain in the diaphragm confuses the brain which doesn't recognise that pain must be coming from there so instead tells the body there is shoulder pain, however this is useful in medicine. Another infamous example is pain from heart disease (angina) which causes pain in the jaw and arm. Perhaps even more interestingly, if a nerve is cut and then grows back linking to the wrong nerve it may lead to the completely wrong part of the body being identified when touched. Also if the brain itself is stimulated in these corresponding areas, a person will feel he or she is indeed being touched in a certain part of the body.


Do humans learn to distinguish different senses?

Mixing up input from different senses is actually a known neurological phenomenon called synesthesia. Synesthetes (ie. adults experiencing synesthesia) might see numbers in colors for example. Some may even "taste" colors as you say.

Now do all infants have synesthesia before some stage in development is another question. It is actually a rather old hypothesis called "neonatal synesthesia". One piece of evidence comes from this study which tested shape/color association in infants. I do not see any other study concerning this hypothesis though. I guess the main reason might be the difficulty to develop an objective experimental design on small infants who hardly communicate...


How did the "serendipitous rediscovery" of Sulfasalazine as an antirheumatic agent after 30 years happen?

Your question led me to:

Pinals, RS (1988) Sulfasalazine in the Rheumatic Disease. Seminars in Arthritis and Rheumatism 17:246-259. I reproduce the introduction to this paper below:

  Most physicians are familiar with sulfasalazine (SSZ) as an agent commonly used to treat inflammatory bowel disease for more than 40 years. In 1978, McConkey et al reported preliminary studies suggesting that this sulfonamide might be effective in rheumatoid arthritis (RA).1 The use of SSZ arose from earlier open and controlled trials with a sulfone, dapsone, which had demonstrable efficacy in RA, but the benefits were accompanied by relatively frequent, often unacceptable adverse effects.2 Dapsone was effective in dermatitis herpetiformis, presumably because of immunosuppressive activity. Another therapeutic agent for this skin disorder was sulfapyridine (SP), a drug with a poor record of gastric tolerance. Therefore, McConkey et al elected to try SSZ, a compound that released sulfapyridine in the bowel after passage through the stomach. Ironically, McConkey was initially unaware that SSZ had been synthesized specifically to treat RA in the late 1930s. In 1980, McConkey et al reported their open experience with SSZ in 74 patients treated for up to 1 year.3 The improvement in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and clinical score (a global evaluation) was similar to that achieved with the disease-modifying antirheumatic drugs (DMARDs), and appeared somewhat sooner, often within 2 months. Moreover, although adverse effects were frequent, they were seldom of sufficient severity to discontinue treatment. This encouraging report led to several controlled trials in the United Kingdom and elsewhere, all confirming the efficacy of this interesting agent. The first study in the United States has been reported4 and, although SSZ has not been approved by the Food and Drug Administration for use in RA, many rheumatologists have used it as an alternative DMARD because of its availability and long record of safety and efficacy in inflammatory bowel disease.

What I have gleaned from this and a couple of papers cited there is that B McConkey, working at a hospital in Birmingham in the UK became interested in developing methods of clinical assessment of rheumatoid arthritis (RA) in the 1960s and this led eventually to the discovery that the drug dapsone is effective as a treatment but with an unacceptable level of adverse side effects. Then, to quote McConkey:

  We had studied dapsone partly because of its effect in leprosy and dermatitis herpetiformis; its mode of action in those diseases may be through its immunosuppressant properties. Another drug used in dermatitis herpetiformis is sulphapyridine;it did not attract us as a contender but it is a constituent of salicyl-azo-sulphapyridine (sulphasalazine), a compound originally formulated for RA and latterly found to have immunosuppressant properties.

  McConkey et al (1980) Sulphasalazine in rheumatoid arthritis. British Medical Journal 1: 442-444

  (This is ref 3 in the Pinals introduction.)

So clearly there was a strand of chemical logic in the rediscovery of the drug; the only serendipitous aspect was that McConkey did not at first know that sulfasalazine was originally designed as a treatment for RA.


Why does the inhibition of translation initiation cause the accumulation of 80S ribosomal monosomes?

It will depend on the drug you are using. There is a pathway that forms the translational initiation complex that starts with binding the mRNA's cap, the small subunit scans to find the AUG, then the large subunit binds, and so on. The 80 S peaks on the density gradients are not vacant, they are poised on mRNAs waiting to initiate (if you removed the inhibitor).


Taking care of Birds: Unwanted species scaring away a less common one from a birdhouse

The best way to foil Mynas is to use an Anti Myna baffle over the nest box. Since Myna always fly directly into the nest box hole, this baffle prevents that while allowing other species to enter the box.


Color van der waals bonds in swiss PdbViewer

If I'm right in assuming you are trying to get colouring like the purple AA VDW bonds then I can only specifically colour VDW bonds in solid 3D view (under display, Render in solid 3D) in SPDBV but not when solid 3D view is not activated, as in the example in your picture. One option is to use POV-Ray but I haven't worked with it.

If the purple colouring is not photoshoped by the authors of the paper you got the picture from, then the chances are they have written a custom script for it in the software, which allows them to do this. So I would just contact the corresponding author and ask them how they managed it and if they have done it through a script or some other software. Most of the time people are happy to share their methodology once they have published it!

Also have you tried the Jalview software? Although it's designed primarily as an alignment tool but it has a nice 3D Jmol view. You can load up your sequence and the associated PDB file and you can play around with it. The graphics output are quite publication friendly. I'm not an expert at it and I've only been playing around with it for a bit but when you get the hang of it, it's quite nice graphically. Although the VDW view is still space fill 3D but it's a bit nicer as it has opacity etc etc. Just download it and as soon as you open it up, you are presented with an example alignment and Jmol view. Just play around with the alignment section and the Jmol view and see if you like the aesthetics. The only tricky part in the software is getting the residues you want selected but once you manage that, you can get the program to display VDW only for the selected residues.

Hope this helps.


Will modern-day insects grow to massive size in a high-oxygen environment?

While @CalendarJ comments "Yep!" above, a quick search suggests that experimental hyperoxia typically only increases insect body sizes slightly. Everything below is from VandenBrooks et al. 2012 (of course there could be other sources that contradict this!)

  A few beetles have been reported to reach larger sizes when reared in hyperoxia, but most of the species examined reach similar body sizes in 40% oxygen as in normoxia (Harrison et al. 2009).

and:

  Here we investigated the impacts of Paleozoic oxygen levels (12–31%) on the development of Blatella germanica cockroaches. Body size decreased strongly in hypoxia, but was only mildly affected by hyperoxia.

and this figure:

These results show that male cockroaches grow much larger under present-day (normoxic; 21% oxygen, highlighted box) and elevated (hyperoxic; >= 24% oxygen) levels than under low (anoxic; 12%) conditions, but the hyperoxia-grown roaches are only a bit larger than normoxia-grown ones. (Similar results for females not shown.)

VandenBrooks, John M., Elyse E. Munoz, Michael D. Weed, Colleen F. Ford, Michael A. Harrison, and Jon F. Harrison. “Impacts of Paleo-Oxygen Levels on the Size, Development, Reproduction, and Tracheal Systems of Blatella Germanica.” Evolutionary Biology 39, no. 1 (March 1, 2012): 83–93. https://doi.org/10.1007/s11692-011-9138-3.


Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?

Excellent question! The answer is actually a really cool and crucially important detail about membrane potentials and the movement of ions. Basically, the electric force is very strong. You don't actually need to move many ions for the membrane potential to fluctuate dramatically. The number of ions that "move" to establish equilibrium is tiny compared to the actual concentrations. That's why the Nernst and GHK equations are so powerful: what really matters is the relative permeability of different ions and the gross concentration differences, not the changes in their concentration that occur when, for example, voltage-gated channels open during an action potential.

You can calculate just how many ions have to move, which depends on the size of the cell. Here is a nice example from the reference I have linked below:

  For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

Therefore to answer your question: why is it allowed to use the resting concentrations? Because the concentrations of the ions don't change by more than 1/100,000 fold with a 100mV swing in potential, and there isn't much impact on the GHK/Nernst equation from a change this small. For example, as the voltage goes from ~-70mV when a fairly typical neuron is at rest (and the membrane is most permeable to K+), up to maybe +30mV at the peak of an action potential (and the membrane is most permeable to Na+), only a "few" sodium ions actually cross the membrane, so maybe the internal sodium concentration changes from 10mM to 10.0001mM. The thing that changes most during an action potential is not the actual concentrations, only the permeability to different ions.

Maybe an additional misconception you have is about the cell "deciding" what the concentrations are. Indeed, if the concentrations of particular ions changed dramatically, it would be necessary to recompute equilibrium potentials. The key concept is that those concentrations don't change much during normal functioning of the cell, and they don't have to change much to observe big changes in membrane potential. An excitable cell uses those swings in membrane potential as the signal, rather than the concentrations of the ions. One exception is calcium, see the note at the end.

Reference:

Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.

(as a side note, movement of ions does matter over a longer time scale, which is why it is necessary for the Na+/K+ pump to constantly operate to keep the membrane potential steady, and some ions like Ca2+ are at such low concentrations normally that the influx of calcium can be substantial relative to the resting concentration, which is partly why calcium is so powerful as a second messenger and why calcium chelating components of the cell are important)


Are microsatellites viable markers for GWAS?

Microsatellites could be used for GWAS. Actually they were the basis for linkage studies and were also used in the first association studies. The main reason why they have been replaced by SNPs is that in the human (or other organims') genome, there are by far more SNPs than microsatellites.
GWAS rely on linkage disequilibrium between the marker and the real causal variant. LD decreases quite fast with distance, thus, the more markers you use, the more likely you are to genotype a marker in LD with the causal variant. In the end, I would strongly recommend to use SNPs to perform GWAS.


What does it mean to share similarities among living organisms "both horizontally and vertically"?

Ben Bolker's comment is correct; the next sentence in the passage helps to clarify (bold added):

  The biggest spin off
  of such studies was the recognition of the sharing of similarities among
  living organisms both horizontally and vertically. That all present day
  living organisms are related to each other and also to all organisms
  that ever lived on this earth, was a revelation which humbled man and
  led to cultural movements for conservation of biodiversity.

The relationship between species in the present day are the horizontal relationships; one can define species horizontally by looking at and grouping organisms existing today (or at any other time "slice"). You can compare species horizontally by, say, looking at the skull of a human and the skull of a chimpanzee.

The relationship between species today and species that have existed in the past are the vertical relationships. For example, you could look at the skull of a modern horse and compare it to the skull of Mesohippus.

I've included a couple sources below that use this distinction, though I'm not sure where it originates.

I'd say the "horizontal" terminology comes up more frequently and may be more familiar, for example in reference to horizontal gene transfer one is talking about genetic material moving between species living at the same time. "Vertical gene transfer" can also be defined as the transmission of genetic information from parent to offspring, but more typically you would just call it inheritance.

Alvarez-Venegas, R., Sadder, M., Tikhonov, A., & Avramova, Z. (2006). Origin of the bacterial SET domain genes: vertical or horizontal?. Molecular biology and evolution, 24(2), 482-497.

Stamos, D. N. (2002). Species, languages, and the horizontal/vertical distinction. Biology and Philosophy, 17(2), 171-198.


Is this formula for calulating the energy requirements of pets applicable to all animals?

No, I would not use this formula for rodents. The "3/4-law" is usually used only for mammals with a mass of m>10 kg and was derived by Kleiber from limited empirical data sets.
For mammals with a bodymass below 10 kg the prefered exponent seems to be 2/3 which was derived from the relationship of volume and surface of the body and heat energy as the main source of metabolic rate. See here.

Either way this are only approximate calculations I would not trust too much as exceptions occure frequently and also the age and/or physical state can make a difference.


How does Yeast-two-hybrid detect interactions between several proteins in one experiment?

You use a library of many yeast in which each expresses only one target, or 'prey' protein. Then you grow each yeast colony separately, for example in different wells.

It's definitely not a high-throughput method if you do it the old-fashioned way, i.e. making your own yeast library, or if you do it with only a few targets.  But these days you can buy pre-made yeast libraries with thousands of target proteins, each separated into a well on a plate, then you run the experiment for all the targets simultaneously. With a visible marker you can then easily see which wells have produced successful interactions, and thus which targets interacted with your bait.


Are the ribosomes specific for each organism

One can prepare rabbit ribosomes from reticulocytes (immature red blood cells), and by providing a few cofactors required for an active extract, create an in vitro system that will translate virtually any eukaryotic mRNA that contains the correct sequence determinants. You can purify mRNA from your cells or tissues of choice, or you can synthesize an mRNA in vitro using a DNA template and an RNA polymerase. Either of these will be translated in a nuclease-treated rabbit reticulocyte lysate.

IVT (in vitro translation) extracts can be prepared from virtually any source (e.g., C. elegans shown by Bob Edgar in Cell ~ 1984). So I would predict that horse ribosomes would be happy translating human mRNAs, and human ribosomes would be happy translating horse mRNAs. The experiment you described, placing a human ribosome into a horse cell would be difficult to interpret because the endogenous horse ribosomes would already be translating the endogenous horse mRNAs, and so detecting activity from one additional ribosome could be challenging (even if you could come up with an experimental approach that gets that foreign ribosome in to the cell).

The take home message is that ribosomes, in general, do not care where the mRNA comes from--because ribosomes, as far as we know, do not have a way of distinguishing "self" from "other".


I believe that it is the vine hawk moth (Choerocampa rosetta).

https://www.whatsthatbug.com/2010/11/20/vine-hawk-moth/


Misophonia

  Misophonia is a relatively unexplored chronic condition in which a
  person experiences autonomic arousal (analogous to an involuntary
  “fight-or-flight” response) to certain innocuous or repetitive sounds
  such as chewing, pen clicking, and lip smacking. Misophonics report
  anxiety, panic, and rage when exposed to trigger sounds, compromising
  their ability to complete everyday tasks and engage in healthy and
  normal social interactions.1

Physiology

The auditory pathways may be functioning normally, but there is an abnormally strong reaction of the limbic (emotional system) and autonomic nervous system (body control system) to which the auditory system is intimately connected.

Several definitions are listed for the disorder, including:

“Abnormally strong negative reactions of the autonomic and limbic systems to specific sounds resulting from enhanced functional connections between the auditory and limbic systems for these sounds.  The auditory system works in a normal manner, without abnormally high activation.  At the behavioral level, sounds specific for a given patient evoke strong negative reactions.  This situation may cause general negative attitude to sound as well.  When fear is dominant emotion (patient is afraid of sound) phonophobia occurs (phobia – fear).  Phonophobia is a specific case of misophonia.”
“Selective sound sensitivity should be considered a type of misophonia, where soft sounds (typically eating and breathing sounds made by emotional attachment figures) are the focus, and the quality of those sounds causes annoyance and rage in the listener.”

“Pre-puberty seems to be a very common age of onset for the majority of those with misophonia, with lifetime persistence for most cases, and there appears to be a genetic component.”
“Misophonia can be considered abnormally strong connections between the autonomic and limbic resulting from enhanced connections between the auditory and limbic systems.  These connections encompass both a high level of cortical level loop with involvement with cognition as well as subconscious connections, most probably involving the link between the medial geniculate body and the amygdale. The functions of these connections are governed by the principles of conditioned reflexes.”

source:

1 Misophonia: physiological investigations and case descriptions
[2] MISOPHONIA 4S Provider Network USA

Great Site: http://lifewithmisophonia.wordpress.com/


Why are mules/donkeys aggressive when faced with predators but horses are not?

So horses, donkeys, and zebras are all of the genus Equus. Mules are not a species, since they are the product of the cross-breed between horses and donkeys, and are sterile (therefore do not comply with the biological interpretation of species).
Given that 2 out of the 3 species from the species of the genus Equus are aggressive against predators (zebras see reference and donkeys), it might be possible that the "aggressive" behavior is the ancestral trait of the genus, and horses evolved afterward the behavior of fleeing before fighting. Furthermore, it looks like the "aggressive" trait is dominant over the "fleeing" trait since mules (cross-breeds between horses and donkeys) inherit the aggressive trait. There are no sources that necessarily say that a dominant trait is associated with ancestral (common ancestor) provenance, but for the case of single genes, this is the most likely scenario.
So if we think that horses evolved the trait of fleeing before fighting (being the "aggressive" trait the ancestral one), then one should ask why did they evolve such behavior (why is a cringy word for evolutionary biologists, but serves the purpose here). And this is probably due to the exposure horses had to different types of predators. I wouldn't be surprised if horses had more contact with human beings than donkeys or zebras, thus they evolved this behavior as a way of coping with extensive hunting.
Alternatively, some traits are not "modular" traits that can evolve independently from other traits. More often than not, complex behaviors, like the "aggressive" trait, are determined by a large number of genes, some of which have phenotypical effects elsewhere. This means that if a species has a "selective pressure" for one trait, other traits can also be modified over time as a causal effect of this selective pressure. Horses were domesticated long before donkeys were, and zebras haven't been domesticated at all. Domestication is usually conferred by a process of selectively breeding individuals that express the least amount of aggressiveness, or show signs/traits of "neoteny". If horses were selected to produce neoteny in the species, the non-aggressive behavior might also have been selected as a causal effect of this selective-breeding.  This would explain why horses, which have been domesticated way before donkeys have, do not show aggressive behavior as donkeys or zebras do.


What makes animal to continually reproduce?

Why organisms reproduce

If they didn't reproduce, they would die out.

More concretely, suppose an animal is born with a mutation that removes the desire to reproduce.  That animal will not have any offspring, so its genes will not be passed on to the next generation.  When that animal dies, that mutation will die with it.

Why some organisms reproduce a lot

Different animals or other organisms have differing strategies for reproduction, based on their ecology.  Some animals, like the Surinam toad, try to have a lot of offspring with relatively little "investment" (of energy, time, effort, etc.) in each one.  Many of the offspring will die, but enough will survive that the organism's genes can persist.  Other animals, like elephants, only have a few offspring but spend a lot of effort in making sure those few offspring survive.

You can read more about this in the Wikipedia article on life history theory.


It would be stressful for cells to be trypsinized 24 hours after seeding. After cells are plated, there is a lag time to start growing. Perhaps, during the lag time, physiological state of cells is stabilized. They have to express proteins digested by trypsin and display on the surface etc. Then you could disturb the state again by trypsinizing cells again if you replate cells after 24 hours.
I would not deny some cells are not affected by trypsin much, but you should be carful.

  if I can treat them with drug the same day I add trypsin for counting.

It is not preferable, but in some cases, such a way is taken actually. If you could, you might want to give us more information about which cells and drugs you are going to use.

PS

If you trypsinize cells to count and do not replate them, you do not need to worry about the cell condition, as WYSIWYG says.


Epilepsy explained by computational neuroscience

Unfortunately, epileptic spiking can occur very easily in many neural modeling studies, and therefore one should be very careful in asserting the possibility of certain aspects of model as a cause for epileptic activity. One possibility, as you mentioned, is the lack of short-term depression which prevents long sustained firing. But again, a simple increase in the global excitatory coupling can also exhibit similar dynamics.

Good luck on your interview.


No — there are both theoretical limitations and experimentally proven ones.

Chemistry in cells is subject to the same laws as chemistry in general. For photosynthesis to take place, certain molecules (e.g. ADP and NADP+) have to be present to transport the energy harvested to the place where carbohydrates are synthesized from this energy. The transport rate of molecules is limited by the rate of diffusion (see Brownian motion) within a fluid at roughly room temperature (where photosynthesis takes place). This limits the amount of energy that can be processed within a defined volume of plant tissue.

There are further limiting issues. Above certain light intensities, some parts of the plant cell suffer heating and destructive effects, which also limit photosynthesis.

See an abstract on this topic

There are also measured limits. Most plants with leaves exhibit stagnant photosynthesis rates at light with $$600 \frac{μmol}{m^2 \cdot s} $$
or higher.


Is Plasmablast a precursor of Plasma cell?

Antigen activated B-cells enter the germinal centre dark zone to form centroblasts which undergo somatic hypermutation. These then form centrocytes in the light zone. The various possibilities/routes the centrocyte can take are shown in the following figure. If the centrocyte undergoes a class switch recombination, it becomes a plasmablast.

A plasmablast is  defined as

  Plasmablast

  The B-cell lineage precursor of non-dividing plasma cells, which has the capacity to divide and that has migratory potential.

Once it matures as a plasma cell, it is out in the blood secreting soluble immunoglobulins or antibodies.

Another important definition to mentioned here would be of antibody secreting cells.

  Antibody-secreting cells

  A term that denotes both proliferating plasmablasts and non-proliferating plasma cells. The term is used when both cell types might be present

So, yes, they indeed are a precursor of plasma cells.

Also, it is necessary to clarify here that although both plasma cells and plasmablasts are antibody secreting cells, plasma cells lack membrane bound antibodies while plasmablasts retain them.

Finally, this is just the germinal centre response that is shown over here. Plasma cells and plasmablasts can also form in an extrafollicular response in extrafollicular sites in the spleen or in the medullary cords of the liver. That's another story altogether!

For a more detailed explanation, have a look at my other answer.

Image and reference: http://www.nature.com/nri/journal/v8/n1/full/nri2217.html


I have 2 doubts here.

You obtain your viruses from the media whereas Actb measurements can be performed only in the cell lysates.
Actb is just a reference to normalize for the cell count: higher the cell count higher will be the viral titre because of higher number of infected cells. But that is immaterial if your aim is lentiviral transduction where you are only interested in obtaining titre values and not measuring the efficiency of its formation.

You can simply do qPCR with the media sample and the standards and regress the measured Ct values of the samples to obtain titres.


How long does it take for a genetic trait to dissipate if its no longer selected for?

There is no way to answer this question as there are way too many factors influencing this time.

It depends on too many factors

It depends on:

whether it is neutrally or negatively selected (and how strongly so)
the population size
mutation rate
mutational variance
level of genetic variance for this trait to start with.

This variance can be calculated at equilibrium (assuming no important demographic change "recently") from the above parameters though.

It may take between 1 generation and a billion generations.

For example

Consider for example that your trait is neutral. Assume that the trait can only take two binary state A and B and that only a single locus affect this trait, which two states are also named A and B for simplicity. Let's say A is the ancestral state and we want to know how much time it takes to have a population of B. Imagine the haploid population size is $N=10^5$. The mutation rate for the locus of interest is $\mu=10^{-9}$.

Slow Case

If at the start there are no alleles B, then you have to wait for a mutation to occur. The time for such a mutation to occur follows an exponential distribution with parameter $\mu=10^{-9}$. Because we assumed neutrality, the probability of fixation (fixation is the state when the whole population carry the same allele) is $\frac{1}{N}=10^{-5}$. Conditioning on fixation, the expected time for fixation to occur is $-4N \left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)=399998$ generations. In consequence, the expected time to fixation in this case is $10^{5}*10^{9}+399998 ≈ 10^{14}$ generations, that is about 77 times the age of the earth assuming there is one generation per day! So Obviously, the environment has time to change again. Note that variance is about $10^{28}$ generations! Of course this example is just an extreme slow case, but I have been using realistic parameter values.

Fast Case

If you have a population size of $N=50$ and the B allele is already present at frequency 0.1 and that the B allele is beneficial with a selection coefficient of 1.5, then it might take about 100 generations.


Why are all human beings not black in color?

First let's look at the difference between light skin and dark skin: darker skinned people have higher concentrations of melanin than those with lighter skin. Africa is located around the equator, a place where the sunlight is very intense. Melanin protects the skin against harsh, damaging rays, which is very beneficial in Africa. But a high concentration of melanin also decreases the skin's ability to produce vitamin D3 (1). Vitamin D3 is a vital nutrient to many physiological processes. Deficiencies in vitamin D3 has been known to cause things like rickets and osteomalacia (2).
So in Africa, having a high concentration of melanin in your skin conferred a great fitness benefit: you could go outside without getting cancer. But when humans relocated to places farther from the equator with reduced sunlight, having a high concentration of melanin in the skin actually became harmful because it would make darker skinned people more likely to have vitamin D3 deficiencies. Given this change in the fitness conferred by the trait of dark skin, individuals with lower concentrations of melanin in their skin were more likely to survive and reproduce in these new conditions. After many generations, the allele(s) that cause lighter skin became more common than those that cause darker skin.
Hope that was helpful!

T.L. Clemens, S.L. Henderson, J.S. Adams, M.F. Holick, INCREASED SKIN PIGMENT REDUCES THE CAPACITY OF SKIN TO SYNTHESISE VITAMIN D3, The Lancet, Volume 319, Issue 8263, 9 January 1982, Pages 74-76, ISSN 0140-6736, http://dx.doi.org/10.1016/S0140-6736(82)90214-8
http://www.everydayhealth.com/drugs/vitamin-d3


In human embryology, what starts ovum cell division?

Actually an ovum doesn't ever start cell division because once it is fertilized by a sperm the combination of the two cells is call a zygote.  In humans, the zygote proceeds with the many steps following fertilization leading to the first division; this takes on the order of 24 to 30 hours.  At that point the set of cells may be termed an embryo or various other technical terms.  The succeeding cell divisions occur by the normal cell division mechanism, which is called mitosis.  In the context of the development of the human embryo, an early stage cell division is often called cleavage.

More details are available from the links in the above.  For greater technical depth on the initial stages of the division of the zygote, you might want to see this article.


Why do brain cells use shuttles that pass electrons from NADH to FAD?

In the absence of unanimous consensus and sources regarding the actual distribution of these shuttles,(wikipedia favours G3P shuttle abundance) let me try to explain the cause if the glycerol-phosphate shuttle is assumed to be prominent in brain cells. Several possible reasons might lead to this:-

1) The existing metabolic pathways are all intertwined to form a complex metabolic net. This means that invariably, the intermediates of any pathway are the products or intermediates of several other pathways. Therefore, the G3P shuttles require Glycerol-phosphate and Glycerol-phosphate dehydrogenase (I and II) which might be naturally abundant in brain owing to its use in strict lipid metabolic control in nervous tissue. This means that tapping the already high G3P for use as a shuttle compared to synthesising and operating a distinct metabolic shuttle is more profitable. Furthermore, operating Malate aspartate shuttle migh require intermediates whose high concentrations (required to maintain the shuttle) might negatively interfere with existing metabolic pathways like protein synthesis and regulation.

2) This shuttle has much faster operation time than Malate-Aspartate shuttle and hence is very useful in shuttling reducing equivalents fast in muscles and brain. Compared to the malate aspartate shuttle, it is shorter and hence faster and less prone to cessation due to unavailable intermediates or enzymatic disruption. Due to several enzymes working in Malate-aspartate shuttle, it has a narrower pH and temperature optima than the G3P shuttle which is shorter and depends on lesser intermediates, and hence is less prone to disruption.

3)The last and the most far-fetched (but relevant)reason is that the loss of one ATP may not cause much of a problem because of already high respiratory rate, high Oxygen delivery to brain and ability of the body to quickly transfer available energy sources to brain at the cost of other parts, at times of energy stress. This means that replacing the shuttle with a more energetically conserving one may not have a strong driving force for evolution to operate on, and therefore the presence of G3P may be because of something like phylogenetic inertia, that is, the prevalence of an ancestral character just because it is neutral and does not influence the fitness in a considerable manner. Therefore, the ancestral G3P shuttle would just not have been replaced here but this is very unlikely as G3P shuttle is prominent in 2 very high energy-demanding organs, muscles and brain.

Except the last outrageously far-fetched reason, all other reasons should be enough to explain its prominent presence (if it is true) in brain tissues.


There's a very simple answer: scale. If a drug company wants to screen a million-compound library to find which ones inhibit the kinase activity of a certain target, they're not about to do a million IPs and a million Western blots. Instead, they'll use recombinant kinase and substrate peptides, with a variety of readout systems to choose from.

Other reasons include not having a good phospho-specific antibody to the substrate, very low expression of the kinase and/or substrate, complicated protocols necessary to activate the kinase in vitro, lack of a good model system, and more.


How long does Lentivirus take to express in vivo mouse neurons?

This depends a lot on what you are expressing (such as how stable it is), and where you need it (soma vs dendrites vs axons, and whether it is trafficked actively in the cell).

For optogenetic constructs, our lab has typically seen near-peak expression around 3 weeks, though expression may be suitable earlier, and toxic later.


I'd like to add to Amy's excellent answer.

Generally, galls are induced by the forced accumulation of plant hormones at different levels to those naturally maintained by the plant, in a localised area. Usually the hormones targeted are auxins and cytokinins which are both involved in the regulation of normal growth patterns; disrupting these patterns leads to disorganised growth, or in some cases a differently organised growth. There are several methods that I know of:

The gall inducer directly synthesising the hormone.
The inducer chemically inducing the host to synthesise more hormone.
The inducer chemically inducing the host to transport more hormone to the site.
The inducer genetically modifying the host to cause synthesis of the hormone in the host cell.

Some examples of the different methods:

Direct production: The bacterium Pseudomonas savastanoi directly produces indole-3-acetic acid (IAA, a type of auxin). This direct accumulation has been shown to be responsible for gall formation in oleander knot disease. Some key papers: Palm et al. 1989, link 1; Glickman et al. 1998, link 2.

Chemical induction of transport: Root-knot nematode worms induce root gall formation in clover. They probably do so by producing flavonoids which up-regulate transportation of auxin into cells (see link 3).

Genetic induction: As already mentioned by Amy, Agrobacterium tumefaciens is a very well characterised example of induction by genetic modification, however, A. tumefaciens is also known to directly produce auxins in large quantities. Another interesting example of genetic modification is in viral gall-inducers. They are not so well studied as their bacterial counterparts, but in some cases (e.g. white clover mosaic potexvirus) it has been shown that virus infection initially leads to a complex change in the types of cytokinins produced by the plant (e.g. Clarke, 1999; see link 4). It has also been shown that if cytokinins are applied exogenously (i.e. injected into the plant) after viral infection, that the virus cannot replicate well. This suggests that the virus is manipulating the host's hormone production in a complex way.

There is also the interesting case of Rhodococcus fascians, which seems to produce a chemical which is not structurally similar to any known cytokinin, and yet has similar effects (Goethals et al., 2001; link 5).

You specifically asked about gall wasps, but unfortunately this mechanism is, as far as I can tell, not completely known. It is speculated (e.g. in Shorthouse & Rohrfritsch, 1992; link 6) that this involves direct injection of phytohormones. The evidence to support this is simply that other insects, particularly aphids, excrete phytohormones in their salivary sheaths when they inject them into a plant.

Finally, I'll just say that the fact that gall induction is carried out by bacteria, viruses, nematodes, fungi and wasps, and that some mechanisms are shared across all those associations,  demonstrates the ability of evolution to converge on the most elegant solution to a problem. It also shows that plants are so great, everyone wants a piece (but I would say that, because I'm a plant biologist).

References:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC209694/
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI.1998.11.2.156
http://www.publish.csiro.au/?paper=PP98157
http://www.plantphysiol.org/content/120/2/547.full
http://www.annualreviews.org/doi/full/10.1146/annurev.phyto.39.1.27
http://www.nhbs.com/biology_of_insect_induced_galls_tefno_3838.html


Infer distance since duplication from tree?

Assuming a molecular clock, the distance between the sequences and the duplication event is 75/2 = 37.5. Ideally, these sequences should have the same distance from the internal node (under a clock), and you could use a model that explicitly assumes a clock -- which will lead to ultrametric trees.  One example is the program promlk (or dnamlk) from the phylip package. A faster alternative would be the  UPGMA method, which also gives you an ultrametric tree.


Where did Neanderthals and Denisovan Man come from?

The topic is reviewed in a freely available Nature article, from which the figure below (I have added the labels ‘Hominid’ and ‘Human’) is taken. As can be seen it is thought that the lines leading to the ancestor of Neanderthals/Denisovans and that leading to modern humans diverged  before humans had left Africa; and that the lines leading to Neanderthals and Denisovans split from their common ancestor subsequently.

You will notice that the article refers to “modern humans”, rather than Homo sapiens, presumably because this terminology is confusing, whereas the picture is clear.


Continuous (yeast) culture system satisfying multiple criteria

A chemostat should satisfy your criteria.
The cell mass balance around a chemostat is the following (assuming no biomass in the feed):
$$F-FX+V_RX\mu_g-V_Rk_dX=V_R\frac{dX}{dt}$$

At steady state there is no change in parameters with respect to time so we set the derivative equal to zero. If we also assume that the death rate ($k_d$) is negligible (for example cells in exponential/log phase) and let:
$$D=\frac{F}{V_R}$$

Where $D$ represents the dilution rate (how quickly the volume in the tank is being replenished). Then rearranging the above equation you get:
$$D=\mu_g$$

This says that the growth rate will be equal to the dilution rate. In other words you can set how fast the cells grow by modifying the flow rate and/or volume of the tank. But there is a limit. Cells grow as fast as they can use the limiting nutrient ($S$) and this relationship is often modeled as:
$$\mu_g=\frac{\mu_mS}{K_s+S}$$
Where $\mu_m$ and $K_s$ are unique parameters for every cell type. $S$ is the concentration of the limiting substrate in the tank (which is also equal to the concentration of the substrate in the outlet stream). The maximum growth rate is $\mu_m$ and if the dilution rate is higher then this value, the cells get washed out of the chemostat. This can be troublesome if you need a flow rate higher than $\mu_m$. In this case a recycle is useful.

To answer your question in the comments regarding medium composition. You probably want to operate at steady-state. Steady state means that there is no change of parameters with respect to time. So if you write the substrate mass balance:

$$FS_0-FS-V_RX\mu_g\frac{1}{Y_{\frac{X}{S}}}--V_RXq_p\frac{1}{Y_{\frac{P}{S}}}=V_R\frac{dS}{dt}$$

And set the derivative to 0. Then you will find the outlet substrate concentration is a function of other constants (biomass, volume, product yield, etc.). You're right in that some substrates get used more than others, but when steady state is reached. They stop changing and the medium composition stays constant in the vessel.


Is there a certain environment where all cellular functions (or at least some) increase their rate?

There are optimal temperature, pressure and substrate concentration for each biochemical process. The optimal temperature and pressure for two or more (but not all) processes may overlap. So there is no SINGLE temperature or pressur where ALL of them will be at their maximum. Please note, by mentioning "cellular processes"  I meant all the biochemical(e.g glycolysis), physiological (cellular micro-transport) as well as physiochemical(transcription) processes. But we can try to provide substrates at reasonably high concentration ( keeping in mind negative feedback phenomena); we may reach the maximum achievable rate. All the above conditions follow bell-shaped curve; so I put the word 'resonably', as after the optimum condition is reached further increasing that condition will lead to decline in "speed" of reaction. We have to create an artificial enviornment using that substrate combination at proper concentration; as there is no such natural condition where that happens(cell always decrease one process while increasing another).

But it may seem to be a paradox - does anabolic and catabolic reactions both will increase simultaneously! E.g glycogenesis and glycogenolysis at the same time......well, as I already said this is not a natural condition; we are forcing substrates of one reaction at "reasonable" concentration keeping in mind the 'opposite' (is it??) reaction. E.g glucose produces glycogen by glycogenesis and that new glycogen is used in glycogenolysis; so we have to consider the concentration of glucose only. Isn't that easy! well, not so soon. Doing this requires lot of ATP, of course we'll get some from the glucose breakdown, but the need is even higher. So we have to provide additional ATP. Then there are second messengers (cAMP, DAG, IP3 to name a few of them). We have to nutralize them all( they favours unidirectional process).....this is a very complicated thing(just for example, we are supplying ATP, so cAMP will be automatically produced; so we should select all the enzyme blockers of cAMP production). But then electrolyte concentration will be disturbed and we need to monitor & regulate that also.

Thus it is clear that such condition requires sofisticated laborarory instruments.

N. B.
1. I considered only a single cell while discussing this.
2. The word "exhausted" was taken as progressive deterioration of cellular architecture, that leads to death.


What kind of larve is this? Found in shed on terracotta pot in Northwest Oregon

They look like the nest and pupae of a mud dauber wasp; the black and yellow mud dauber is a common species to your area and elsewhere, though I can't personally identify the species clearly from the larvae themselves they certainly are consistent.

A nice view of the nest building process

These wasps have a characteristic very skinny abdomen, and they pack their nests with spiders before laying an egg there. They aren't typically a bother to people because they don't have any communal nest to defend, except for building nests on troublesome places like airplanes.


The quote (which you more likely got from Wikipedia) discusses multiple types of matrices.

Let's break down the quoted definition:

The general definition of a matrix would be "an environment or material in which something develops; a surrounding medium or structure." In biology, we think of a matrix as a material, tissue or area in which more specialized structures (molecules, cells, organisms, etc.) are embedded.

In animals or plants, the matrix is often describing a material or tissue.

The nail matrix is the layer of cells that your fingernail or toenail sits on that actually produces the nail.
The extracellular matrix (or ECM) consists of a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding [more specialized] cells. One very familiar example of "matrix" tissue is connective tissue.

Here's a video from Khan  Academy's Youtube channel to walk you through this a bit.  And here's a more graphical walk-through explaining extra-cellular matrices.

The cytoplasmic matrix (aka cytosol) is the liquid found within cells in which organelles reside. It constitutes most of the intracellular fluid (ICF)

The mitochondrial matrix, a type of cytoplasmic matrix, is the fluid within the inner membrane of a cell's mitochondria that splits it into numerous compartments. This viscous "space" contains the mitochondria's DNA, ribosomes, soluble enzymes, small organic molecules, nucleotide cofactors, and inorganic ions; it is also the site in which oxidation of organic molecules occurs.

So whats this look like under a microscope? Here's an image of a mitochondria and surrounding cellular cytosol under an electron microscope:

In ecology, a matrix is the general area in which your population, community, or habitat "patch" exists within. In other words, Matrix is the "background ecological system" of a landscape with a high degree of connectivity.


How does the immune system "learn" from a vaccine?

Vaccines work by introducing an attenuated strain of the pathogen (or alternatively the antigens that are normally present on the pathogens surface) into the body, whereupon the body mounts an immune response.  As this will (hopefully) be the first time that the body has encountered the antigens on the pseudo-pathogen's surface, the response is called the primary response.

This consists of two main divisions: the cell mediated pathway and the humoral pathway.  In vaccination it is the humoral pathway that is important.  This is where a division of white blood cells (B-Cells) produce antibodies that are complementary to the antigens on the pathogen surface, causing a negative effect to the pathogen (death, inability to reproduce, de-activation of toxins, etc.).  However as each B-Cell produces a different antibody, there needs to be a mechanism to select the correct one:

Antigen Presentation (technically part of the cell-mediated-response) - a phagocyte engulfs the pathogen and displays the pathogenic antigens on its own surface.
Clonal Selection - B-Cells that are attracted to the invasion site attempt to bind their antibodies onto the pathogen's antigens.  It takes time for this to occur successfully as you are essentially waiting for the correct mutation to happen.
Clonal Expansion - Once a complementary antibody producing B-Cell has been found it is then activated with the help of a T-Helper cell.  This causes it to divide rapidly whereupon these cloned specific B cells can secrete their antibodies which will cause detriment to the pathogen.

It's at this point that I can start to answer your specific question.  The large clone of B cells will then sub-divide into two types.  Plasma Cells remain in the blood and produce antibodies to fight the infection.  The other type, much smaller in proportion, are called Memory Cells.  These cells have a very long lifetime and move to lymph nodes across the body (including the spleen), where they remain dormant until the same pathogen is found again.

When this is the case, the memory cells are activated by T-helpers so that they can divide into massive numbers of plasma cells to fight the infection the second time.  This secondary response is a much faster as the clonal selection stage does not have to wait for the right mutation - they are already waiting in the lymph nodes.  The response is also much stronger as each memory cell can produce large numbers of plasma cells - i.e. you can start with multiple activated B-cells (as many as you have memory cells) rather than just the one that has mutated into a complementary shape in the primary immune response.

The aim of the vaccine is for the secondary response to be so quick that potentially life threatening symptoms do not occur; the body has time to find and store the correct antigen in a safe environment as the pathogen has been deactivated.


What does the "cov" mean in a velvet assembler generated contig name?

It means k-mer coverage. From the velvet manual:

  4.2.1 The contigs.fa file

  This fasta file contains the sequences of the contigs longer than 2 k
  , where k is the word-length used in velveth.  If you have specified a
  min_contig_length threshold, then the contigs shorter than that value are omitted. Note  that  the  length  and  coverage  information
  provided  in  the  header  of each contig should therefore be
  understood in k-mers and in k-mer coverage (cf. 5.2 ) respectively.
  E.g.  for a 500bp contig and a k-mer length of 21, the length in the
  header will be 480.


What is the correct classification of population groups of homo sapiens?

Basically all the genetic variation of humans is inside the native african populations.  A norwegian and a australian native are more closely related  to each other than two random native Africans are. So the only accurate way to do it would not only group those two asians together but also group them with europeans and native americans. If you split people up enough to get two groups of "asians" then you end up with more than a hundred races the vast majority of whom would be split among the native african populations.

Humans have very low genetic diversity in the first place, and most of our diversity is within our populations not between them, so splitting us up does not make a lot of sense. We end up doing it mostly on superficial variations.
Source


The picture looks like it's from the Cerastes genus. It looks similar to a head shot of Cerastes Cerastes (Saharan horned viper) shown on Wikipedia:

In fact, the incident you describe is also reported in Wikipedia's Cerastes Cerastes article since it could be the first sighting in Pakistan. However, I sincerely (and respectfully) doubt that this snake was producing the "baby crying sounds". According to Wikipedia they produce a "rasping sound" when threatened.

I'm not sure that the specimen in your photograph is actually Cerastes Cerastes but the genus should be correct.


Cell-type specific methylation profiles: original reference finding?

Note: This is not my field, and only the result from a quick  database search

Doing a quick search in the Web of Knowledge, I found the paper Ehrlich et al (1982), Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells, which is relatively well-cited. This in turn mentions that:

  Recent studies indicate that for many genes associated with vertebrate development, there are tissue- or cell-specific differences in the extent of DNA methylation.

The oldest studies referenced in this paper that seem to refer to tissue-specific methylation are Vanyushin et al (1970), Rare Bases in Animal DNA, Nature and Vanyushin et al (1973), The content of 5-methylcytosine in animal DNA: The species and tissue specificity, Biochimica et Biophysica Acta. The 1973 paper is also one of the earliest papers cited in another well-cited paper from 1983 (Gama-Sosa et al, 1983)), so it might be the best bet. However, Gama-Sosa et al also mentions Kappler (1971), The 5-methylcytosine content of DNA: Tissue specificity, which is clearly relevant. In total, Gama-Sosa et al has references to 13 early papers on DNa methylation, so you might want to check them all out, and backtrack from there. Also, Vanyushin seems to have published in smaller, more obscure journals around the same time (e.g. DOKLADY AKADEMII NAUK SSSR), so there might be earlier papers that express the same ideas. The earlier papers seems to deal with bacterial DNA methylation though.

A couple of other references are:

Van der Ploeg & Flavell (1980), DNA methylation in the human gamma delta beta-globin locus in erythroid and nonerythroid tissues,
Mandel & Chambon (1981) DNA methylation: organ specific variations in the methylation pattern within and around ovalbumin and other chicken genes
McGhee & Ginder (1981), Specific DNA methylation sites in the vicinity of the chicken beta-globin genes


Having a lot of trouble identifying this insect

Other's are right, some genera in the subfamily Reduviinae, I don't think it's an adult though. Very close to this.


I'm going to give this question a blind attempt, assuming you are talking about PCR (since you are talking about genomic DNA and cDNA) and not RT-PCR or qPCR, since I know very little about them. This answer is not necessarily optimisation for annealing but checking some basics and potential solutions. In my work I had to do a lot of site directed mutagenesis and genotyping and there are some important rules you have to follow in your primer design. First try to keep your primer length between 25-30 for sequencing (at least thats what I do) and for site-directed mutagenesis between 25-45 since anything above 45 bases increases the likelihood of secondary structure formation. Primer melting temperature (Tm) should be >=78 oC (Tm= 81.5 + 0.41(%GC)-675/N [with N being primer length in bases]). Also primers should have a minimum CG content of 40% and should ideally start and end with a C or G. So check your primer CG% since if its too high then it will make a few problems including increased Tm and possibility of primer-dimer formation due to CG triple hydrogen binding. This document has some nice information (http://www.genomics.agilent.com/files/Manual/210518.pdf)

In my opinion if all else fails and you are still struggling with your primers, then re-design a new primer set, if possible. Now getting back to the annealing temperature issue, in my experience for cDNA, annealing temp of 50 oC works best and for genomic DNA, annealing temp of 55 oC works best, which is about the range most people work with and I have so far had no problems. I'm more than happy to share my genomic DNA PCR cycle information with you if you wish through an edit.

Hope this helps!


Is there a mechanism by which mammals lose interest in a partner after mating?

Well from what I have been taught, and have studied, is that multiple partners for men does not equal more of their DNA persisting, because they are needed to provide for the offspring. So if they impregnate 10 different females and don't stick around, that really doesn't help them pass on their DNA because most would die. So having a family with the same partner does ensure more offspring survive. Humans are picky selecting their mate for the reason of wanting to get the best genetic combination possible to have the most offspring survive. A human child takes a lot of effort to raise to reproductive age, we aren't like some animals who are off and running. So our bodies invest a lot in making sure that happens, being flooded with bonding hormones after sex, women's bodies changing to nurse (and then not being able to hunt/gather/protect themselves) etc. So there is a hormonal cascade that happens to ensure you are going to stick around after mating.

I am really talking about our ancestors, but obviously some of their behavior has carried to us.

However having multiple partners DOES benefit the female. Males can't tell they are the father to a child until much later, after they have supported the pregnant mother, etc. Females can then have their DNA pass on in multiple combinations to ensure survival of more children. Pubic hair in women is thought to have evolved to hide any physical evidence of a recent mating with different males outside of the family. And if current statistics say anything - just as many women cheat on their spouse as men. And when cheated on women want to go after the other woman, because that's our competition and they may be taking the mate we worked so hard to get.

Humans are hard to compare to other animals because we can manipulate so much of what happens to us. But if the ultimate goal is to ensure the passing of DNA then that hypothesis (to me) doesn't fit with humans.

But then again, I am a woman and therefore could be biased haha. If you read an animal behavior textbook it will go into this in in detail, and state it much better than I can, and with supporting scientific evidence. As a biologist the term "anecdotal evidence" makes me cringe :)


Pneumonia in children after abdominal operations

Abdominal surgery results in a painful wound that affects the abdominal muscles, which are important for coughing. The Lungs and respiratory tracts constantly secrete mucus that flows upwards to the Trachea then down the Oesophagus. The trachea is lined with a moist mucous-membrane layer composed of cells containing small hairlike projections called Cilia. The Cilia project into the channel (lumen) of the trachea to trap particles. The Cilia constantly move in a manner that pushes the mucus up to help clear the respiratory tract of pollutants, debris and bacteria. Here is a link to show the Cilia Movement:

https://www.britannica.com/science/cilium/media/117814/16442

Abdominal Surgery reduces the efficiency of the cough reflex due to abdominal wound pain, while the Anaesthetic results in an increase in mucus due to the upper respiratory tract trauma, with some anaesthetic drugs also increasing these secretions and suppressing Cilia movement. All that eventually results in secretions being produced at a higher rate than being evacuated leading them to accumulate and resulting in an increased risk of lung infection.


Have there been any "chopstick gene" mistakes in genetics?

Have a look at this time article from a couple years ago.

A concept that you should think about is nature vs nurture. You can think of nature (your genetics) as controlling part of the potential of what you could become (for example, many long distance athletes have genetics that are beneficial for their sport) where as nurture encapsulates the environment that you grow up in (a nutritionally deficient child will not reach maximum potential height that you might predict based on genetics alone).

When scientists are studying a gene in relation to a phenotype, they statistical methods to determine how much a genotype contributes to a phenotype. This process would minimize these types of fallacies since different alleles in different populations would be considered. However, sampling biases can occur and most human variation studies are done on people of european, asian, and african descent.