Mithradates - Developing immunity to poison?

Welcome to SE. Edit: The answer is in two parts based on the mechanism of action of the toxin. Courtesy: @David and @jamesqf

Immunity

The white blood cells in the body are responsible for recognizing self or non-self peptides and form the adaptive compartment of the immune system. The B lymphocytes have a receptor that can bind to various peptides. Upon recognition of foreign peptides in the body, they go through a reaction (somatic hypermutation) to become further specific to the foreign peptide. They also differentiate into Plasma cells which can now secret another protein (antibodies) which neutralizes the foreign peptide.

Small amounts, which are non-lethal, but in enough concentration to drive the B cell reaction creates an immunological "memory". This memory allows a faster response to the same peptide compared to the reaction. This in order allows the body to withstand a higher concentration of toxic peptide, which otherwise would have been lethal as its being neutralized.

Vaccines work on a principle very close to this.

Homeostasis

Every toxin interacts which some biological process and drives it out of balance. The body actively tries to restore the balance by some means.

For example, if a ligand is depleted the body can increase the number of receptors to counter the effect and vice versa.

By ingesting small amounts of toxins body can adjust the equilibrium by very small amount at a time adjusting the concentration of relevant ligands or receptors.

Again, the person who has been through this process can withstand a higher dosage of the toxin compared to a person who hasn't.


Expected reproduction rate of a dandelion and/or fern

Dandelions may have "from 54 to 172 seeds per head and a single plant can produce more than 2000 seeds" (https://fyi.uwex.edu/weedsci/2002/11/12/dandelion/), but the number of inflorescences depends, for example, on the age of the plant. It should also be remembered that some individuals repeat the blooming in autumn, although it is not so abundant (usually only one inflorescence). That, what is called a dandelion (Taraxacum officinale) is a collective species, which actually consists of several hundred microspecies, which may differ in the amount of seeds produced. Thus, the given data is only quoted.


Each eye is controlled separately. Three cranial nerves emerge at the brain for each eye to control the so called extraocular muscles. That we usually move both eyes in one direction is due to that our brain is trained that way. Nonetheless, we sometimes move each eye individually, for example when looking at an object that is very close to our face (convergence). I wonder that you have not noticed it on yourself, since it is a pretty common eye movement. Further, you can train your brain to perform other, rather unusual movements, as you can see in this video.


I'm not aware of any confirmed cases of melanism in snow leopards either.

There are some relevant studies on the evolution of melanism on Felidae. Melanism seems to occur only in two extant species of the genus Panthera (Panthera onca and Panthera pardus). There is a direct correlation between melanistic colorations and enviroment (especially humidity):

  Moist forests (especially in Southeast Asia) presented very high
  frequencies of melanistic leopards (e.g., 39 of 71 individuals [55%]
  in Southeast Asia), and more than 80% of the black animals in our
  database, a fivefold increase relative to the expected number based on
  the overall number of records. Furthermore, we found no confirmed
  melanistic leopards in the Middle East, Arabian Peninsula, Central
  China, and Russian Far East, nor any mention in the literature as to
  the presence of melanism in these regions, indicating that this
  polymorphism is really absent from these areas. Overall, there was a
  significant reduction in the frequency of melanism in some biomes that
  consist of open habitats or temperate forests. There thus is a clear
  pattern in which melanism tends to increase in tropical/subtropical
  moist forests and decrease in open/dry or temperate habitats

References:

https://www.sciencedirect.com/science/article/pii/S0960982203001283
https://www.intechopen.com/books/big-cats/ecology-and-evolution-of-melanism-in-big-cats-case-study-with-black-leopards-and-jaguars


Please identify this moth from Bangladesh

I think I have found the identification. It is a planthopper from ricaniidae family. Most likely Ricanula stigmatica.

Image source: https://en.m.wikipedia.org/wiki/Ricanula_stigmatica


Rejection of valid theories of biology on theoretical grounds

The idea that organisms with mitochondria derive energy from respiration through a proton motive force was considered controversial at the time.

This is the best reference I could find at the time:

  His theory explained that it was the energy captured from those protons
  returning to the matrix and not energy stored in an undefined
  high-energy covalent chemical intermediate that was then used to drive
  ATP synthesis. This Nobel Prize-worthy concept (1978) was so counter
  to the leading theories of the day that the field spurned it for the
  better part of a decade.

Pagliarini, D.J., Rutter J. Hallmarks of a new era in mitochondrial biochemistry 2013  Genes Dev.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877752/


What is the difference between a graded potential and an action potential?

Short answer
An action potential is a binary all-or-nothing event, while a graded potential is an analog signal.

Background
Action potentials, once initiated, are basically all-or-nothing events. Amplitudes may admittedly be variable, but basically it is the spike rate that is relevant to the neural code (Gerstner et al., 1997).

In contrast, graded potentials code information mainly by amplitude. A notable example of the significance of graded potentials is the function of the inner hair cells in the cochlea (the inner ear). The mechanoreceptors on the hair cells open when deflected in one direction, while they close in the other. This is important, as that property depolarizes the cell on one phase of an input sinusoid, while it hyperpolarizes the cell in the subsequent phase. Also, stronger (louder) input increases the response, while softer stimulu generate less response (Fig. 1). In the auditory nerve this graded potential is translated into spike rates (Fig. 2). Basically the hair-cell and auditory nerve system is an analogue-to-digital converter.

Fig. 1. Cochlear microphonic: a graded potential that increases amplitude with increasing loudness. Source: Juaristi & Martínez-Conde, 2014

Fig. 2. In the auditory nerve amplitude is coded as action potential (spike) rates, low frequencies as burst-repetition rate. Source: NY University

References
- Gerstner et al., PNAS (1997); 94(24): 12740–1
- Juaristi & Martínez-Conde, Acta Otorrinolaringol Española (2014); 65(04)


does order of genes in a chromosome matter?

is the difference between humans and mice due primarily to the
  different order of the genes or to the slight differences in the genes
  themselves?

The latter.

  This question was raised from a claim here which seems to imply it
  does not matter.

You are talking about two different things.  Gene expression is often controlled by nearby DNA sequences that don't code for protein.  Moving a gene away from the DNA that controls it can change its expression a lot, and have huge consequences on the organism.  But in many cases, you can move a whole gene, including its controlling sequences, to another place, and nothing much will happen.

People were bringing up synteny as evidence of evolutionary relatedness, not as the cause for all primates looking similar.


Correlation between genetic distance and birth defects

For humans the closest argument may come from observational studies (since experiments aren't possible due to ethical reasons).

One example for the correlation of genetic distance and "defects" comes from a recent study of Chagnon et al. PNAS, 2017 http://www.pnas.org/content/114/13/E2590.full . Rather than asking for birth defects directly they however survey the number of children, and survival of children to age 15 (which would be one example of the term "inbreeding depression" that is more general than "birth defects")

Note that their study also sheds some light on the underlying big question, why certain types of kin relationships can be common despite their effect on the creation of healthy offspring - and why certain types of cousin relations are different from others.


Do camels pose an environmental threat to kangaroos?

Feral camels have environmental, economic and cultural impacts in Australia's Northern Territory (Dept of Land Resource Management, Australia).

In central Australia, camels feed on more than 80% of the available plant species. Feral camels severely defoliate and suppress the recruitment of some shrub and tree species, with such impacts being greatly exacerbated in drier years (Dept of Land Resource Management).

Feral camels have a noticeable impact on fragile salt lake ecosystems and waterholes, which are important sites for Aboriginal people and for native fauna (Dept of Land Resource Management).

However, its impact on kangaroos may be the last of our worries. There are other, typically smaller, marsupials that cover the endangered species list in the NT, including the Western quoll, bandicoots and wallabies (Dept of Land Resource Management). Kangaroos thrive in the agricultural farmlands that now dot the nation.


There is some chance for that. Look at this chart with some probabilities:

Its from this webpage, which also gives some background information.
There is also an online calculation tool available, which takes the grandparents into account as well. It can be found here.


Physiology of skin and leather: why do salt borders occur?

The two processes are quite different: On leather shoes no active transport takes place. The salt either comes with the snow (most likely most of it) when the streets get salted to avoid ice. Your shoe soaks up the salt-water mixture and when the water dries up, the salt stays behind. The other possibility (more for new leather shoes) is that water goes into the leather and dissolves salts, which remain from the tanning process of the leather. With older shoes I have never observed this "snow marks" in the summer when the shoes got wet in rain.
Using a wet cloth removes the salt, subsequent treatment of the shoe prevents that water can enter the leather.

The skin is quite different: Here we have living cells and an active transport of water through pores when you body get warm. This is to cool you and prevent overheating and since the body fluids contain salt, so does sweat.


Disproportion in cranial nerve innervation?

We can somewhat rule out reason 1 because fingertips are also highly sensitive to sensory stimulus. Moreover innervation is not solely about sensory inputs but also motor functions, visceral control etc. All the nerves required for the motor function and a significant portion of visceral control nerves connect to spinal cord.

Therefore in my opinion reason 2 is the most appropriate which automatically rules out reason 3.
Spinal cord is an advancement of neural organization in the chordates. Spinal cord can be viewed as a central cable in which all power lines merge (they still maintain their individuality [the spinal tracts]; they just get clustered to form an organized bundle). Evolution of spinal reflexes must have been a secondary event.

The case of vagus nerve and cranioaccessory nerve suggests that this is an ancient pathway to control the heart. Heart with a closed circulatory system is found in molluscs as well. Apart from the functional significance of the heart (which might to some extent justify direct cranial innervation), it is decently proximal to the brain as well.


Genotype to phenotype map and the G-matrix

From the pheno-geno map and the genotypes frequencies, you have the whole distribution of phenotypes in your population. The mean of the phenoype $n$, $P_n$ is the

$$\bar P_n = \sum f_{G_i} P_{G_i}$$

, where $f_{G_i}$ is the proportions of individuals having genotype $G_i$ and $P_{G_i}$ is the phenotype of the individuals with genotype $G_i$. Therefore, the variance of $P_n$ is

$$var(P_n) = \sum f_{G_i} (P_{G_i} - \bar P_n)^2$$.

The covariance between the phenotypic traits $n$ and $m$ is

$$cov(P_n,P_m) = \sum f_{G_i} (P_{G_i} - \bar P_n)(P_{G_i} - \bar P_m)$$

The only assumptions you need is that there is no environmental variance. I don't think the above calculations required any other assumption. $G$ can be defined at the haploid or diploid stage, it doesn't change anything.

The above calculations however give you the genetic variance and covariance but not the additive genetic variance covariance. I think (but I might be mistaken) that the additive genetic variance would be equal to

$$\sigma_D^2 = \sum_i f_i^2(1-f_i)^2(2 \cdot P_{n,i,12} - P_{n,i,11} - P_{n,i,22})^2$$

$$\sigma_A^2 = \sum_i 2f_i(1-f_i)(f_iP_{n,i,11}+(1-2f_i)P_{n,i,12} - (1-f_i)P_{n,i,22})^2$$

, where $f_i$ is the frequency of the allele $A$ at the locus $i$ (you should get those data by reformatting your geno-pheno map matrix) and $P_{n,i,11}$, $P_{n,i,12}$ and

$$P_{n,i,22} =\frac{1}{l-1} \sum_j P_{n,i,j,22}$$

is the $n^{th}$ phenotypic trait for the genotype $22$ and locus $i$ averaged over all other genotypes. There are $l$ genotypes in total. Of course, this works only for biallelic loci. I don't know what it would look like for more alleles.


Are all antibodies against a common antigen identical?

Alright, there are two major questions:
(a) Are all the antibodies that are produced against a specific antigen necessarily identical?
Not in most cases. Antigens can either be monovalent or polyvalent, meaning that they can either have one epitope or various different epitopes (an epitope is the site of the antigen that binds to a T-cell receptor or a B-cell receptor). Most antigens are polyvalent, which implies that a single antigen may interact with several different T and B cell lineages. Each B cell lineage is only able to produce and export one type of antibody. Because the antigen will interact with different lineages, it will promote the production of different types of antibodies. These multiple antibodies produced against one antigen are called polyclonal antibodies, since they arise from multiple clonal lineages. When the antigen only has one kind of epitope, it will induce the production of only one type of antibody, which are called monoclonal antibodies, because they arise from only one clonal lineage.
(b) Do the antibodies produced against a certain antigen differ between members of the same species or between species?
Yes, in both cases. There is an important genetic variability surrounding immunoglobulins and T cell receptors.
Reference: Karp, G. (2009). Molecular and Cellular Biology: Methods and Concepts. Wiley. New York.


What is this strange sea creature we found on the beach?

You have a Dosima: Also known as a Buoy Barnacle. A gallery of observations of these can be found here:
https://inaturalist.ca/taxa/462188-Dosima/browse_photos
They are found in the coastal UK and Spain area, New Zealand, and east and west N.America:

(source: iNaturalist observations)
These barnacles attach themselves to things that float, and if they don't have access to one, they will grow one themselves. Your image looks like five individuals attached to a central float that one of them (or a dead relative) constructed.


What are some examples of coupled reactions in the cell?

All the anabolic reaction inside our body require energy. The majority of those reactions use the hydrolysis of ATP as source of energy.

To cite a few reaction that require ATP:

Gluconeogenesis where 4 ATP, 2 GTP and 2 NADH2 are consume to produce glucose from pyruvate.
Formation of peptide bond between two amino acids.  Here the amino acid have to be first activate by binding to the tRNAc consuming ATP, as explain here (from wikipedia)

  Polymerization of amino acids is what creates proteins. This condensation reaction yields the newly formed peptide bond and a molecule of water. In cells, this reaction does not occur directly; instead, the amino acid is first activated by attachment to a transfer RNA molecule through an ester bond. This aminoacyl-tRNA is produced in an ATP-dependent reaction carried out by an aminoacyl tRNA synthetase

Ubiquitin ligase, that require ATP to activate ubiquitin for conjugaison and it transfer to an E2 enzyme. This pathway is mediate by the E1 enzyme, as suggested here

  There is one major E1 enzyme, shared by all ubiquitin ligases, that uses ATP to activate ubiquitin for conjugation and transfers it to an E2 enzyme. The E2 enzyme interacts with a specific E3 partner and transfers the ubiquitin to the target protein.

Hope that it helps.


Why are there no multicellular prokaryotes?

From a Molecular Cell Biology introduction course web resource from the University of Illinios, which explains the general sentiment in microbiology over this question:

There are lots of unicellular eukaryotes, including amoebas, paramecium, yeast, and so on. As to whether there are multicellular prokaryotes, the standard answer is No, but there is a lot of evidence that some bacterial species can aggregate together and divide labor so that the "colony" is working more efficiently. This is characteristic of any traditional multicellular organism, but there's still a lot of resistance to the idea of calling these prokaryotes "multicellular."

Here's a Scientific American article on the subject, which is good for the layman and will add to your understanding. Note that the most complex 'multicellular prokaryotes' known do not form comparably large or complicated structures when contrasted with eukaryotes. Even though prokaryotes have more biochemical tools available to them, their largest multicellular specimen pales in comparison to our small multicellular eukaryotes, let alone out large eukaryotes like the Armillaria ostoyae fungus in Oregon (nicknamed "the largest organism on Earth"), giant sequoia trees, the dinosaurs, or blue whales. But I digress! Total organism size is not a requisite for multicellularity, which is why some bacteria can be termed so.

Here is a paper I found in the literature on the first reported 'true' multicellular prokaryote, from 2004. Similar organisms have been observed since. See Pubmed link.

The same question has also been answered extensively by specialists on Quora and on ResearchGate.

  What made eukaryotes to become multicellular?

Your question implies external influence. Biological evolution does not proceed teleologically, with an end goal in mind. Instead, traits gradually accumulate if they are not detrimental to the replication of the genes. The evolution of multicellularity is a complex and active field of research but there is no reason behind this major switch in cellularity other than that it works as a strategy for the replicating organism and its genes. Multicellular organisms survive. That's all.


Is there a database of pollen-seed distances across plant species?

In my searching I didn't find a comprehensive database of this information. There are biologists interested in analyzing seed dispersal distance as a trait however.

Vittoz and Enger (2007) used plants with known seed dispersal along with characteristics about these species to predict dispersal distances for other species.

There is another study here that examines the relationship of plant height and seed dispersal. They provide interesting background information as well on the trade-offs associated with a particular dispersal mode. For example,

"It is often assumed that there is a trade-off between maternal provisioning and dispersal capacity, leading small-seeded species to disperse further than large-seeded species."

It is certainly an area of research actively being pursued but there doesn't seem to be a list or database of these dispersal traits by species. There is information on dispersal distance by mode in the appendix of the second link I've provided.


The roots respond to gravity, not to light.  They display what is called a geotropism (aka gravitropism).  It has nothing to do with the light..  The roots grow TOWARD the force of gravity so the roots exhibit positive geotropism.   The stem grows AWAY from the force of gravity so it exhibits negative geotropism.   Think about a tree planted on a hill.

Phototropism is a plant's response to light.  It has nothing to do with the direction of room growth.  The stem may lean toward the sun (because of it's positive phototropism) but will still grow upward because of its negative geotropism.

**If the light was below the plant, the roots would still grow downward.


Use of restriction endonucleases to analyse Variable Number Tandem Repeats (VNTRs)

The general situation regarding using restriction endonucleases to analyse Variable Number Tandem Repeats can be explained with (as well as without) reference to the illustration below.

The original region of DNA in which the insertion occurs will in general be complex (rather than repeated) and conserved to a reasonable extent among H. sapiens. The complex conserved sequence is represented by a gradient of colour in the upper part of the diagram so that the point at which the original copy of the repeat inserted can be identified in different individuals (or alleles), A, B and C, where, for the sake of argument, two, three and four copies have been generated.
The individual repeat unit is relatively short (typically 10–100 bp), so it is relatively easy to find conserved sites for at least one commercially-available restriction endonuclease on either side of the original insertion, but not within the repeat.
The mathematics of this reasoning are quite simple, and I provide exercises on my University website. However, as an example, consider a 4-base pair sequence that is the target for a restriction enzyme. It need not be palindromic, but as most Type I restriction endonucleases are, let’s choose GGCC. The chance of finding this in any tetra-nucleotide is 1 in 256 (4x4x4x4), or, in other words, it should occur in any 256 bp stretch of DNA. (Of course this is just an average of what may be a normal distribution, and overall base composition will affect the actual frequency.)
The net result will be that it will be possible to generate fragments of an overall size such that the flanking regions are not so large that they make it difficult to distinguish differences reflecting different numbers of repeats.
And today?
The polymerase chain reaction (PCR) might well be used instead of restriction endonuclease digestion as, given that the DNA sequence of the region has been determined, one could choose appropriate positions in the flanking regions to generate DNA fragments for analysis. See, e.g. Richie et al. (1999).


Summary

Messenger RNAs that are recruited to the ribosome for protein synthesis in vivo, need to satisfy particular structural requirements and must interact with the protein initiation factors that deliver them to the ribosome. Generic single-stranded DNA (ssDNA) does not have these structural characteristics and so cannot be translated on ribosomes under natural conditions.

A single reported attempt to translate deoxyribose-based analogues of these mRNAs under conditions equivalent to those within the cell was unsuccessful. Thus, although experiments suggest that ssDNA may be able to bind transfer-RNA and allow some polypeptide synthesis under non-physiological conditions, this reflects only those aspects of protein biosynthesis that involve base-pairing interactions between the message and other RNAs involved in translation. In contrast, the stages involved in the selection of the first initiation codon and the recognition of termination codons involve interactions between protein factors and the message, where recognition of a hydroxyl group in the 2ʹ-position (and discrimination between thymine and uracil) may well occur and would prevent translation of a synthetic ssDNA message.

If, in fact, no discrimination against DNA has evolved for the ribosomal- and transfer-RNA components of the translation apparatus, this may be because the system arose in an ‘RNA World’ before DNA evolved, and because free ssDNA in the cell has never been a competitor with mRNA for ribosomes, especially after sophisticated protein-based systems arose for the selection of the appropriate initiation codon.

Contemporary physiological interactions of mRNA with ribosomes

Translation of mRNA by ribosomes (protein biosynthesis) is a complex process which can be divided into a number of stages, each generally involving a variety of RNA and protein molecules — initiation factors (IF), elongation factors (EF) and termination or release factors (RF). The reader who is not familiar with this is advised to read a text-book account such as that in Chapter 29 of Berg et al.. However, to summarize briefly, they are: selection of the correct AUG (usually) on the mRNA for initiation, IF-dependent binding of the initiator-tRNA to the P site, EF-dependent and codon-directed binding of an elongator-tRNA, peptide bond formation catalysed by the large ribosomal subunit, EF-dependent translocation, and eventually stop-codon directed and RF-dependent release of the completed polypeptide chain.

The first step, is crucial for the binding of natural mRNAs — the subject of this question. Under natural cellular conditions prokaryotes and eukaryotes have different methods of ensuring that the ribosome interacts with the correct mRNA codon to start translation. In prokaryotes a specific ribosome-binding signal (Shine and Dalgarno sequence) must interact with the 16S rRNA and a particular initiation factor protein is involved in this step. In eukaryotes the main method is recognition of a modified 5ʹ structure on the mRNA and unwinding of secondary structure, also modulated by protein initiation factors.

I am aware of one report of an attempt to translate a DNA-based analogue of such natural mRNA structures under any conditions. This was by Damian et al.  (Biochim. Biophys. Res. Commun 385, 296-301 (2009)), and was unsuccessful, even though physical methods indicated binding to the ribosome. I imagine that recognition by the protein initiation factors did not occur but I cannot be sure that base-pairing to the 16S rRNA was also hindered.

Regardless, one can answer the question posed:

  The fact that ‘random’ single-stranded DNA would lack the structural features for selection of the correct initiation codon
  explains why it would not be translated under natural
  conditions — it could not bind to the ribosome.

Artificial systems of protein synthesis

The full details of the reactions on the ribosome only emerged gradually. Nevertheless the lack of understanding of the features of natural mRNA required for binding to the ribosome did not prevent either the dissection of subsequent steps of protein biosynthesis, nor the use of ribosomal systems to decipher the genetic code. This is because it was possible to bypass the initial steps by using suitable unphysiological conditions, that allowed polynucleotides or oligonucleotide triplets to bind to the ribosome, where further reactions were possible, albeit generally less efficiently than in the cell. Such conditions included high concentrations of magnesium ions and certain antibiotics that affect the accuracy of protein synthesis. It has been suggested that the neutralization of the charge on the backbone phosphates of the RNA by Mg2+ enhances (non-specific hydrophobic interactions at the mRNA-binding channel, and that the antibiotics stabilize a state of the ribosome in which amino-acyl tRNA can bind more easily (and hence promote the binding of polynucleotides by base pairing). Once bound with the codons hydrogen-bonded to the cognate anticodons of tRNA, subsequent elongation reactions depended on components of the ribosome other than the artificial messenger.

Thus, it was that the genetic code was deciphered using bacterial cell-free systems to which were added simple synthetic polynucleotides, lacking Shine and Dalgarno sequences or start (or stop) codons; and by experiments in which amino acyl-tRNAs were bound to triplet codons in the absence of both IFs and EFs. Other partial reactions of protein synthesis were similarly dissected artificially — the peptidyl transferase reaction was studied on isolated 50S subunits using just a fragment of tRNA and puromycin by conducting the reaction in 50% ethanol!

Experiments with single-stranded DNA

Understanding that ribosomes can be induced to bind and translate ‘non-mRNA’ oligo-ribonucleotides under certain artificial conditions, we are in a position to consider the significance of reports of translation of oligo-deoxyribonucleotides — ssDNA.

The original experiments in this area by McCarthy and Holland in 1965 showed that denatured DNA from various sources (including animal cells) could stimulate the incorporation of radioactive amino acids in a bacterial cell-free system, but this depended on the presence of antibiotics. Furthermore, it was shown in Khorana’s lab that only certain synthetic poly-deoxynucleotides  (analogous to the poly-ribonucleotides he used to decipher the genetic code) were active. Thus, it would appear that under the non-physiological conditions that favour promiscuous binding of poly- and oligo-ribonucleotides, there is some binding of ssDNA, and subsequent translation.

A paper by Ricker and Kaji mentioned by @Mesentery — reports that oligodeoxynucleotides could function in some partial reactions (fmet-tRNA binding) although not in others. In particular it was not possible to perform RF-dependent termination reaction with oligonucleotides containing termination codons, but — in the presence of antibiotics — termination independent of release factors did occur.

It is, thus, obvious that these experiments in which ssDNA is translated on ribosomes have no physiological significance. However it is still pertinent to ask the complement to the question of the poster, why does the system work at all?

Why are deoxyribose (and thymine) not discriminated against under artificial conditions?

Enzymes of synthesis and degradation of nucleic acids — RNA and DNA polymerases; ribonucleases and deoxyribonucleases — are specific for either RNA or DNA (or in some cases DNA/RNA hybrids). This is both important to ensure they fulfil their specific functions, and perhaps an inevitable consequence of the nature of their reactions — the making or breaking of sugar–phosphate bonds. Here we are dealing with catalysis by a protein enzyme that binds these structures at its active site.

In contrast, those reactions of protein synthesis for which certain requirements may be relaxed under non-physiological conditions involve base-pairing interactions. In modern ribosomes they may be optimized by associated proteins, but it is thought that the latter only evolved later. Artificial conditions, such as high concentrations of magnesium ions or antibiotics, may be thought of as allowing the essential interactions that existed in ‘ur-ribosomes’. And, of course as DNA/RNA hybrids readily form, the participation of DNA in such interactions is not so surprising. (In the RNA world of ‘ur-ribosomes’ — or even an RNA/protein world — there would be no need to discriminate against DNA, because it had not yet arisen. And chemically, the substitution of a hydrogen for a hydroxyl group could not hinder an interaction — at the worst it would only weaken it.)

It is pertinent that the contemporary AUG-selection and termination reactions depends on RNA–protein interaction. These might well involve recognition of ribose as well as base sequence, explaining the observations by Ricker and Kaji, and by Damian et al., mentioned above.


Which aspects of renal physiology are standing in the way of an artificial (mechanical) kidney?

The problem is that real organs are just damn complex - yes the kidney's prime role is just to be a filter, but in order to do so it must be plugged in to a dozen regulation mechanisms - osmotic balance, ion management, protein management and a plethora of more subtle ones. Moreover it is a part of body, so it must also follow all the standard protocols to live with immune system, obtain necessary resources to its function and maintenance, cooperate with nearby tissues...

Currently we only have rough knowledge about major processes, deciphering them all is a work for many, many years (if it is not futile at all).  Finally, our technology will be long not capable of implementing all those protocols; in peaks of perfection we can serially do simple parts in 100nm scale (microprocessors), while this is a scale of a complete molecular device.


Are there statistics on Sickle Cell Traits based on country of origin?

For "where does it come from and how does it spread?", why not read Wikipedia?  Short answers: (1) malarial regions of sub-Saharan Africa; (2) movement of people and genetic introgression.

Googling 'sickle cell "country of origin" turns up, for example:

"Sickle cell disease in areas of immigration of high-risk populations: a low cost and reproducible method of screening in northern Italy" Blood Transfus. 2014 Jul; 12(3): 346–351. doi:  10.2450/2013.0188-13 PMCID: PMC4111816

Country    Selected     Enrolled/   Enrolled/
                        negative    Hb variant
-----------------------------------------------
Ghana      241 (51.4%)  112 (47.1%) 53 (57.6%)
Nigeria    152 (32.4%)  77 (32.4%)  29 (31.5%)
Guinea      15 (3.2%)   8 (3.4%)    4 (4.3%)
Cameroon    13 (2.8%)   10 (4.2%)   1 (1.1%)
Senegal     12 (2.6%)   8 (3.4%)    1 (1.1%)
Ivory Coast 10 (2.1%)   9 (3.8%)    1 (1.1%)
Other       26 (5.5%)   14 (5.7%)   3 (3.3%)
Total      469 (100%)   238 (100%)  92 (100%)

"The burden of sickle cell disease in Cape Town", South African Medical Journal 102(9), 2012 Wonham et al. http://www.samj.org.za/index.php/samj/article/view/5886/4421

Distribution of sickle cell disease patients by country of origin. Up to 93.1% (n=54) of the patients were originally from other countries in Africa, mainly from the Democratic Republic of Congo (62.1%, n=36).


Are there any online resources one can use to access raw clinical trial data without having to contact those involved in the study?

See these three sites:

ClinicalTrials.gov
NIDA
ClinicalStudyDataRequest

For clinical trials conducted by other agencies (in different countries), you may have to contact those authorities.


They seem to be rotifers, the fuzzy (supposedly rotating) mouthparts are part of what convinces me. The behavior you mentioned of latching on the moss with their 'tails' is also a characteristic behavior of rotifers. They are also able to retract their bodies just as you mentioned.
Here are some images of rotifers that might support the argument.

I am least certain about the last image but I am making the assumption for now that it is either some variety of circular/retracted rotifer or a completely different kind of microorganism.
Stay curios!


Do green algae form obligate symbioses with fungi?

Yes, Lichen are composite organisms of green algae (or cyanobacteria) living togther with fungi.

In most cases the fungi-part is completely dependent on that symbioses and is completely dependent on the symbiosis. For the algae it seems that some species can survive on their own, but not necessarily in the same enviroment as the lichen, while other species may again be completely depedent on the symbiosis (see also the comments).


Why my proteins are migrating like this on SDS-page?

It's a guess, as I haven't run a algae sample on SDS-PAGE, but your migration problems might be due the algal polysaccharides that are present in your sample. Check if your protein purification protocol is specific for algal proteins and see if there is any step dealing with the algal polysaccharides.


Why are there no known animals with an odd number of legs?

It depends what you mean by 'leg'.

The instinctive way to define a 'leg' is based on its functional use: we use legs to walk on. But if we adopt that definition of 'leg' then there certainly are animals with odd numbers of legs: kangaroos, for instance, have a five-legged gait, functionally using their tail as a fifth leg. There is no developmental process that stops an animal from growing an odd number of appendages, and if one of those appendages happens to be used as a leg, evolution and development will have no problem with that.

However, there is another way to define 'leg', and that is by homology - 'legs' are the appendages derived by evolution from the legs of a common ancestor. Under this definition, (for vertebrates, at least) you're a bit more hard-pressed to find examples of animals with an odd number. This is because those legs are paired appendages, and the developmental pathways for the leg on one side of the body are tied into the developmental pathways for the leg on the other side of the body, so it is hard to evolve an odd number of legs from these appendages.

Hard is not the same as impossible, though. A comparable piece of evolution is the severe reduction in size of fins from one side of the body in flatfishes (flounders, sole, etc). I am struggling to think of terrestrial examples, but it is certainly evolutionarily possible to lose one appendage from a pair but keep the other.


Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Not that much, because fibers from both sides are fused, so each nerve carries about a 50% of fibers originated from the one side and about 50% from the contro-lateral. Consider that fibers are rewired after each plexus.

References:

 wikipedia page about vagus nerve

 wikipedia category about vagus nerve


Its there a gene or genes for intelligence?

Is IQ heritable?

Let me start by saying that there is no commonly agreed upon method to measure IQ (thank you @mdperry). Keeping this in mind...

Yes, studies have shown that IQ is heritable. Or rather, IQ has a heritability that differs from both 0 and 1, meaning that both environment variation and genetic variation plays a role in determining an individual's IQ. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref). For more information, please have a look at this post.

To understand the concept of heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

  What are the genes that contribute to it?

IQ is a polygenic trait, meaning that many loci (locus = position in the genome) are affecting the variation in IQ. For more information about those loci, please have a look at this post.

  What I don't understand is if only some people have this 500 genes or all human population has this genes?

Your misunderstanding comes from a misunderstanding about the concepts of gene and allele. You should start by having a look at the definition of the three following terms

gene
allele
locus

Below, I will not comment about the 500 genes claimed in this popular article and will just consider them as valid without considering the complication behind the methodology used for such estimation and about what original articles this popular article is citing.

With the exception of eventual copy number variation, the entire human population share these 500 genes but not everyone has the same allele at these 500 loci.


how to find accurately the closest species to my plant species?

If you know the species name, you can search TreeBase to find previously published phylogenetic trees which will point you towards close relatives to your species. Depending on how obscure your taxon is, though, you might not find much.


Do cancer cells give off specific chemical signatures?

The answer is it depends.  First, take a step back from the definitions of "cancer" versus "normal" cell and recognize that cells and tissues can undergo a variety of changes in their growth.  A solid cancer/tumor (as its usually defined) is something that grows and invades the surrounding tissue.   A spectrum of possible cell growth can be :

normal -> hypertrophy -> hyperplasia or dysplasia -> hamartoma -> benign tumor -> carcinoma in situ -> invasive cancer -> metastais

(this list is NOT suggesting these are the actual steps to cancer, but instead they are useful for the next paragraph):

The point of this list is that from a human perspective we can see something odd happening when we see a tumor, but the view from inside a cancer cell is basically "things are fine, I'm just doing my cell thing".

But, that said...when a tumor grows and cancer cells invade tissues a few things happen which can give rise to differences between cancer cells and normal tissues and which can be detected.
First, it needs energy, and cancer cells often switch to aerobic glycolysis (a phenomenon called the Warburg effect). As the link shows, a special form of labelled glucose can be used to detect this in the body.

Secondly, a tumor invades the surrounding tissue and generates new blood vessels, and so enzymes that break down extracellular matrix  are released.

Some tumors over-express and secrete markers (usually proteins) that can be detected.  The prostate specific antigen (PSA) and carcinoembryonic antigen are two examples.

Other things secreted by certain tumors may include volatiles that can be detected by dogs.

The challenge with any 'signature' detection is the sensitivity and specificity  which often limits the use of tests that show some early promise.

Cancer cells DO have specific changes to their DNA that can be used as very specific signatures for detection.  Tumor DNA is shed into the blood and possibly the urine.

Finally, tumor biology overlaps with many aspects of normal biology, including wound healing and pregnancy and this continues to make it challenging to identify tumor specific markers that have high sensitivity and specificity.


Which proteins are part of the most different protein complexes?

This answer does not address the number of complexes that a protein participates in, but rather a related question -- With how many proteins does a protein interact?
I acknowledge this  is a fundamentally different question, though I think it's a good starting point on which other people can build a better answer.

Taking the data from STRING v11 for all protein-protein interactions (PPIs) in Escherichia coli str. K-12 substr. MG1655, we can subset these PPIs to include only those of action type "binding".  This database provides PPI scores between 0 and 1 based upon experiments (co-purification, co-crystallization, Y2H), textmining, co-occurence, co-expression, and co-localization of coding genes across genomes.
If we set no cutoff for the confidence in these binding interactions, we see that 2585 proteins have ≥1 binding partner, and one protein has an astonishing 273 binding partners (pfo, a putative pyruvate-flavodoxin oxidoreductase).  Also, this database states this E. coli strain has 4127 distinct protein-coding genes, so approximately 63% (2585/4127) of genes encode a protein that interacts with at least one other distinct protein.
If we limit the interactions to those with a "high confidence" score (≥0.900), only 656 proteins (~16%) are seen to have ≥1 binding partner, with a maximum of 55 binding partners seen for 4 proteins.  Unsurprisingly, and consistent with the comment from Maximilian Press, these proteins are all associated with the ribosome (sra, rpsP, rpsI, and rpsR).  The spike in the graph below at 54 interacting partners for the high-confidence PPIs is a group of of ribosomal proteins, most of which are annotated as co-interactors.

Two important notes on interpretation of interactions in this database:

splice variants and post-transcriptionally modified proteins are collapsed into single nodes in the interaction network, so all gene product variants are represented by one coding sequence
self-interactions (e.g. dimerization) are not counted, which are a valid type of protein complex per the question


List of genes across species (or just for humans)

In principle there are a LOT of these databases and depending on your specific questions you may want to look into different ones. Like already mentioned NCBI hosts basically all of the available information, however it's not always easy to find the bits you care about.

The database I personally use the most is biomart (hosted by the ensembl consortium). It doesn't just contain all known for genes for pretty much all organisms, but is also able to link this to a ot of different information sources.
I usually access the database directly via the biomaRt R package, so I can't really say how good the actual website this. However, this link should allow you to download a table of all human genes with names, (unique) identifies & descriptions (I selected these from the 'Attributes' section).


Note: not my area of expertise

First of all, heterochromia can be congenital (found at birth) or acquired, and from your question it is not clear if you are asking about one specific type or the overall frequency (if so, at what age?). Since acquired heterochromia is often due to injury or disease, the overall frequency is likely to increase with age. Also see answers to the question "Is it biologically possible for an adult's eye color to change?" for more on reasons for acquired heterochromia.

According to an Austrian study (Stelzer, 1979), the overall frequency in the Vienna population was 0.26% (males: 0.16; females: 0.37). However, Medicine.net reports a frequency of 0.6% for only congenial heterochromia, but this number lacks a clear reference. A thorough review of different reasons for heterochomia can be found in Rennie (2012).


Well nerve crossing or misinterpretation of nerve signal by the brain does not happen all the time. In case it happens frequently then I guess it would be Multiple Sclerosis or might be Fibromyalgia syndrome. In multiple sclerosis, the Myelin sheath surrounding neuron when gets damaged causes certain problem with nerve signal transmission to the brain. But that is not the main cause. The main cause can be found in Neuropathy:

When nerve cells are damaged, perhaps by a temporary restriction in their access to oxygen, they too atrophy or shrink a little, thus the synaptic junctions widens.  Just like with a spark plug in your car or lawn mower, if this gap gets too wide, the spark cannot make the jump. A normal sized nerve signal cannot jump this enlarged gap either, so the signal either does not get through or it gets misdirected to another part of the body and is misinterpreted as pain.

So I can say that the nerve cells in the place where you feel real pain fails to transmit the signal to brain via its neighboring nerve cell instead that signal passes through some other node randomly (or it might take the same path every time you touch the pain area) and signal the brain which gets misinterpreted and make you feel that you have pain in the misinterpreted region.


Mathematical/statistical models for forecasting population distributions of age, sex, weight, and height

The term you are looking for is demography - there are literally thousands of papers published on this topic.
Each of your topics mentioned has its own models and prevailing theories, so without an exact question it is very hard to answer as to which model you might find best.
Having said that there are well established models of things like geometric growth of populations (proposed by Thomas Malthus in 1798). The United Nations does a lot of modeling of populations and the like. You might be interested in their freely available publications and information here.


Proteins: Post translational modification

1) Is the attachment of zinc regarded as a type of post-translational
  modification?

It is not really considered a post-translational modification because the zinc atom is not covalently bound to the protein. Binding to zinc is adsorption.

  2) When carbonic anhydrase is denatured, is the zinc ion released in
  the medium?

Yes, but it depends on the extent of denaturation too. Metal ions can be removed using chelating ligands like EDTA, without actually denaturing the protein.

  3) Will the amino acid sequence (primary structure) be changed after
  denaturation? If yes, are amino acids removed after denaturation, if
  yes, which?

Denaturation does not include cleavage of covalent bonds. There won't be change in the amino acid sequence.

  4) I guess Zinc will be removed after denaturation. Is the remaining
  structure the primary protein structure?

Yes; just the polypeptide.


Recommended sequence clustering algorithm for transcriptome data

It does sound like you have a lot of data.

I would first try Robert Edgar's other newer tool UPARSE which is faster and can handle more data using the free 32-bit version.  I think you'll mainly be limited by machine memory though, right?

Did you try CD-Hit?


Difference between Category, Rank and Taxon

A taxon (plural taxa) is any taxonomic unit. For example, the class Mammalia is a taxon which includes all mammalian species. Similarly, a species is a taxon, Panthera tigris being the tiger. This taxon contains lower taxa, which are sub-species, such as Panthera tigris tigris (Bengal tiger) or Panthera tigris sumatrae (Sumatran tiger).

Rank is simply the level of a taxon in the taxonomic heirarchy. For example, the taxa Mammalia and Aves both have the same rank since they are both classes. Panthera tigris sumatrae is of a lower rank than Panthera tigris because the former is a sub-species and the latter a species. Use of the term rank is only truly meaningful when comparing two taxa.

Taxonomic category is usually – for better or worse – used interchangeably with the term taxonomic rank. A Dictionary of Biology (6 ed.) certainly indicates that the terms rank and category are equivalent. The major taxonomic categories are domain, kingdom, phylum, class, order, family, genus, and species. A category can contain one or more taxa.

Another example, to summarize:

Carnivora is a taxon, which contains many species including Vulpes
vulpes (red fox)
Carnivora is in the category of order
Carnivora (order) is a higher rank than Vulpes vulpes (species)


How could I identify whether given RNA-seq data is paired end or single end

To find out whether a dataset was paired-end or single-end, go to SRA, click on a run, and look under "Library". Paired-end datasets will typically have "Layout: paired". Note that people don't always mark this correctly, which causes no end of headaches.

Regarding lines like "CCCFFFFFGFHHHGJJJJI#1?FEIGGI", that's the quality score line. Look at the fastq article in wikipedia for more details.

Edit: Regarding the updated portion of your question, no you can not increase this length. The sequences produced by Illumina machines are a fixed length and that length (or whatever length was submitted) is what you're getting. As a general rule, you'll get whatever sequence was updated (unless you forget the --split3 (or whatever it's called) option).


Yes. Below is a link to a review of ncRNA (non-coding RNAs) and their role in disease. There are many examples in this review in all sorts of diseases, one of which is miR-200, which is thought to play a role in some cancers.

There are also some tables in the paper that list the miRNA and the disease they are linked to. They also have a reference for each one, so you could read more about that particular miRNA and its function, including the gene it regulates.

http://www.nature.com/nrg/journal/v12/n12/full/nrg3074.html

Im not sure if that article is open to the public or not. If you cant access it you could always check out the wikipedia entry for miR-200

http://en.wikipedia.org/wiki/Mir-200


Does the Valsalva maneuver require a completely closed airway? How do the effects compare to exhalation against partial resistance?

The eustachian tubes exit into the nasal cavity superior to the glottis.  Thus restricting the glottis while exhaling cannot increase pressure in the nasal cavity / eustachians.  Only by closing the nostrils can that be achieved, and only while exhaling.  Even a technique like circular breathing cannot maintain pressure in the nasal cavity since that's necessarily the entry point for every new breath, be it mouth or nose.


Which countries do not feature mosquitoes?

According to India.com, Chris is right and Iceland has been declared mosquito free.

The science behind this is quite interesting and there are various hypotheses regarding as to why Iceland doors are shut to mosquitoes. The most preferred hypothesis by scientists, according to New York Times is >>

  When mosquitoes lay eggs in cold weather, the larvae emerge with a
  thaw, allowing them to breed and multiply. Iceland, however, typically
  has three major freezes and thaws a year, creating conditions that may
  be too unstable for the insect’s survival.


This is Libellula quadrimaculata, which is a common and very widespread species (North America, Europe, Asia at least). This is based on the relatively wide and flat abdomen (hard to judge due to the angle though), which suggests Libellula, brown/golden colour and a brownish wingbase. The main problem I have with the pictures (which makes my suggestion more uncertain) is that it is really hard to see the wingspots in your pictures, due to sun glare. Libellula quadrimaculata is one of the few European species that has four wing-spots (hence the english name Four-spotted chaser), which is why the wing-spots are important to see. However, I think I see hints of wing-spots at the middle of the wing (greyish patches on the top picture), which suggests four spots on each wing pair.

Edit
The distinctive four spots vary greatly in size among individuals and though small they are clearly present. The yellowish tint in the wings and the hairy thorax are also distinctive. The shining wings suggest this individual just emerged (from its larval stadium).  Colors may be less distinctive in these young individuals.

There are no similair species.

(picture from wikipedia)

More pictures of the species can be found here


Is the reason that flies can perceive things faster because their brains are smaller?

Fly neurons aren't like human neurons. They have different nerves that transport signals faster than human nerves. So they can see your hand moving towards them faster than we can see for ourselves, which makes them able to avoid being squashed (most of the time).


Does Amphibian embryo's blastocoel become a primitive yolk sac without yolk?

Amphibians are produced externally so they do not get proteins and ATP from the mother during their maturation and differentiation. This means that they must have some way to get those things to protect themselves and survive.

The way that they get these things is yolk. Amphibians start to have yolk-filled endoderm during blastulation, [page 9, Gilbert, Developmental Biology].

I am considering the frog here as an example of amphibian. To know that things need energy to survive and that they must get it somewhere, you can deduce this solution. So nutrition and external "hatching" or development outside of female is the key here.

The overall answer to the question:
The organism must have a yolk sac, since it has yolk.

The second question seems to be an idealized one.
Without blastocoele but with yolk-sac suggests me that the blastocoel has developed already to yolk-sac. If that is the case, then I would call the thing gastrula, since for instance some species' ectoderm develops into yolk-sac. I assume that the question refers with "yolk-sac" to complete yolk-sac, not to the developing one during gastrulation.

If it is about developing yolk-sac, I would say that the cell is still blastula but is developing to gastrula. The yolk sac is not ready until gastrulation is complete.


What method would you use to genotype SNPs in low quality samples?

I agree with @gchadwick that more infor would help.

However, based on my understanding of what you are trying to do (SNP genotyping on several genes), I suggest.
1) Enrich your DNA with DNA from the organism you want
2) Enrich your DNA with DNA in the desired regions (if any).

Solution: Target enrichment. You are probably aware that companies such as agilent, nimblegen and illumina offer target enrichment kist for next generation sequencing.
However, if your DNA is soooo bad, I suggest performing target selection with PCR.


Why do smaller mammals move intermittently?

Short answer
Intermittent locomotion can increase the detection of prey by predators (e.g.  rats), while it may lead to reduced attack rates in prey animals (e.g., rats and chipmunks). It may also increase physical endurance.

Background
Rather than moving continuously through the environment, many animals interrupt their locomotion with frequent brief pauses. Pauses increase the time required to travel a given distance and add costs of acceleration and deceleration to the
energetic cost of locomotion. From an adaptation perspective, pausing should provide benefits that outweigh these costs (Adam & kramer, 1998).

One potential benefit of pausing is increased detection of prey by predators. Slower movement speeds likely improve prey detection by providing more time to
scan a given visual field.

A second plausible benefit is reduced attack rate by predators. Many predators are more likely to attack moving prey, perhaps because such prey is more easily detected or recognized. Indeed, motionlessness (‘freezing’) is a widespread
response by prey that detect a predator.

A third benefit may be increased endurance. For animals moving faster than their aerobically sustainable speeds, the maximum distance run can be increased by taking pauses. These pauses allow the clearance of lactate from the muscles through aerobic mechanisms.

PS: If you mean with 'snappy' not only that small animals move intermittently, but also 'fast', then Remi.b's answers nicely covers the story why small critters are quick. Basically, it comes down to Newton's second law, namely acceleration is inversely proportional to mass (a = F/m), but the size of muscle power is not. Hence, bigger animals have more mass and need a lot more force to build up to accelerate at the same speed. That build up of force needs time (ever witnessed the vertical lift-off of a space shuttle?) Hence, small critters accelerate quicker and allow them to move 'snappy'.

Reference
- Adam & kramer, Anim Behav (1998); 55: 109–117


Why doesn't the cytosol dissolve the polar structures?

Many cell components are not simply hydrophobic or hydrophilic, but have dual affinities. Proteins typically have structures which result in the interior of the protein being hydrophobic and the exterior, which is exposed to the water in the cytosol, being hydrophilic. Thus, differences in polarity between different regions allow proteins to be dissolved in the cytosol while still maintaining a stable structure.

Similarly, the lipid bilayer is composed of phospholipids, which can be described as "tails" of hydrophobic carbon chains connected to hydrophilic phosphate "heads". The phospholipid bilayer is organized so that the phosphate heads are on the surface of each side of the bilayer, with the carbon chains from each side of the bilayer intertwined with each other in the interior.


Do antibiotics attenuate immune response on subsequent exposure to same bacteria?

A quick search on ISI Web of Knowledge yielded this paper:

  R J North, P A Berche and M F Newborg (1981) Immunologic consequences of antibiotic-induced abridgement of bacterial infection: effect on generation and loss of protective T cells and level of immunologic memory. Journal of Immunology 127: 342-346

The authors investigated the effects of ampicillin treatement in mice infected with Listeria monocytogenes. They reported an abridgement of T cell-mediated antibacterial immunity and in particular an effect upon the development of memory:

  Moreover, Ampicillin-induced abridgement of infection, either before or at the time of peak primary response, resulted in the expression of greatly reduced levels of immunologic memory at a later time. This indicates that memory cells are generated throughout the entire course of the primary anti-Listeria response, including the period of its decay.

Presumably any treatment that reduces the need for an immune response will have an effect upon the production of useful memory T cells.


Mutation in axillary buds of trees overcoming self-incompatability?

Recently, samples from different parts of cottonwood trees have been sequenced (Nature News). The conclusion:

  “The variation within a tree is as great as the variation across unrelated trees,” says Ken Paige, an evolutionary biologist at the University of Illinois at Urbana-Champaign, who led the team that made the discovery.

This doesn't say anything about overcoming self-incompatibility, and it probably depends on the mechanism of self-incompatibility if it can be overcome by accumulating mutations.


What is difference between "Syngonium" & "Pothos"?

Pothos is a common name for Epipremnum aureum, which, like the genus Syngonium, is in the monocot family Araceae.

From Wikipedia:

  E. aureum is an evergreen vine growing to 400 m (1,312 ft) tall, with stems up to 4 cm (2 in) in diameter, climbing by means of aerial roots which adhere to surfaces. The leaves are alternate, heart-shaped, entire on juvenile plants, but irregularly pinnatifid on mature plants, up to 100 cm (39 in) long and 45 cm (18 in) broad; juvenile leaves are much smaller, typically under 20 cm (8 in) long. The flowers are produced in a spathe up to 23 cm (9 in) long. This plant produces trailing stems when it climbs up trees and these take root when they reach the ground and grow along it. The leaves on these trailing stems grow up to 10 cm (4 in) long and are the ones normally seen on this plant when it is cultivated as a potted plant.

 Source: Wikipedia

Syngonium species, on the other hand, can have broader stems, stems that lose their chlorophyll, and different leaf shapes, to anme a few descriptions. From Wikipedia:

  juvenile leaves, whole ovate or elliptical; mature bisector leaves up to 11-secant and fan-shaped

Wikipedia also mentions some unique traits of this group of plants:

  The climbing stalks have elongated internodes and are elastic to some extent, however, after bending the stem's skin often breaks and peels off, turning brown or yellowish. The stem in section shows a distinct layer of the plant directly under the skin of the stem. The border between the colenchyma and stem stem is poorly scratched. In the parenchyma, starch grains are randomly distributed. The tissue of the stem also contains idioblasts with calcium oxalate crystals and drusen. The stem also contains secretory cells, containing tannins and milk juice, which solidifies in the air.


Reproduction number of a SIR model with mortality

The only answer that makes numerical sense is 1. The product of two rates beta and delta (recovery * death) doesn't mean anything in SIR. And in answer three you're doubling the rate of infection (alpha). Looking at the other way, for R_0 it doesn't matter how people leave the Infected class, once you're either dead or recovered you no longer are transmitting the disease. Therefore you can say that some value Zeta is the exit from Infected class and Zeta would be the sum of all rates which remove a person from being Infectious


Genotypic distribution of a population with two characteristics and linkage

You are...  done. You fully answered the question; if I were you, I might just put it in ratio format instead of probability, just to be safe.

The three times thing is a bit weird, but I have seen it before. First, let's look at the phenotypic ratio of the progeny: 9:3:3:1 for Dominant Both:Dominant A Recessive B:Recessive A Dominant B: Recessive Both.

Let's find out how many dominant and recessive there are for each trait. For the dominant A trait, you add up the 9 and 3, because they are the only two types of dominant phenotypes, and find that 12 different organisms of the 16 possible are dominant for Trait A, so the probability of getting trait A is 3/4 or 75%. This means that 4 of the 16 orgamisms are recessive for Trait A, so the probability of being recessive for Trait A is 4/16, or 25%. Therefore, the ratio of Dominant Organism probability:Recessive organism probability is 75% to 25%, or 3:1. This means that it is 3 times as likely to get the dominant trait than the recessive trait. Make sense?


Can the heart generate its own rhythm independent to the SAN?

Your textbook and review guide are correct, but the missing details may be a little confusing. Yes, the heart has the property of automaticity, meaning action potentials fire on their own at a certain rate, without input from the nervous system. Yes, the SA node typically controls the overall rhythm of the heart because it overrides the rhythm of the rest of the heart.  However, not all cardiac muscle cells have automaticity. Cells in the SA node, the AV node, and to a certain extent, the conducting system all exhibit a physiologic automaticity, that is, they have ion channels that carry what is called a pacemaker current (or sometimes "funny current"), that slowly depolarizes their membranes after each action potential. When this slow depolarization reaches the threshold voltage, another action potential fires. The SA node drives the rate of the heart because an action potential reaches these other automaticity centers, or latent pacemakers, before they would fire on their own. Normal, non-conducting atrial and ventricular myocytes do not exhibit a pacemaker current (except in certain pathological situations), so do not contract independently. So, while the heart muscle is, as your textbook describes it, "myogenic", normal cardiac myocytes (in an intact organ) are not.

This becomes important in cases where the SA node is unable to generate an action potential, is suppressed (is generating an action potential at a slower rate), or other cells with a pacemaker current have increased their rate of firing. In these cases, you can experience an escape beat (a single action potential from a latent pacemaker propagates through the conducting system to cause a heart beat), or an escape rhythm (a series of escape beats).

These are general textbook level principles. You can refer to the wikipedia entry linked above. They are discussed, perhaps more authoritatively, in Lilly's pathophysiology of heart disease. Chapter 1, under electrophysiology, discusses the general principles of automaticity, pacemakers, and latent pacemakers. Chapter 11, under native and latent pacemakers, alterations in sinus node automaticity, and escape rhythms, goes into more detail about the circumstances in which latent pacemakers drive the heart.


Predict if a given protein is recognized by antibodies

First of all: It is important to appreciate tha antibodies do not recognize antigens, they recognize epitopes borne on antigens.

There are several software (online) that allow to predict these epitopes with high accuracy. I´m going to describe some of them next:

Prediction of B-cell epitopes:
You have to be in mind that B-cell epitopes can be continuous and conformationals.

Continuous epitopes can be predicted using Bcepred. This prediction methods is based on physico-chemical properties on a non-redundant dataset. The dataset consists of 1029 B-cell epitopes obtained from Bcipep database and equally number of non-epitopes obtained randomly from Swiss-Prot database. The prediction accuracy for models based of various properties varies from 52.92% and 57.53%. Also It achived highest accuracy of 58.70% at threshold 2.38, when  combined four amino acid properties( hydrophilicity, flexibility, polarity and exposed surface).

Conformational epitopes can be predicted using DiscoTope 2.0. This method predicts discontinuous B cell epitopes from protein three dimensional structures. The method utilizes calculation of surface accessibility (estimated in terms of contact numbers) and a novel epitope propensity amino acid score. The final scores are calculated by combining the propensity scores of residues in spatial proximity and the contact numbers. Besides, Using the benchmark data set from the original DiscoTope paper, has been demonstrated that the updated method has a significantly increased predictive performance.

Important: Discotope allows to get a 3D structure of this epitopes.

I propose to use DiscoTope for prediction of discontinuous epitope residues for several reasons. First, I have shown on a data set of discontinuous epitopes that the average predictive performance of the DiscoTope is significantly higher than the Parker propensity scale and marginally higher than the surface localization score defined by the NACCESS RSA score. Second, several authors have shown that DiscoTope correctly predicts residues in epitopes that have been identified using different techniques such as phage-display, point mutation, and sequence analysis. Third, the DiscoTope prediction method is publicly available on www.cbs.dtu.dk/services/DiscoTope, and the output of the method is easily interpreted.

I would recommend you to check if this epitopes borne on the protein have possible allergenic sites that can contain experimentally proven IgE
epitope. For this you can use Algpred


How pronounced is the difference if we would change the running direction for runners?

Been a sprinter for 12 years, so from that perspective, I don't think it would matter. The angle that you take when turning is not drastic enough to have a musculoskeletal difference; step height differs only a few inches. Additionally, turns never account for more than 50% of a race (barring a couple distance events, where turns act much more like straightaways anyway due to the lessened speed), so a bigger imbalance would be disadvantageous for straight sprinting. In practice, I think it would take a little bit to get used to, but not more than a year.


How does a baby deer stand the day it's born?

If you compare placental mammals in how much time they need to start walking, you'll see that deer are no exception. Humans are an exception.

Hypothesis of Obstetrical Dilemma

The hypothesis of Obstetrical Dilemma states that humans are born premature. We very much think this is because if we were to be born more developed (like other mammals), our big brain would not be able to make its way through the pelvis. Also, bipedalism leads to a narrower pelvis making the passage of the big brain even more problematic. For this reason, human babies are very dependent on the care of their parents for a long time. This hypothesis is called the Obstetrical dilemma (see Rosenberg 1992, Weiner et al. 2008 among many other papers as well as several books such as Ancient Bodies, Modern Lives for example).

Counter arguments to the Hypothesis of Obstetrical Dilemma

Note however that this hypothesis comes with a few potential contradictions, such as the fact that human gestation is no shorter than the gestation of humans' sister species. Indeed, in chimpanzees, for example, gestation lasts 243 days on average against 280 days on average for humans. These counter-arguments can be found in Dunsworth et al. 2012.

Thanks to @MattThrower and @AdamDavis for their helpful comments.


Can PolyA tails be within Expressed Sequence Tags?

The CATGTC sequence at the end of the poly A tail is an artefact of the method used in constructing the original cDNA library.

According to https://www.ncbi.nlm.nih.gov/nucest/EE485195.1 this EST comes from a library constructed in the Clontech vector pDNR-LIB

The Clontech SMART cDNA cloning system manuals are linked to from here
and the general manual descibes the use of a primer for 1st strand synthesis:

  CDS III/3' PCR Primer  5'-ATTCTAGAGGCCGAGGCGGCCGACATG-d(T)30N-1N-3'

  (N = A, G, C, or T; N-1 = A, G, or C)

If you look carefully at the primer you will see that the oligo dT portion, designed to anneal to the poly-A tail of the mRNA is preceded by the sequence GACATG and a SfiI site that is used in some clever cloning strategy that I don't fully understand. What is clear however is that the use of this primer will put CATGTC immediately after the poly A in the cDNA:

           .....SfiI....
5'-ATTCTAGAGGCCGAGGCGGCCGACATGTTTTTTTTTTTTTTTTTTT...
   TAAGATCTCCGGCTCCGCCGGCTGTACAAAAAAAAAAAAAAAAAAA...5'

>>> turning bottom strand around -  5' ...AAAAAAACATGTC


Why will happen if plant phloem does not contain sieve plates?

First of all, phloem sieve cells (opposing to xylem vessels) are live cells. In the phloem, a transport occurs not like in water pipes (with free movement of liquids) but through cells transport structures, particularly through plasmodesmata. As live cells, sieve elements need all standard structures, including cell wall, to sustain functionality.

Moreover, the phloem transport is (at least partially) an active process. I.e. to transport something you have to spend some energy. Today the most supported hypothesis of phloem transport is Pressure Flow Hypothesis . According to Wikipedia:

  While movement of water and minerals through the xylem is driven by
  negative pressures (tension) most of the time, movement through the
  phloem is driven by positive hydrostatic pressure. This process is
  termed translocation, and is accomplished by a process called phloem
  loading and unloading. Cells in a sugar source "load" a sieve-tube
  element by actively transporting solute molecules into it. This causes
  water to move into the sieve-tube element by osmosis, creating
  pressure that pushes the sap down the tube. In sugar sinks, cells
  actively transport solutes out of the sieve-tube elements, producing
  the exactly opposite effect. The gradient of sugar from source to sink
  causes pressure flow through the sieve tube toward the sink.

So, a plant needs live cells to support such mechanism.

Here we come to sieve plates. In plants, live cells interacts by means of plasmodesmata. In simple words, they are extensions of endoplasmatic reticulum which connect the cytoplasm of two cells and act as transport channels. And sive plates are simply places of highly hypertrophied plasmodesmata region.

So in conclusion:

Phloem transport is a partially active transport which occurs with
an involvement of cells transport structures like plasmodesmata.
The region of hyper-developed plasmodesmata on sieve elements wall
appears as sieve plate.
That is why an absence of such structure will not provide any gains in conductivity.

UPD. In response to Jim Young comment.
Damage protection is not a major role of sieve plates. Again, sieve plates are areas where plasmodesmata penetrate cell wall. Plasmodesmata act as the main vector of intercellular transport. So, the transport is the main purpose (or a reason) of sieve plates.  The damage protection is an additional property and not an aim of these structures. As to tyloses, yes it is a common mechanism of vertical transport prevention in xylem. But xylem vessels consist of dead cells. They are literally pipes. Therefore it is possible to cork up xylem vessels by simply inserting packs of fibre. BTW, that is why cavitation in vessels can cause embolization.  In contrast, phloem cells are live cells (with cytoplasm and EPR). They conduct water and sugars not by free flaw but with an involvement of intercellular mechanisms. That is why mechanical embolization is not a case for phloem cells.


late Maastrichtian is probably it.

Part of the problem you are running into is the Triceratops genus is in flux, there is debate about whether certain species belong in the genus. Such as whether triceratops and torosaurus are the same species.

The other problem you are running in to is the accuracy of dating methods, many fossils are dated indirectly, by bracketing (distance in section) with ash beds but this means they have a decent margin of error, 69MYA +/- 2mya is completely possible. Many were collected before such dating was even done or suche detailed measurements were taken leading to an even wider error bar. Especially given the best dates for the Hell Creek Formation itself has an date range error of about +/- 0.7MY and begins with a unconformity. Many studies are just going not going to calculate a date that has a high degree of uncertainty. The date for the end is more solid because it is an ash bed, thus directly datatable.

The most recent analysis of triceratops I know of is here many of the specimens were collected in the 1800's so late Maastrichtian is about the best you are going to get for an uncontroversial date.


Do bisexuals have any evolutionary advantage over straights and gays?

Like many things, whether bisexuality is advantageous for an individual's reproductive success or not depends on the environment. The fact that a wide variety of sexual systems and behavior exists in the animal kingdom suggests that. Also, "advantageous for an individual's reproductive success" doesn't necessarily imply "will spread via the processes of evolution"; for a trait to spread via natural selection+random mutation you need the trait to promote the individual's reproductive success, and for it to be reliably passed down to its offspring. And as the causes of sexual orientation in humans aren't well understood there is always the possibility it isn't strongly or genetically inherited.

As far as bonobos go, I am given to understand they use sex as a social tool, much more so than we do. In that context it does seem like bisexuality would be advantageous; it's silly to only be able to use your most powerful tool for conflict-resolution and social bonding on half of your community. This particular advantage won't be true, or will be much reduced, in species that don't use sex in the same way, i.e. all or most other species that we know of.


In short: base pairs are not composed of amino acids but nucleotides. Base pairs are parts of the DNA, while chains of amino acids forms proteins.
Certain parts of the DNA (called genes) are transcribed to messenger RNAs (mRNA) which are sequentially translated to amino acids and the chains become proteins. 3 bases (called a codon) code for 1 amino acid.

Please look up the Central dogma, DNA, mRNA, protein and translation for further information


What are the functions of magnetic bacteria?

You can find a detailed discussion of this topic here.

Magnetic bacteria contain chains of magnetic crystals (magnetite or greigite) which cause the cells to be oriented in a magnetic field.

It was originally proposed that magnetic bacteria use their magnetosomes to ensure that they swim downwards into the sediment (everywhere on earth, except at the equator, these lines of force have a downward component vector.) However, the current view is more complex than this: magnetic bacteria are microaerophilic and occur in stratified aquatic environments (i.e. ones where there are zones of oxygen concentration at different depths). In this view the magnetic "sense" is not a true taxis, but rather is used to keep the cells oriented in the magnetic field while they adjust their position by sensing oxygen (aerotaxis). As you may be aware, the standard way that Gram-negative bacteria operate is to perform a biassed random walk in three dimensions. The alignment of cells with the magetic field will reduce the dimensionality of the movement, which is more efficient.


Different Mutations Leading to Same Allele?

You are looking at high school biology books. if that.  I'd be shocked if a high school text didn't mention blood group genes, for instance.
The simple genetics that Mendel elucidated only applies to a very small number of situations.
In real life, very few situations are explained by the interactions of only two different alleles, one of which is classically dominant to the other, within a single gene.
So sure, you could have many alleles which break a gene, but where the presence of one working allele is enough to be functionally indistinguishable from having two working copies.  You could also have slight sequence differences that are functionally identical.
Here's a random example; all the variants ensembl knows about for a random gene.  Note that these are only variants which have been found, obviously private individuals and families might have their own variants that are not documented
http://uswest.ensembl.org/Homo_sapiens/Gene/Variation_Gene/Table?db=core;g=ENSG00000280165;r=13:61409685-61415522;t=ENST00000409204
Most of these are in the 3' UnTranslated Region, and likely have no functional significance.


Can soap kill cockroaches and/or ants? If so, how?

I'm not completely confident that the aforementioned post is a duplicate, because the question explicitly asks "Why do cockroaches burst from soapy water?" While this question explicitly asks "Can soap kill cockroaches and/or ants?"

The short answer to your question is yes.

According to this website:

  The soapy water kills [cockroaches] by forming a thin film over the
  roach's breathing pores that stays in place due to surface tension,
  causing the roach to suffocate.

Ants are killed in a similar manner (see this archived Reddit post).

For a more scientific read, check out this paper: Behavioral Responses and Mortality in German Cockroaches (Blattodea: Blattellidae) After Exposure to Dishwashing Liquid.


Survival of streptococcus after my scarlet fever

The Streptococci are a part of the normal human flora.

  The streptococci are widely distributed in nature and frequently form part of the normal human flora (seeTable 29-1). Approximately 5-15% of humans carry S pyogenes or S agalactiae in the nasopharynx.

Please see:http://www.ncbi.nlm.nih.gov/books/NBK7611/#!po=51.4706 for more details on epidemiology of streptococci.

As 5-15% humans have it in their nasopharynx, it is not really possible to maintain streptococci free environment. It will get repopulated quickly.

Usually the reason you get infected is because of some alteration in your normal flora.

  S pneumoniae and, to a lesser extent, S pyogenes are part of the normal human nasopharyngeal flora. Their numbers are usually limited by competition from the nasopharyngeal microbial ecosystem and by nonspecific host defense mechanisms, but failure of these mechanisms can result in disease. More often disease results from the acquisition of a new strain following alteration of the normal flora. (From the same article, under pathogenesis)

So basically disinfecting wont help much as humans have the streptococci as a part of their normal flora. And it is very likely that the people you live with or come in contact with regularly have the streptococci already in their flora (either they got it from you or they originally had it themselves).


Why are bacteria immune to snake poisons?

Short answer
Many snake poisons target specific proteins not present in unicellular organisms.

Background
The question is admittedly broad but the idea behind this question is pretty much what you indicate in your post - many venoms target specific proteins and do not simply destroy their target by, e.g., disrupting gross cellular structure (like alcohol does for example). Instead, they target specific molecules that are essential for the survival of their prey.

Snake toxins can be categorized according to the organ systems they target, namely :

the central nervous system
the cardiovascular system
the muscular system
the vascular system

Central nervous system toxins are carried by elapid snakes like cobras, kraits and the taipan. Typical targets are the nicotinic acetylcholine receptor and the muscarinic acetylcholine receptor. Blockade of these receptors at the neuromuscular junctions resulting in death by asphyxiation. Acetylcholine receptors are not present in bacteria.

Cardiovascular toxins are pretty diverse and include things like angiotensin-converting enzyme inhibitors (leading to a drop in blood pressure) and glycosaminoglycans (the sulphated carbohydrate moieties that occur abundantly in cells of cardiovascular tissues) binding proteins that lead to cardiotoxicity. Again, the targets are specific molecules involved in heart function and hormones, stuff not present in bacteria.

Muscular toxins include those that bind specifically to the sarcoplasmic reticulum of muscles or interfere with specific second messenger systems messing up muscular function. Again, quite specific targets not present in bacteria.

Lastly, typical vascular system toxins include anti-coagulants such as protein C activators and inhibitors of prothrombin complex formation. Again, specific targets.

Reference
Koh et al., Cell. Mol. Life Sci (2006); 63: 3030–3041


What other cognitive behaviors in bees, outside of navigation, are affect by neonicotinoids

It is assumed that this effect of locomotive behavior IS an effect on cognition (1-4). Navigation requires snapshot memory, learning, and attention (2-4). You asked if this effect of neonicotinoids on cognition manifests itself through other vital behaviors. The short answer, yes. Specifically neonicotinoids are shown to effect mating, queen behavior, and foraging short and long distance (5-7). It is suggestive that neonicotinoids are a contributing factor in collapsing colonies with both meta analysis and direct evidence of effects on behavior (5-8). I think you are more questioning why people have not done anything about this issue or more definitive in their action against colony collapse. That is more of a political issue. Since the pesticide does not have as many human health effects at levels that cause bee collapse, the policies to resolve this issue are not as clear. EPA has discussed making restrictions regarding use the use of neonicotinoids, but they will still be used. However, they have actually been banned in France due to these effects. Hope that answered your question!

Sources

Honey Bee Behaviors  doi:10.1016/S1364-6613(00)01601-6
Bee Navigation and Memory          doi:10.1006/anbe.1997.0574
Learning and Memory in Bees doi: 1146/annurev.ne.19.030196.002115
Behavioral Neuroscience ISBN: 978-0-87893-092-0
Bees, neonicotinoids, and Dance Behavior Effects doi: 10.1242/jeb.068718
Bees, neonicotinoids, and Foraging Behavior Effects  DOI: 10.1046/j.1365-2435.2000.00443.x
Queen and Colony Effects   DOI: 10.1126/science.1215025
Colony Collapse meta study DOI: 10.1007/s10646-010-0566-0


Which extinction event killed the highest proportion of organisms?

This is a great question. I decided to research it and here is what I found. For some reason the GOE is not on lists of the "big 5" mass extinctions. The question is why?

I think it's due to the pace of the event. The event is described as happening 2.45–2.32 billion years ago.

This is a timescale in billions of years. So it isn't really a proper mass extinction. Little is known about the time scale of the evolution of cyanobacterial lineages.


If a gene is located on the X chromosome, does that mean males are never heterozygous for these genes?

There is a specific term for this called hemizygous / hemizygote - meaning that only one allele of the gene is present. Therefore males cannot be heterozygous for genes on the X or Y chromosome (not counting for gene duplication or other chromosome disorders) since they naturally carry only one copy of these chromosomes.


Can nitrate be an electron acceptor for NADH generated in the citric acid cycle?

Yes, many microbes can use electron acceptors other than oxygen.

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

https://www.sciencedirect.com/science/article/pii/S0168165611000289


methods for targetted deletion of genomic regions?

I can only provide you with a few pointers from memory, as an ad hoc search for "review of dna cutting techniques" was not prolific.

Please consider the provided information with precaution and only for pointers to help you do literature research.

cre/lox system and variants (best known), belong to SSRs (Site specific recombinases)
various Restriction enzyme based systems (see Homing Endonucleases)
meganuclease based tools
aptamer based
based on hybridizing n-mer probes which yields a reactive species nicking the DNA at the probe's-site when introduced to certain chemicals such as oxoacids
light twizzers and lasers /purely proof of concept (perhaps already commercialized?)
ZFNs and variants / protein based-probes . http://en.wikipedia.org/wiki/Zinc_finger_nuclease

There are definitely published reviews on this exhaustive topic, notwithstanding the dozens of books.
I would estimate that there are at least 10 commercial methods, and almost 100 methods in total when theoretical and proof-of concepts are included.

Naturally (literally!), the vast majority of methods will be based on the noncovalent interaction of an n-mer "homing construct"/probe a)attached to an nuclease or b)an
attachment site for a nuclease or c)participate in the reaction for the formation of a reactive chemical species to break the sugar-phosphate backbone.

I would speculate that most other methods are likely not practical in terms of either efficiency and/or affordability.

To learn about the applicability of the respective methods relating to your field of research, and be provided with an overview of the pros and cons of the methods, you will still need to find a good review paper.


Your body exists at a certain pressure, determined by your surroundings; usually, this is about 1 atmosphere of pressure, but it can go up or down (e.g. when you fly on an airplane, or when you go diving). The pressure that your surroundings put on your skin is transmitted throughout your body, and your body "pushed back" against it.

However, this means that all your blood vessels have that pressure weighing down on them along their length. Normally, when they're full of blood, the pressure of that blood will press the blood vessel outwards to counter-act this. Without the blood, however, that pressure within the blood vessel is no longer sufficient to withstand the pressure being exerted on it from the outside.

Since the walls of the blood vessels aren't thick enough to have enough structural integrity to withstand that pressure differential, they then proceed to collapse.


Calculation of the bacterial growth rate from a spectrophotomer growth curve

This is a common experiment for microbiology courses and you can find instructions on the internet , here is an example from University of Wisconsin: http://inst.bact.wisc.edu/inst/index.php?module=Book&func=displayarticle&art_id=114

But the general method is measure optical density at regular intervals and plot them on a semilog graph, which has the normal linear scale on the X axis for time, but a base 10 log scale on the Y axis for optical density. You can set this up in microsoft excel or libreoffice calc by right clicking the y axis and going to format axis, there should be a logarithmic scale option somewhere depending on the version.

After you have the data plotted, the exponential growth phase should appear as a line with positive slope. The logarithmic scale on the Y axis will automatically transform the exponential curve into a straight line. To determine growth rate in terms of generation per hour, you need to get the optical density at time 0, which is the beginning of the exponential phase, and time t, which is just some other time on the exponential phase. Use this equation to determine growth rate: $k =\frac{log(X_t) - log(X_0)}{0.301t}$

Once you know the growth rate, you can determine the generation time with $t_{gen} = \frac{1}{k}$, which gives time for 1 generation in hours. To convert to minutes, just multiply by 60.

As a side note, remember to blank your spectrophotometer with sterile media. Also, if the optical density goes over 2 it won't be as accurate, so dilute the aliquots to make the optical density go below 2. Remember to record the dilution factor so you can multiply the density by the dilution and get back to the "original" optical density for plotting.


Can a bacterium express a virulence gene and not produce toxins and what may be the cause of this?

To expand a bit on @Mohamed's answer, there are several mechanisms by which virulence gene products can be up- or down-regulated without changes to mRNA expression.
Post-translational modifications
Adenylate cyclase-hemolysin (AC-Hly) is a toxin produced by the Bordetella pertussis, the causal agent of whooping cough.  There are very few amino acid differences between the AC-Hly of B. pertussis and closely related Bordetella species.  Palmitoylations of lysine residues on the C-terminus of the B. pertussis AC-Hly are necessary for its specific cytotoxic activity.  [Bouchez 2017]
RNA secondary structures
After transcription, mRNAs can form secondary structures by base pairing, preventing ribosome binding and translation.  For some pathogens, virulence gene mRNAs forms these structures, which melt at human body temperature, allowing for fast production of toxins without the need to increase virulence gene transcription. [Narberhaus 2010]


How to reduce/eliminate cell clumping in suspension CHO cells, without using an anti clumping agent?

After looking around for a bit, I came across a few potential solutions however they are not a definitive answer to your question and requires testing under your experimental conditions to see which works best.

This page contained one excellent suggestion and that is to select for cells that do not clump during the passage, by pooling the cells in 15ml of media in a tube and letting the clumped cells to settle down by gravity for 5 minutes and afterwards taking the top 1ml and passaging it and after 20 passages using the exact same technique, you should be able to get single cell suspension. The main caveat is the heavy selection for non-clumped cells, which might harbour certain properties that might be undesirable for the procedure you are interested in so it might be nice to do some RNA expression profiling to observe the differences and perhaps even publish it! Amongst the suggestions on this page included using different concentrations of Mn2+, Mg2+, and Ca2+ in your (custom?) media since cell adhesion is regulated by integrins, cadherins, and selections and in general, Mn2+ increases ligand affinity, Mg2+ promotes adhesion to cells, and Ca2+ decreases cell adhesion as referened here. You can also try heparin, as tested by this paper on CHO cells and it impotent to note that in the study, heparin did not reducing cell growth, antibody secretion, and antigen-binding activity although I'm unsure as to whether heparin would be classified as an anti-clumping agent and whether it interferes with the ability of the cells to get transfected but that can be simple tested by a GFP transfection and looking at the transfection efficiency of the heparin treated and control cells treated with whatever heparin is dissolved in.


identification of differentially expressed genes in RNA-seq analysis

Unless you have a good reason, stick with the ones that the community at large uses most frequently: EdgeR or DESeq2.


Which concentration of BSA is recommended for dynamic light scattering experiments?


Why is marginal reconstruction "more correct" than joint reconstruction in some cases?

I know this is too late, but since this is something I'm struggling with too I thought I'd post here in case others also find there way here. I don't have an answer but, here are some quotes that might help (I found them at least partially helpful).

Yang (2004): "Marginal reconstruction is more suitable when one wants the sequence at a particular node, as in the molecular restoration studies. Joint reconstruction is more suitable when one counts changes at each site."

http://aracnologia.macn.gov.ar/st/biblio/Yang%202006%20Computational%20Molecular%20Evolution.pdf

Revell (2014):

"Joint reconstruction is finding the set of character states at all
nodes that (jointly) maximizes the likelihood."

"Marginal reconstruction is finding the state at the current
node that maximizes the likelihood integrating over all other
states at all nodes, in proportion to their probability"

http://www.phytools.org/eqg/Lecture_5.1/Revell.ancestral-state-reconstruction.pdf

Joint reconstruction is "not (necessarily) equivalent to picking the state at each node with the highest probability" (Revell 2014), but is the method of picking the tree with the overall highest MLE.


How effective is water purification by boiling?

To be precise, boiling water would not remove all bacteria as there are certain extremophiles that thrive at higher temperatures.

However, boiling of water is known to get rid of harmful pathogens. Boiling of water is a method of pasteurization, which means killing those organisms that can cause harm to humans.

Quoting from New York State - Department of Health >>

  Boiling water kills or inactivates viruses, bacteria, protozoa and
  other pathogens by using heat to damage structural components and
  disrupt essential life processes (e.g. denature proteins). Boiling is
  not sterilization and is more accurately characterized as
  pasteurization.

  Cooking food is also a form of pasteurization. For pasteurization to
  be effective, water or food must be heated to at least the
  pasteurization temperature for the organisms of concern and held at
  that temperature for a prescribed interval.


How do cold conditions help organ transplants?

This paper actually goes into the whole history of organ transplants.

In short it seems to have the following effects:

preservation - usually with a specific solution to help.
slows down extracorporeal ischaemic damage
slows down hypoxic damage
slows down the metabolism (energy consumption) and thus the need for oxygen that blood provides.

Remember that the cooling doesn't allow the organ to live indefinitely, and may only work for a few short hours depending on the organ.

I highly recommend reading the paper if you'd like to know more about organ transplant. They went into great detail about the past and present and the abstract also says they discuss new techniques about to be don't in clinical trials.


I am afraid you may have to read your textbook more closely. The question on page 29 states that this equation models the proportion of infected humans. If $I$  $≥1$ that would mean that there are more people are infected than there are people in total - e.g. 3/2 of people are infected - this clearly doesn't make sense.

Thus $1≥I$ when using this model.


What makes an animal/species suitable for domestication/training?

The ability of an animal to be trained or domesticated appears to be genetic. A quick Google search revealed this Review: http://rspb.royalsocietypublishing.org/content/278/1722/3161.full.pdf