This is a good question. Firstly, let's get the terminology straightened out: The terms recessive and dominant are not actually used to describe genes, but rather alleles. The term allele is used for alternative forms of the same gene.(1) Many genes have two or more alleles, and some genes have alleles that can be described as dominant or recessive.

It is also useful to be familiar with the terms genotype and phenotype. Genotype refers to the form of the genetic material (DNA), while phenotype refers to the observed effect of the genotype.

Secondly, it's important to realize that the concept of "dominant" and "recessive" is a human-made abstraction. The concept of dominant and recessive genes were invented (or discovered, if you like) before we reached a good undertanding of how genetics works at the molecular level. Thus, genetics in the early days had a much cruder understanding of how different phenotypes depend on the genotype.

The dominant/recessive concept is useful in cases where there is a limited number of possible allele pairs and one or several alleles can mask the effect of other alleles. This is a very limited set of cases. Many genes have many different alleles, and it's hard to account for all of them. Many alleles also do not have a clear observable effect, in which case any "masking" effect is not prominent. To quote Wikipedia (2):

  The most common basis of dominance and recessiveness is that the
  dominant allele codes for a functional protein and the recessive
  allele for a mutant, non-functional protein.

A further important point is made in the following passage:

  Dominance is not inherent to an allele. It is a relationship between
  alleles; one allele can be dominant over a second allele, recessive to
  a third allele, and codominant to a fourth. Dominance should be
  distinguished from epistasis, a relationship in which an allele of one
  gene affects the expression of an allele at a different gene.

Let's consider your example: A single gene with two different alleles, T and t. Let's assume the T allele codes for a more powerful version of the growth hormone than the t allele, or that the t allele produces a non-functional hormone. Furthermore, we assume that production of the T hormone from a single allele is enough to make the plant grow tall, and that production of T or t from a second allele has no further effect. Then, we can say that the T allele masks the effect of the t allele. However, as you can probably imagine, one allele fully masking the effect of another is rather rare. So recessive/dominant allele pairs are rather the exception than the norm.

Thus, the that place for the two alleles in the genome of the plant is definitely not empty. Note that a mutation could in principle cause one of the genes to be deleted in its entirety from one of the chromosomes of the plant during reproduction. The "place" for the gene on that chromosome would then indeed be empty. This has nothing to do with how dominance and recessiveness usually works, except that a recessive gene could become expressed if the dominant allele is deleted.

So, at the molecular level there is no concept of recessive or dominant alleles. Some genes have allele pairs that can be described as dominant/recessive in relation to each other, most others do not. The effect of different combinations of alleles determines whether the relationship between the alleles is described in terms of dominant/recessive.


True examples of common variation due to Mendelian Inheritance

Earwax consistency is an example of a monogenic trait with dimorphic phenotypes in humans -- "wet" and "dry" -- where both phenotypes are globally common, though allele ratios are highly variable between human populations.  The population genetics and molecular basis of this trait are discussed at length by Dr. John H. McDonald as part of a series on the myths of human genetics (archived version here).  I reformat his discussion in my answer.

In The dimorphism in human normal cerumen, Matsunaga summarizes 30 years of research into the earwax of Japanese families, with two major observations:

Dry earwax parents never have wet earwax children, suggesting the genetics underlying the wet phenotype are dominant to those underlying the dry phenotype.
Because the allele for wet earwax is relatively rare in the sampled families, it is likely that most wet earwax parents are heterozygotes.  Following from this, if the trait is monogenic with two allele variants, we expect a 3:1 ratio of wet to dry children in wet × wet parent crosses, and a 1:1 ratio of wet to dry children wet × dry parent crosses.  Indeed, this is observed.

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 35 & 12 \\ \hline
\text{w×d} & 205 & 195 \\ \hline
\text{d×d} & 0 & 634 \\ \hline
\end{array}$$

These results were later corroborated in Native Americans --
Cerumen in American Indians: Genetic Implications of Sticky and Dry Types

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 32 & 6 \\ \hline
\text{w×d} & 20 & 9 \\ \hline
\text{d×d} & 0 & 42 \\ \hline
\end{array}$$

And in a different Japanese cohort --
Distribution and inheritance of earwax types: a study on inhabitants in Awa District, Chiba Prefecture

$$\begin{array}{c|c|c|}
\text{parents} & \text{wet children} & \text{dry children} \\ \hline
\text{w×w} & 27 & 3 \\ \hline
\text{w×d} & 137 & 109 \\ \hline
\text{d×d} & 0 & 345 \\ \hline
\end{array}$$

In the early 2000s, the molecular basis of human earwax consistency was elucidated in three major publications.

Toshida et al. mapped a single locus on chromosome 16
Yoshiura et al. identified a SNP at position 538 in the coding region of ABCC11.  At this site, G corresponds to a wet earwax phenotype, whereas A leads to a dry earwax phenotype.  A less common allele representing a deletion of 27 nucleotides in exon 29 also yields a dry phenotype.
Toyoda et al. found that the 538G>A transition encodes arginine in place of glycine, resulting in a loss of glycosylation in the mutant protein, leading to deficient cellular localization, rapid degradation, and loss of function.

To directly address your question,

  Are there any examples of human phenotypes that are due to mendelian inheritance where all of the phenotypes are common?

I point you to the tables above, as well as Table 1 from Cerumen Phenotypes in Certain
Populations of Eurasia and Africa, which shows that the frequency of the dry allele ranges from 59% to 89% across diverse human populations --

To conclude, human earwax consistency is a dimorphic trait controlled by a single gene, where both phenotypes are common across human populations.


With an excess supply of nutrients, in how much time will the number of algae cells double in full sun?

I am presuming this a Blue Green Algae(BGA) Identify your algae

Growth rate for N1, N2 biomass at t1 and t2 time respectively, can be give as,

Growth rate:   $K'$ = $\ln \frac{(N_2 / N_1)}{(t_2 - t_1)}$

(source: csiro.au)

So, by this equation it is easy to calculate the doubling time of your algae.

For BGA normal doubling time is 6-8 hours.$^2$

Source:

http://www.marine.csiro.au/microalgae/methods/Growth%20rate.htm
https://sites.google.com/site/biomonstaaar/algae


How is circadian rhythm of gastric acid secretion regulated?

I'd suggest reading wiki first.

Autonomic nervous system, the one that regulates breathing rate, heart rate and other physiological processes as a function of circadian time, regulates secretion of gastric acid. Vagus nerve, part of parasympathetic nervous system (the one responsible for "rest and digest" part of behavior, opposite to sympathetic "fight or flight") stimulates secretion of gastric acid and regulated through circadian mechanism.

See also here, Circadian variation in gastric vagal afferent mechanosensitivity:

  Thus, gastric vagal mechanoreceptors display circadian rhythm, which may act to control food intake differentially at different times of the day.

This is another interesting review: Gut clock: implication of circadian rhythms in the gastrointestinal tract. It states that GI tract has its segments set their own circadian clocks, different for various segments. But all of them are operating and adjusted by main clock, regulated by, as I know, melatonin and orexin hormones.

Surprisingly, not much seems to be known about this connection. Pineal gland seems to be very important in this process, because it produces melatonin.


I am interested just in the nature of the results as described here.

By aligning this sequence to all nucleotides of all organisms, we would realize that the given (short) sequence occurs in various organisms besides humans. Therefore it might come from a species with only one chromosome see NCBI Blast !

For the sake of the example, let's assume that the species had multiple instances of each chromosome (e.g. one by human mother, and one by human father), and look at "the results as described here". As no detail is given on the protocol, let's further assume the most common scenario - namely that there was no experimental distinction or separation of the individual instances of chromosomes.

Looking at the results, we would realize that is not "next generation sequencing", but Sanger-sequencing.

Now we look at the provided scheme again (note: this is not real experimental data): clearly the bands on the left side only occur for one letter/base, and at a given position of the sequence, there only is one very clear peak on the right hand side (as opposed to the possibility, to have multiple peaks corresponding to different bases).

We would have to conclude that every instance of the chromosome has an absolutely identical sequence. Thus we would conclude that it would not be important to distinguish individual instances.

But wait - aren't maternal and paternal chromosomes different? Absolutely, the given example however only looks at 25 bases rather than the full chromosome - and it would quite possible that they are absolutely identical. (note: there are various experimental techniques to select only specific regions of DNA or RNA for analysis).


There are quite a lot of articles(1,2, etc.) which have investigated this, I think this article did a great job to give a visual representation of the specificity, reliability and coverage:

also this article noticed the following:

  Compared to electronic annotations, it is not surprising that curated
  annotations have a considerably lower average coverage (Fig. 8,
  vertical lines). Indeed, the main appeal of electronic annotations is
  precisely that they scale efficiently to large quantities of data. But
  in terms of reliability, and contrary to current beliefs, curated
  annotations that use evidence other than experiments from primary
  literature do not fare better than electronic annotations (Fig. 8,
  horizontal lines, Fig. S9 in Text S1). In fact, we observed a higher reliability for electronic annotations than for curated annotations (0.52 vs. 0.33). the figure blow is figure 8 from the article

I don't know if you are just curious in the reliabilty of GO or if you are searching for an other kind of hierarchical annotation method, but e.g. for enzymes there are also EC numbers.  I can continue citing the article but I would suggest to read the article from which I used the figures ( Quality of Computationally Inferred Gene Ontology Annotations). Secondly this article is more recent and  something similair was done here. Among other things they also compared the computional annotation from 2008 with manual annotation in 2010 for the same set of GO terms:

So I would also recommend to read The what, where, how and why of gene ontology—a primer for bioinformaticians. This article and the previous mentioned article will give you a good insight in GO terms.


Relationship between bacteria size and temperature?

There is a negative correlation between growth temperature and genome size for prokaryotes, which may be driven by selection for smaller cell size overall in warmer environments. Sabath et al., 2013 provide a good discussion:

  Smaller cells tend to have smaller genomes in both prokaryotes and unicellular eukaryotes (Shuter et al. 1983; Lynch 2007), for reasons that are not fully understood (but see Dill et al. 2011). This correlation suggests that cell and genome size are functionally related, such that an evolutionary change in one would induce an evolutionary change in the other. Previous studies have hypothesized that reduction in cell size could be advantageous, either to optimize surface-to-volume ratio for uptake of scarce nutrients (Dufresne et al. 2005; Giovannoni et al. 2005; Moya et al. 2009), or to decrease predation by bacterivores or bacteriophages (Yooseph et al. 2010). Similarly, we speculate that bacteria adapted to high temperature could be subject to selection favoring smaller cell size, which also requires smaller genome size—regardless of gene content.


In a population of mice, the presence of black spots is the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.15, what is the approximate percentage of heterozygous genotypes in this mouse population? (Assume that the population is in Hardy-Weinberg equilibrium.)

We know the frequency of the allele (0.15) and we're looking for the frequency of the heterozygotes. $2\cdot 0.15(1-0.15) = 0.255$.

  (ii) In a population of giraffes, dark brown spots are the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.10, what percentage of the individuals in the next generation would be expected to be homozygous dominant?

Yes, you are right it is 0.81

  (iii) In a population of monkeys, the allele that causes long hair at the tip of the tail (H) is dominant, while the allele that causes short hair at the tip of the tail (h) is recessive. If 67% of the monkeys have long hair at the tip of their tails, what is the frequency of the dominant allele?

Although the notation is wrong ($p=1-\sqrt{q}$), the result is correct.

  [last question]

As both genotypes GG and Gg are grey, we know that $p^2 + 2pq ≈ 0.45$ (Rather looks 0.48 from the figure though), where $p$ is the frequency of the G allele. From that you can calculate $p$ and $q$ and therefore calculate the frequency of the double homozygous gg


"Love" is a subjective phenomenon that can't really be applied to non-human animals because we can't ask them about their subjective experiences. However there is some clear evidence, especially in more social mammals, of caring behavior and social bonds for other conspecifics.

As far as biological basis, I suppose you could consider it biochemistry, the peptide hormone oxytocin is correlated with formation of social bonds between animals of many species (although Wikipedia isn't the greatest source, you will find this particular page is saturated with links to scientific literature). I would caution against the popular press treatment of oxytocin as "the love hormone" and caution against simplifying a complex set of behaviors to the action of one peptide, but certainly the evolutionary conservation and broad applicability suggest that this is indeed an important hormone in social relationships.


Why and how does uniprot list around 150,000 proteins in the human genome?

Well you are assuming one sequenced genome/proteome per NCBI tax id. That is no longer true. So if you click on the proteome filter it decreases by half.
Which gets you into the 60,000 range. Now not all of these are "different" conceptual proteins, many are artifacts from the way GenBank/EMBL/DDBJ interact with the TrEMBL section of UniProtKB i.e. they are not normalized in db speak.

So for the human case you also want to add the Swiss-Prot filter to get a decent proteome that gives you about 20,000 proteins. Corresponding to the predicted/confirmed human gene count.

In all bioinformatics databases you need to pay attention to difference between database records and biological concepts. They rarely map cleanly one to one. In this case an UniProt record is not a protein, but information about a protein and a different record could have information about the same "protein". Or at least the same under some definitions of "same".

See the announcement of the draft human proteome in UniProtKB

The known isoforms are most often stored in the alternative products section of an UniProt entry. In some rare cases when the splice variant has a completly different biological function they are described in separate UniProt entries. For UniProtKB/Swiss-Prot Human there is a near 1 to 1 relation between genes and proteins. Cases as above and fusion proteins are the exceptions to this rule.

TrEMBL tries to automatically reduce redundancy in INSDC by auto merging entries in the same taxid and now proteome that have an identical reported sequence. However, variations of single gene products due to mutations and or limit what auto merging can do. For example there are 8 records for the P53 gene in TrEMBL today. Many of them from mutants, i.e. cancer genomes etc...


Significance of the resequencing of the chimpanzee genome

The effect of re-sequencing the great ape genomes (orangutan as well as chimpanzee) without the use of a human genome as a guide to assembly has in general been to correct mistakes and improve the ape genome sequences so that they can be compared better with the human genome.

As far as I am aware, it appears that in a broad sense the same genes are present in humans and great apes, i.e. each will have a similar (orthologous) gene for, e.g. insulin, trypsin, keratin, generally at the same position on the chromosome. As the species are different these differences are thought to come from differences in these orthologous genes or in the regions of the genome that control their expression as RNA and then protein. The differences could also affect their activity, where they are expressed in the body or whether different variants occur (by differential splicing of transcripts).

So with improved and independent genome sequences it was possible to identify a greater number of variants in these orthogonal genes.

The focus of this work was on genes that are expressed in brain cells, because a key feature that distinguishes man from the great apes is brain size. The interest was in genes that were found in separate experiments to have significantly different expression when glial or neuronal cells of human or non-human species were compared. The authors report mutational variation in 252 genes with such differences in glial cells and 123 in neuronal cells.

To quote the discussion:

  These improved genomes yield a comprehensive view of intermediate-size
  structural variation among apes. As we focused on SVs (structural
  variants) that potentially disrupt genes or regulatory sequences, we
  began to address potential functional effect. Differential gene
  expression, especially in cortical radial glia, has been hypothesized
  to be a critical effector of brain size and a likely selective target
  of human brain evolution. Nearly 41% of the genes down-regulated in
  human radial glia, when compared to chimpanzee radial glial analogs
  from cerebral organoids, associate with an fhSV (fixed human-specific
  structural variants) and most often as a deletion or a retroposon
  insertion. These findings are consistent with the “less-is-more”
  hypothesis, which argues that the loss of functional elements
  underlies critical aspects of human evolution.

So, they haven’t found what makes us human yet, but have laid the foundations for studies that may at least find out why we have bigger brains.


There are actually a lot of these sites available, I have used some of the one listed below. Additionally there are some huge list of other services available in this field from ExPASy, you can find it here and the Center for Biological Sequence Analysis, which can be found here.

ExPASy - FindMod
The Eukaryote Linear Motif resource for Functional Sites in Proteins
Phosida


How do I know whether or not a nuclear gene is single copy?

The simple way to do this is to use blast to search the genomes your interested in for sequences similar to your gene. If there's another copy it'll turn up in the blast results (so will orthologous genes - but they'll have lower scores than an actual copy). That relies on the annotation and genome being correct, of course.


Can anyone identify this creature that looks like a stick?

It may be a Caddisfly (Trichoptera). Though my guess is a moth (Lepidoptera). Specifically one of the Psychidae family, also known as "bagworm moths." They are common pests in most parts of the world and while they're typically seen fixed in place they spend much of their life mobile. Both of these groups spin a case from silk and attach detritus to the outside so without a better look at the resident insect it is basically impossible to distinguish them from a photograph. However, as a general rule (with some exceptions), Caddisfly larva tend to be aquatic.
Here are a couple of links to descriptions of the groups (with pictures!) as they appear on BugGuide:
Psychidae

Trichoptera


Investigating rare variants in ethnically different populations (European ancestry & African ancestry)

Too long for a comment, but sort of:

Mainly you do this because these populations have segregated long time ago and developed differently, so it is more likely to identify these polymorphisms. It is also helpful to use populations for this which mixed not too much with other populations (thats why north-americans are usually not used here, as America was kind of a melting pot).

You will find rare SNPs for pigmentation in europeans that are not present in the more ancient african population (and must therefore be occured after the populations divided), examples are the so called "golden mutation" in SLC24A5 (rs1426654) or a polymorphism in IRF4 (rs12203592).


What’s the term used to define a terrestrial being that moves by using six limbs?

Hexapedal. From wiki > Hexapedal

  Having six legs

Note that Hexapoda is a taxonomic group including insects and the smaller groups that are Collembola, Protura, and Diplura.


Perception of white in the absence of rods

Short answer
Cones mediate the perception of white in photopic conditions. Rods mediate the perception of white in scotopic conditions. The rod system is not needed for cones to mediate white perception and vice versa.

Background
Cones code for red, green and blue. The remaining colors, as you rightfully state in the question, can be generated by mixing these three colors, as shown in Fig. 1.

Fig. 1. Color mixtures. Source: Davidson College

The millions of different color hues that we can perceive are generated by the retina and the brain by mixing colors and adding the weight that each cone class adds to the color percept (Fig. 2).

Fig. 2. Color Triangle. Source: Wikipedia

As you can see in Fig. 2, when all three basic colors are present in equal amount, perceptually a white color is perceived (the middle point of the color triangle). That is, the combination of co-activation of each cone class yields the perception of white, i.e., without the need for rod activation. Rods are not needed for color vision, including the perception of white or black. In fact, under photopic (well-lit) conditions the rods are adapted to high light levels and are less responsive; their photopigments are said to be bleached and the rods become unresponsive to light. Hence, under photopic conditions the contribution of rod-mediated vision is low (Ambler, 1974).

Rods mediate vision in low-lighting conditions (scotopic vision), as opposed to photopic vision where sufficient amount of light is present to feed the photon-hungry cones. While rod-mediated vision operates at much lower lighting conditions than cone-vision, it only mediates the perception of low-resolution gray-scale images.

References
- Ambler, Perception & Psychophysics (1974); 15(3): 586-90
- Gouras, Color Vision. In: Kolb et al. (eds). Webvision. The Organization of the Retina and Visual System. Utah (2012)


So, your blank is everything but the enzyme? That is, substrate and DNSA with 100 uL water? If yes, measure, as negative controls, substrate alone and DNSA alone. If one of them is also highly absorbing light, it may be contaminated, and a new vial should be ordered. If both are highly absorbing, it may be the water you are using, or the spectrophotometer.

Alternatively, you may try to measure a time course. If blank's absorbance is increasing as time goes by, there is contamination, and reordering reagents may help you. If absorbance stays constant, you are not looking at an enzyme contamination, that is, the culprit is spoilt water, or broken spec, or even wrong protocol. (That is, reordering or repeating won't help.)


What's the mechanism or structure responsible for new species genetic code generation?

I strongly advice to have a look at an introductory source of information on evolutionary biology (such as Understanding Evolution by UC Berkeley). It will give you much more information.

Locus and Allele

Here are two definitions to start with:

A locus is a location on a chromosome. This location can be of any size. It can be a single nucleotide, a codon, a whole gene or even longer.
An allele is one variant at a given locus. When considering relatively short loci (say 1 nucleotide or 1 base pair (bp)), then the majority of loci have only one allele.

What is evolution?

Evolution is defined as any change in allele frequency in a population over time.

There are a number of "forces" that affect evolutionary processes. I picked the 3 most commonly considered: Mutations, Natural Selection and genetic drift

Natural Selection

Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.

Natural selection occurs whenever the three following conditions are respected

Individuals in a population varies in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such situation natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.

You may want to have a look at this post (although it might be too advanced) to understand the concept of heritability.

Mutations

In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen that other but in any case the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to raise in frequency in the population.

Mutations can be a simple a "small change" such as nucleotide substitution, an nucleotide insertion and deletion or can be a "bigger change" such as a chromosomal duplication/deletion, a whole genome duplication and the duplication/deletion of a long sequence.

Mutations create the genetic variance on which natural selection selects the best variants. As a consequence natural selection decreases the genetic variance while mutations increases genetic variance.

Genetic drift

If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo more random change in frequency of their genes than are big population.


Is the coronavirus getting less dangerous?

The issue is using the number of positive tests as a measure for the total number of active cases at a given time. At least in the U.K., the early testing capacity was much lower than it was now:
Because of this, many people who were infected were not being tested and so weren't included in the total number of infections. Therefore, the total number of infections in April/May time was likely a large underestimate. It's been estimated that there was something in the range of 150,000-200,000 new cases per day in that time period.
On the other hand, testing capacity in the U.K. at the moment is much higher and will catch a much higher proportion of the total cases.
Therefore, your crude calculation of 'death rate' = deaths / cases is skewed by the error in the estimated number of cases, making it appear the 'death rate' is going down because we underestimated the total number of cases early in the pandemic.
The other thing to note is that the 'death rate' is dependent upon demographic factors, most obviously age. Early in the pandemic in the U.K., a large number of cases occurred in care homes, where the residents were particularly vulnerable. On the other hand, cases are high in students at the moment, who are a low-risk group. If the age distribution of cases is relatively skewed towards older people, then the 'death rate' will appear higher than vice versa, even though nothing may have biologically changed with the virus.
Note: Sorry, I don't have citations for a lot of this. I will try and find them and add them at a later point.


Designing degenerate primers using alignment of protein sequences from other species

Try going through this tutorial: http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
It is a nice introduction on how to use multiseq and identify conserved domains from AA or nt sequences across many taxa.

Also check out http://fungene.cme.msu.edu/
The RDP staff at Michigan State University are the masters of doing exactly what you're trying to do.


How much is local blood non-Newtonian in Pathophysiology?

According to this conference proceeding blood is very nearly newtonian at normal shear rates. More accurately blood is very thick and a shear-thinning fluid, but the shear-thinning effects don't scale with a power law like other non-Newtonian fluids.

In terms of blood changing viscosities, I suspect that in living patients blood viscosity is quite constrained, not only by physiological feedback but by the fact that if the blood viscosity changed very much the patient would become nonliving. Blood circulates constantly, and when it stops circulating it coagulates(which complicates efforts to measure its viscosity, I imagine). Any local effects on blood viscosity would be 'washed away' by the fresh blood arriving every heartbeat. If there's no or very limited blood circulating to the muscular pathology you're interested in the blood viscosity is probably not as significant as the ischemic tissue death that's just about to happen.


Fish are definitely evolving to avoid fishing pressure. For example, largemouth bass evolve toward avoiding hooks.  More broadly, since fishing selectively removes larger fish from the population, there's selection toward fish evolving smaller size.  A brief review, linking to many studies demonstrating this, is Evolutionary impacts of fishing: overfishing's ‘Darwinian debt’.


Does the edge effect promote biodiversity?

EDGE EFFECT PROMOTES BIODIVERSITY.
EDGE EFFECT OCCURS IN ECOTYPE.
ECOTYPE IS THE TRANSISSION ZONE WHERE TWO COMMUNITIES MERGE.
HENCE SPECIES RICHNESS IS FAIRLY HIGHER THAN THAT OF THE SURROUNDING ECOSYSTEMS.
IF ANY OF THE SPECIES TENDS TO EXPLOIT THE RESOURCES OF THE ECOTYPE IT WHOULD HAVE TO MODIFY ITS CHARACTERISTICS BY THE PROCESS OF  ADAPTIVE RADIATION AND EVOLUTION .
HENCE NEW SPECIES EMERGES PROMOTING BIODIVERSITY.


Why are human children more likely to get lice (nits) than adults?

Children generally don't care about their hair as much as adults do. So unless parents insist, they don't care for their hair as much (reference). Kids generally get lice because they are in close contact with each other during play-dates, slumber parties, and sports activities. They are also prone to exchange hair brushes and other personal items more often than adults (reference).

An interesting difference I came across between articles is that one article says that its

  theoretically possible to get infested if your hair makes contact with
  items such as hats, combs, or brushes (reference).

Another article insists that

  You’re extremely unlikely to get head lice by sharing hats, combs or
  pillows – a louse’s lifespan is very short once it’s removed from your
  head (reference).

Between the two, I believe that it is extremely likely that lice would spread if you use a infected hairbrush immediately after it was used by someone harboring the parasite since the time span is short.


How close to Earth's core can organisms live?

There's a lot we don't know about life in deep caves, but we can bound the deepest living organism to at least 3.5 kilometers down, and probably not more than 30 kilometers down.

The worms recovered from deep mining boreholes are not particularly specifically adapted to live that far down: they have similar oxygen/temperature requirements as surface nematodes.

The Tau Tona mine is about 3.5 kilometers deep and about 60˚ C at the bottom. Hydrothermal vent life does just fine up to about 80˚C, and the crust gets warmer at "about" 25˚C per kilometer. It's entirely reasonable to expect life to about 5 kilometers down, but further than that is speculation.

Increasing pressure helps to stabilize biological molecules that would otherwise disintegrate at those temperatures, so it's not impossible there could be life even deeper. It may even be likely, given that the Tau Tona life breathes oxygen.

I am certain no life we might recognize as life exists in the upper mantle.


Do the effect of inbreeding depression disappear after the first generation of outbreeding?

This depends on if you are talking about animals in the wild, such as isolated populations, or humans, or whether you mean research animals. Inbreeding tends to breed homozygosity, so as you said, if you have a recessive disease causing allele within a bloodline, then even if only one of the founders was a heterozygous carrier, then inbreeding can give rise to afflicted homozygotes. However, for lab strains, it is actually desirable to use completely inbred lines where all animals are as near to 100% identical (from a DNA sequence perspective) as you can get. This makes genetic mutational analysis far easier (possible).

It also depends on the alleles in question. Not every mutation is purely dominant or purely recessive. You can have situations, such as with some tumor suppressor genes, that diversifying the population by outbreeding to someone with a functional tumor suppressor, will still cause the offspring to have only a single working allele, and therefore an increased probability that they can sustain a random mutation that will knock the working gene out. You can also have cases where having one functional copy of the gene isn't enough, so the offspring are haploinsufficient. You need two doses of both working copies of an allele to display the non-afflicted phenotype, though the afflicted heterozygote has a better time of it that the afflicted homozygote, who has none of the working allele.

You also have X-Linked conditions. If the maternal lineage is inbred, then all of the males will be afflicted and females will be carriers.

Another possibility is that the outside breeder is a carrier of the mutant allele so the offspring remain homozygous or the outside breeder has an allele of the gene that comes with its own defect. They may not be afflicted, as they could be heterozygous for a working copy, but their offspring with the inbred line could be heterozygous afflicted because neither of the alleles they inherit are functional, it is just that they are not functional in different ways.

Sexual reproductions main advantage is that it is supposed to increase diversity in the population and increase survivability of the species. When you have isolated populations or inbreeding by choice, then this can circumvents the benefits. Not all inbreeding, as seen with laboratory strains and selective breeding of domesticated animals, is deleterious. It is just that the breeder needs to be careful of the choices made and cognizant of how the genetics can work. Animals displaying a diseased phenotype should not be allowed to produce offspring, and you need to evaluate the siblings of that animal as well as the parents to insure that you do not have problems in that lineage.


How can birds disperse seeds when they are able to digest them?

Birds may indeed digest seeds under conditions of rest. It has been postulated that almost all current knowledge on mechanisms of internal seed dispersal has been obtained from experiments with resting animals.

A study with the mallard Anas platyrhynchos (common wild duck), claimed to be quantitatively one of the most important seed dispersing animals in aquatic habitats in the Northern Hemisphere, has shown that physical activity affects gut passage survival and retention time of ingested plant seeds. The authors fed seeds of nine common wetland plants to mallards trained to subsequently swim for six hours. They compared gut passage survival of seeds against a control treatment with resting mallards.

Intact gut passage of seeds increased significantly with mallard activity (up to 80% in the fastest swimming treatment compared to the control), and hence revealing reduced digestive efficiency due to increased metabolic rates. This enhances the dispersal potential of ingested seeds.

An extensive work-out after a meal generally slows down metabolism, as blood is redistributed to the musculature and away from the digestive tract.

These findings imply that seed dispersal potential by mallards calculated from other experiments with resting birds may be underestimated.

Reference
- Kleyheeg et al., Oikos (2015); 124(7): 899–907


Is there any definition of life which makes viruses undeterminable?

Your last sentence is the key: defining life really is just finding a dictionary definition that we can agree upon. Biology is something that defies discrete definitions at times: "What is it to be alive?" "What is a species?" maybe even "What is the wild type allele of a gene?"
I would recommend not looking at viruses as a challenge to determine if they are alive or not so much as an excellent opportunity to discuss what we think are important characteristics of life.
Life can alternately be described as:
"Comprised of self-replicating cells" (a paraphrase of the "Cell Theory of Life"
or
As things that embody at least most of the following characteristics:
1. Self-Replicating
2. Metabolizing
3. Growing
4. Showing signs of adaptation
5. Being organized
6. Respond to their environment
7. Being comprised of cells

I like to think that we should focus on extraterrestrial forms when we define life. i.e. what would we want to see in an extraterrestrial in order to call it 'life'? While some are troubled by calling viruses alive here on earth, the same people might be willing to say that we have found extraterrestrial life on another planet if it was similar (granted, it's hard to imagine this kind of life existing without a host...)

as an aside: You might also ask whether this question is fit for this stack as it can not be supported by literature references (at least none that would actually support a conclusion). So should this be posted as 'Biology' or 'Philosophy'?


Why are mice with a single X chromosome and no Y chromosome males?

Almost all mammals (including mice and humans) have two sexes where the males have a Y chromosome and an X chromosome (whereas females have two X and no Y chromosomes).  This is not the only way organisms can determine sexes, but it's the way mammals evolved to do it.

So how does having a Y cause an individual to be male?  The Y has only a few genes (less than all other chromosomes), but it has genes that occur only on the Y.  One of these in particular, the one called SRY, is the main gene that causes the individual to develop male characteristics.  It mostly does its job indirectly, by making a protein that affects many other genes on other chromosomes that in turn do the work of building and maintaining the male form.

In the experiments reported by the article mentioned in the question, they managed to cause mice without a Y chromosome to develop many male characteristics.  They did this by faking one or two of the actions of SRY.  One of the many actions of SRY is to turn on a gene called Sox9 (which is on a non-Y chromosome), and it turns out Sox9 causes most of the things that make the male mouse form.

So the experimenters found a way to turn on Sox9 without using SRY or anything else from a Y chromosome.  This got them mice that looked male, but didn't produce sperm.  So they did something further that substituted for a Y chromosome, and caused a weak gene on the X to work at many-times strength to do the job that a strong Y gene normally does.  This caused the special "male" mice to produce sperm.  But these sperm were not fully functional (they couldn't swim and enter the egg), so they showed they were essentially sperm by simply using a tiny needle to inject the semi-functional sperm into mouse eggs and have those eggs develop into viable baby mice.

Bottom line, if you use artificial methods to do what the Y chromosome does, you can make male mice which do not have a Y chromosome (and learn some things in the process).


Do tRNAs that recognize multiple codons have any preference for one over another?

There is an extensive literature on synonymous codons and their usage in different organisms. I shall assume that the question concerns relationship between strength of codon–anticodon interaction and the efficiency (speed in this case) of translation.

It is not disputed (I am aware of few experiments on this) that the strength of codon–anticodon interaction depends on the number of hydrogen bonds made.
It was predicted that for optimal rate of translation one needs a balance between association and dissociation of the codon–anticodon pair. Hence weak interactions (all AU) — which would disfavour association — or strong interactions (all GC)  — which would disfavour dissociation — would not allow a rate of protein synthesis as fast as that for intermediate interactions (mixed AU,GC).
This appeared to be borne out
in the codon usage patterns of rapidly growing organisms such as Escherichia coli, something subsequently confirmed by more extensive studies. To be precise, the more highly expressed proteins (e.g. ribosomal proteins) were encoded by mRNAs containing the intermediate  codon–anticodon interactions predicted to allow rapid translation. In contrast, poorly expressed proteins (e.g. repressors) were encoded my mRNAs predicted to produce slower translation.
One should be aware, however, that there are other factors that influence the codon usage in different organisms, and that these can overide the effect of codon–anticodon interaction strength.


Online Molecular and Cellular Biology Video Lectures?

MIT OpenCourseWare provides very interesting material, and not only on biology.

You may be interested in seeing the video lectures from some of the Introductory biology courses, such as this one, this one or this other one.

There is, however, much more, check out the index of the available material for biology.


Is it a medical condition to not able to recall the word in a language while having a conversation

The phenomenon you describe is known as tip-of-the-tongue phenomenon, where you know there is a word, and you feel it's "right on the tip of the tongue, but doesn't come out".

The phenomenon is normal and tends to worsen with age. Only in case it becomes so strong that it seriously interferes with daily life, it can be considered a medical condition (anomic aphasia) that may be indicative of damage to the brain, such as stroke, head trauma, dementia, or tumor.


What is the most effective way to eliminate silverfish (g. Thysanura) from walls and floorboards?

They feed on fungi, which grow wherever there's high humidity levels. So the best way to get rid of them would be to lower the air humidity. For example, by increasing the temperature in your (presumably) bathroom.


Sharks sense their prey with the normal senses, they see, hear and smell them.

They have a remarkable sensitive sense of smelling, which enables them to sense highly diluted traces of prey. They can also use their smelling to determine the direction where a certain smell comes from. This is achieved by the timing in which the senses arrive in different parts of the sharks nose. See references 1 and 2 for more details.

While sharks have eyes which are similar to that of vertebrates, they have an additional reflective tissue called "tapetum lucidum" behind their retina, which reflects the light back and therefore raises the sensitivity of the eye. It seems that a lot of shark species are either colorblind (because they only have rod cells but no cones) or they had only one kind of cone cells which allows them only to see one color. For sharks it is obviously more important to detect objects than to see colors. See references 3 and 4 for more details.

The sense of hearing of sharks is also highly sensitive and is able to detect sounds from far away. See also references 5 and 6 for more details.

The most interesting sense of sharks is their electrosensory organ. This is also called Ampullae of Lorenzini which is a number of sensory cells along the head and which are able to detect the weak electric fields that exist around living animals. This sense only works on a very short distance. See references 7 and 8 for more details.

Finally sharks have the so-called lateral lines (which are present in most fish), which is an organ which detects movements and vibrations in the water around the shark. See the Wikipedia page for more information.

And for the sake of completeness (already quite nicely answered by @Susan in the comments), sharks do get cancer. All cures which are made from shark and claim to be able to treat cancer are pseudoscientific nonsense. This also endangers many shark species as they get radically overfished. See references 9 and 10 for more details.

References:

Smell and Taste
The Function of Bilateral Odor Arrival Time Differences in Olfactory
Orientation of Sharks
Microspectrophotometric evidence for cone monochromacy in sharks.
Vision and a Carpet of Light
Hearing and Vibration Detection
Functional anatomy of the auditory system in sharks and rays
The Shark's Electric Sense
Electroreception
Mythbusting 101: Sharks will cure cancer
Shark cartilage, cancer and the growing threat of pseudoscience.


Why do Alu repeats form secondary structures?

Single-stranded RNA can easily form secondary structures, a very important example of this are tRNAs.

From a quick look at the article you read it seems that these Alu repeats work similar to riboswitches in the 5'-UTR. They can form secondary structures that block translation initiation, riboswitches commonly do this by hiding the Shine-Dalgarno sequence in a stable helix.

This kind of regulation of translation can obviously only work in the 5'-UTR as that is the place where the translation starts. The 3'-UTR can't affect translation in this way as the translation starts at the other end of the mRNA.

The Alu repeats still can form secondary structures in the 3'-UTR, and the article suggests that those might have an effect on mRNA stability.


Ants can usually learn patterns, colors and sequences. Species that do not use pheromone trails rely heavily on landmarks for navigation, that is they perform learning walks during which they look backward and circle around the nest to learn what the landscape looks like so they can easily return to the nest after foraging.

  Harris, R. A., de Ibarra, N. H., Graham, P., & Collett, T. S. (2005).
  Ant navigation: Priming of visual route memories. Nature, 438(7066),
  302.

  Chameron, S., Schatz, B., Pastergue-Ruiz, I., Beugnon, G., & Collett,
  T. S. (1998). The learning of a sequence of visual patterns by the ant
  Cataglyphis cursor. Proceedings of the Royal Society of London. Series
  B: Biological Sciences, 265(1412), 2309-2313.

This is usually the case in large ants that tend to rely less on pheromones and more on visual cues to navigate. Studies commonly focus on species such as Gigantiops destructor or Myrmecia spp.

  Macquart, D., Latil, G., & Beugnon, G. (2008). Sensorimotor sequence
  learning in the ant Gigantiops destructor. Animal Behaviour, 75(5),
  1693-1701.

  Jayatilaka, P., Murray, T., Narendra, A., & Zeil, J. (2018). The
  choreography of learning walks in the Australian jack jumper ant
  Myrmecia croslandi. Journal of Experimental Biology, 221(20),
  jeb185306.

The type of learning you are referring to may be termed habituation, and habituation has been shown in ants, for example some ants tend to be less aggressive to other colonies that they encounter frequently.

  Langen, T. A., Tripet, F., & Nonacs, P. (2000). The red and the black:
  habituation and the dear-enemy phenomenon in two desert Pheidole ants.
  Behavioral Ecology and Sociobiology, 48(4), 285-292.


Do axon grows after cutting/damaging of some of its part?

Well look at this picture from Junqueira histology book:

In an injured or cut peripheral nerve, segments of axons distal to the injury lose their support from the cell bodies and degenerate completely. The proximal segments can
regenerate from their cut ends after a delay. The main changes that take place in an injured nerve fiber are shown in the picture above.
In the nerve segment distal to the injury the axon and myelin, but not the connective tissue, degenerate completely and are removed by macrophages. While these
regressive changes take place, Schwann cells proliferate within the connective tissue sleeve, giving rise to rows of cells that serve as guides for the sprouting axons
formed during the reparative phase.
The axon grows at the rate of 0.5–3 mm/day


I got $26$% as the answer.

To get a recombination between C and E, there are two possible mechanisms:-

C and D produce a recombinant, but D and E remain linked, therefore the final genotype will be a recombinant considering C and E(Chiasmata between C and D). Here $P_1=P_{CD}\times P'_{DE}$ where $P$ is the probability of recombination and $P'=1-P$ is the probability of linkage.Hence $P_1=0.08$
C and D remain linked but D and E undergo recombination (Chiasmata between D and E). Here, $P_2=P'_{CD}\times P_{DE}=0.18$

If there is a chiasmata between both C and D, and D and E, the resultant will not have a recombination in C and E locus due to double crossing over. If there is no crossing over, there will be no recombination at either loci.

The net probability of recombination $P_{CE}$ will be the sum of these two, as any of these possibilities can occur to give a recombination between C and E. $P_{CE}=P_1+P_2=0.26$

And Biogirllajja, your calculation (the Edit) was almost correct, but you have to subtract $2$% from both $10$% and $20$%, because, both of them include the probability of crossover at one loci, including the case where the other loci has also crossed over. Hence, you need to subtract it from both, and then add to get $26$%. Tell me if you want me to expand on my explanation or provide some clarifications.

If we simply add the map distances, we get the actual map distance which disregards the possibility of double recombinations. All map units greater than 10cM have significant chances of double crossovers between them, and hence, the observed recombination frequency would be less than the expected 0.1. Hence, for distances greater than 10cM, the observed frequency of recombination will not be the same as (map distance/100).


I think I found it. It can be Lacewings:

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


Do ions in the medullary interstitium just hang out, or go into the circulatory system and leave the kidney?

Both!

You've grasped one of the fundamental principles of the renal physiology -- the medulla must stay salty. Lets start there and see if we can't work out what happens.

As the filtrate flows through the tubule, solutes are removed from the lumen at the thick ascending limb and added to the medullary ECF. This concentrates solutes in the medulla, producing the corticomedullary gradient (the medulla must stay salty). This is called countercurrent multiplication, and explains how such a large osmolar gradient occurs between the cortex and the medulla.

At steady state, with an established corticomedullary gradient, what happens? Solutes continue to be reabsorbed by the tubular cells in the thick ascending limb. In order for it to be steady state, each ion reabsorbed into the ECF needs to go somewhere. One of three things could happen to these ions:

Secretion or diffusion into the collecting duct (and excretion as urine)
Diffusion into the cortex (dissipating the corticomedullary gradient)
Diffusion into the capillaries in the medulla, the vasa recta (exiting the kidney through the renal vein)

In fact, all of these things happen to a certain extent.

Secretion and diffusion into the collecting duct (1) are regulated by changes in the expression of pumps and channels. Diffusion into the cortex (2) is kept to a minimum by diffusion into the vasa recta (3), what we call countercurrent exchange.

  I always assumed that those ions were then entering blood vessels for another purpose.

So this does happen, but remember, the main reason for concentrating solutes in the medulla is so that the kidney can, if it needs to, excrete a very concentrated urine. Ions enter the blood vessels for the same purpose, in order to prevent them from diffusing back to the cortex, dissipating the corticomedullary gradient.

The concepts of countercurrent multiplication and countercurrent exchange were proposed in the 1940s and supported by a series of experiments in the 1950s. The landmark 1959 paper by Gottschalk and Mylle in The American Journal of Physiology was reprinted in 1997 by JASN and available for download without a paywall. It's an excellent read! As they predicted, we've learned a lot more, but this model still holds up, and is what we teach in renal physiology to this day.

This is their figure:


For a luekemia patient - how does the chemotherapy fixes the bone marrow to not produce immature cells

Chemotherapy in general works by killing (hopefully all) cancerous cells, while leaving the patient / healthy cells alive.
The drugs used for this usually are in principle toxins/poisons, but are more deadly to cancer cells, since these cells are growing very quickly compared to healthy cells. This general strategy is true for a lot of different types of drugs (and cancers). However, because the drugs are still generally toxic they are hard to dose correctly and also the reason why chemotherapy often has quite strong side-effects.
Additionally cancer can quickly evolve to gain resistance to specific drugs, which is why nowadays often a combination of multiple drugs at once is used.

In leukemia - which is a form of cancer where the blood and immune cell precursor cells in the bone marrow become cancerous - additional ways of selectively killing the cancer are radiation therapy (of the affected bones) and in some cases complete bone marrow transplants (which have their own issues, so they are not usually  used as first option).


How many cells are there in the apical meristematic tissue?

Meristem size is a very controled, highly genetic feature. It doesn't change between big or small branch/root (The SAM and RAM are obviously different).
There are very levels of potency in the meristematic tissue, so you should explain more which section of the meristem is of interest.
SAM (shoot apical meristem)
In *Arabidopsis thaliana* there are 9 long-lived meristematic cells, 3 in each lineage (L1, L2, L3) (https://www.sciencedirect.com/science/article/pii/S0012160609013840)
But the whole meristem is somewhat larger. If you consider the organizing center and cells that react to wushell by creating CLV1, CLV3 you get a few dozens.
If you consider cells that express miR156, miR172 or AP2-like genes you can get a few hundereds.
The scale is similar between species but the number and genes used to asses it vary.
RAM (root apical meristem)
I know less about the RAM but we can consider there the Quiescent center and also the Intial cells togheter called the promeristem.
THe Quiescent center consists of 10-20 cells and there is one (sometimes more) initial per file of cells in the root giving 20-30 cells in the promeristem.
The meristematic zone is somewhat bigger than the promeristem but the cells are pluripotent with relative small mobility.
 Roughly speaking
The most meristematic zone of each meristeme has no more than 50 cells.
The full area considered a meristeme can have a few hundered cells, depending on the research goal.


Please identify this tree in the Netherlands

I suspect this is a hazel (Corylus avellana) based on:

the leaves
the male flowers (not mature in your photo)
the fact that it is a common tree in Europe)

This one has twisty branches, so it could well be of a particular variety called "contorta".

According to
https://en.wikipedia.org/wiki/Corylus_avellana#Cultivation_and_uses

  A selection with twisted branches has been propagated horticulturally as Corylus avellana 'Contorta'.


Chromosome naming convention: Why are there chromosomes named "1" and "1A"?

I would suggest looking at some of the reference genome papers. My guess is that the chromosomes are named as such based on their synteny to the chicken genome; e.g. look at Accessory Figure 3 here for your zebra finch, and note that chromsomes 1 and 4 are split in the zebra finch relative to Gallus.

The direct comparison from that paper is to an Accessory Table 1 that I can't actually find.

I would guess that in most cases it's because of a synteny comparison to some reference, in this case chicken that splits a chromosome in the new genome. For example sequences homologous to the chicken chr1 are on two finch chromosomes 1 and 1A.


How do we know that everybody's DNA fingerprint is unique?

First, remember that identical twins actually have the same genotype. So its not exactly true that everyone has a unique genome.

But to get at the heart of it, you're asking how I can be sure that I have a different genome than you, or even than say my brother. And moreover you're asking how these differences are obvious enough that they can be detected without whole genome sequencing.

The answer is that there is no mechanism to ensure differences, but that the differences arise from the enormous variability of our genome. Look at the major histocompatibility complex, or MHC, a cluster of genes that affect our immune system.

Just to simplify things, lets focus in on four genes in this cluster: HLA-A, HLA-B, HLA-C and HLA-DRB1. According to this site there are 2579, 3285, 2133 and 1411 alleles for each, respectively. If we make a naive assumption that each of us received a random assortment of these genes, that makes 2579 x 3285 x 2133 x 1411 = 25,549,791,000,000 possible combinations. The chance that we both have the same combination is then about 1 in 25 trillion, just considering 4 genes.

But wait, you say, surely some of these genes are not equally likely and surely they segregate together, making this chance much smaller. You would be right. But this consideration stops mattering very much when you account for the rest of the variable regions. They combine multiplicatively, so considering a fifth gene with only 2 possible alleles brings the possible combinations to 50 trillion.

If you consider just a few more genes, the numbers get unthinkably high. This pretty much ensures that, even considering a small sequence, we can be sure that the genetic fingerprint is unique.


What is the role of lamellar bodies in lung cells?

Well, The paper published in Nature 2003:

Despite two decades of progress in understanding the role of LGs and
their contents in epidermal barrier function, almost nothing is known
about the mechanisms responsible for the assembly of these unique
organelles.source: http://www.nature.com/jid/journal/v120/n4/full/5601763a.html

Since then the word "Lamellar Granule" appeared only 5 more times in journals:

1: Sando GN, Zhu H, Weis JM, Richman JT, Wertz PW, Madison KC.
Caveolin expression and localization in human keratinocytes suggest a
role in lamellar granule biogenesis. J Invest Dermatol. 2003
Apr;120(4):531-41. PubMed PMID:
12648214.
2: Akiyama M. The roles of ABCA12 in epidermal lipid barrier formation
and keratinocyte differentiation. Biochim Biophys Acta. 2014
Mar;1841(3):435-40. doi:
10.1016/j.bbalip.2013.08.009. Epub 2013 Aug 15. Review. PubMed PMID: 23954554.
3: Sakai K, Akiyama M, Sugiyama-Nakagiri Y, McMillan JR, Sawamura D,
Shimizu H. Localization of ABCA12 from Golgi apparatus to lamellar
granules in human upper epidermal keratinocytes. Exp Dermatol. 2007
Nov;16(11):920-6. PubMed PMID:
17927575.
4: Lee WS, Oh TH, Chun SH, Jeon SY, Lee EY, Lee S, Park WS, Hwang S.
Integral lipid in human hair follicle. J Investig Dermatol Symp Proc.
2005 Dec;10(3):234-7. PubMed PMID: 16382672.
5: Kelsell DP, Norgett EE, Unsworth H, Teh MT, Cullup T, Mein CA,
Dopping-Hepenstal PJ, Dale BA, Tadini G, Fleckman P, Stephens KG,
Sybert VP, Mallory SB, North BV, Witt DR, Sprecher E, Taylor AE,
Ilchyshyn A, Kennedy CT, Goodyear H, Moss C, Paige D, Harper JI, Young
BD, Leigh IM, Eady RA, O'Toole EA.  Mutations in ABCA12 underlie the
severe congenital skin disease harlequin ichthyosis. Am J Hum Genet.
2005 May;76(5):794-803. Epub 2005 Mar 8. PubMed PMID: 15756637; PubMed
Central PMCID: PMC1199369.
6: Ishida-Yamamoto A, Deraison C, Bonnart C, Bitoun E, Robinson R,
O'Brien TJ, Wakamatsu K, Ohtsubo S, Takahashi H, Hashimoto Y,
Dopping-Hepenstal PJ, McGrath JA, Iizuka H, Richard G, Hovnanian A.
LEKTI is localized in lamellar granules, separated from KLK5 and KLK7,
and is secreted in the extracellular spaces of the  superficial
stratum granulosum. J Invest Dermatol. 2005 Feb;124(2):360-6. PubMed
PMID: 15675955.

According to the last mentioned paper[6]:

LG(Lameller granule) constitute a specialized secretory system within the epidermis.

LG are seen as isolated oval-shaped granules in post-embedding methods, whereas they appear as parts of beaded tubular structures in cryo-ultramicrotomy

Result highlights the biological significance of LG in regulation of protease activities.

LEKTI labels were aggregated and not evenly distributed throughout the LG system, indicating the heterogeneous nature of the LG  (Ishida-Yamamoto et al, 2004).

Biologically active fragments derived from LEKTI are released extracellularly (Bitoun et al, 2003).

LEKTI labels were seen in the extracellular spaces in the superficial granular layers and the first cornified layer with release from the apical side of upper granular cells. Aggregates of LEKTI immunolabels were also closely associated with the TGN46-positive trans-Golgi network .

Double labeling with antibodies to glucosylceramide, a well-known LG molecule, showed that each occupies a distinct domain of beaded tubular structure

The ultrastructural localization of LEKTI was compared with that of KLK7. As reported previously (Sondell et al, 1995; Ishida-Yamamoto et al, 2004), KLK7 was localized in the LG system but was not co-localized with LEKTI within keratinocytes.

This finding suggests that LEKTI is expressed and released earlier than its target proteases, which is consistent with a role in preventing premature proteolysis of extracellular matrix proteins or cell surface adhesion molecules, and in controlling the timing of desquamation.

Source: [6]. http://www.nature.com/jid/journal/v124/n2/fig_tab/5602696f4.html

(source: nature.com)

Caption: Lympho-epithelial Kazal-type-related inhibitor (LEKTI) is
transported through the lamellar granule (LG) system. Post-embedding
immunoelectron microscopy using Lowicryl HM20 resin (A, D) and a
cryo-ultramicrotomy method (B, C, E). (A, B) LEKTI signals (black
arrows) are detected in the LG using polyclonal antibodies against
D8–D11 in (A) and D1–D6 in (B). Note that LG are seen as isolated
granules in the post-embedding method (A), but appear as beaded
tubular structures in the cryo-ultramicrotomy (B). Lamellar internal
structures are seen in both methods (white arrows). (C) LEKTI is
secreted from the apical side of upper granular cells (arrows). d,
desmosomes. Polyclonal antibody to D8–D11 and desmoglein 1 monoclonal
antibody were used and were labeled with 5 and 10 nm immunogold,
respectively. (D) LEKTI antibody to D8–D11 labels are closely
associated with those of the TGN46-positive trans-Golgi network. (E)
LEKTI (monoclonal antibody, 5 nm gold labels) and glucosylceramides
(GlcCer, 10 nm gold labels) are localized within the same continuous
beaded tubular structure of the LG system.


More basic answer; the asbestos crystals have hooks. So the cilia in the lungs have difficulty moving them out with the other dust. This irritates the tissue causing the effects of the first answer. So it is a matter of time and number of asbestos particles that increases the probability of a cancer. Decades ago , the asbestos miners in Africa typically worked for years ( eg 20 years) before getting cancer.


What is the difference between eugenics and evolution by natural selection?

Selection is a mechanism of evolution which favours specific forms of traits over others, this can cause the spread of beneficial mutations through a population.

Natural selection is the spread of beneficial traits/genes through populations as a result of the natural variance in their effect on reproductive output (a function of life history traits like lifespan aging and reproductive rates). A classic example is that of Darwin's finches, where different variants of bill length and shape have evolved in populations based on what food resources (types of seed) are available to them and their ability to utilise those resources.

Artificial selection is selection imposed on a population by humans to deliberately affect specific traits. Examples of this would be milk yield in cattle (we want more efficient production and better quality milk), dog breeds (selection on a whole host of traits like colour, beardedness, height, length) and crops like wheat and barley (selected for higher efficiency and  quality output).

Eugenics, coming from the greek for "well-born" or "good" race, is the application of artificial selection principles to humans. Just as with cattle or crops, there is an aim, it may be to increase height, remove genetic diseases, or promote a certain set of traits like blonde hair and blue eyes. Historically we can associate with a number of radical political ideologies, such as Nazism. Even here in Sweden (people tend to think of it as a very progressive and equality driven country) there was a program of eugenics until very recently, achieved by forcibly sterilising or coercing people in to it, for various reasons (racial purity, health, and antisocial behaviour). Here's an interesting example of a girl designated as being genetically inferior because her family had a history of alcoholism (that page gives a good history of eugenics too). The social and ethical problems of eugenics are obvious.

Under normal conditions a persons reproductive output is largely determined by their own choices and actions whereas under eugenics that choice is taken away and made by someone else and specifically with the aim of "improving" the quality of the population.

So in summary:

natural selection is the result of natural variance in fitness linked to traits
artificial selection leads to a change in traits, in a specifically targeted direction, decided and imposed by another organism (usually humans, I know of no other species which does this)
eugenics is practice of artificial selection on humans enacted by humans with the specific aim of improving quality: often for social, economic, or political reasons and is generally accepted as being against human rights these days.


tetrads in meiosis are held together by what

A recombinase only active during meiosis - Dmc1 and a general recombinase Rad51 coat the single-stranded DNA to form nucleoprotein filaments. These filaments hold the homologs together at the chiasma, the point of attachment during crossing over.


What are these structures inside a cut open Allamanda blanchetti?

The third photo gets to the heart of the matter. Here's an enlargement:

The gold-colored areas are the anthers of some of the stamens, the filaments of which are fused with the tissue of the petal.  (This is typical of the Apocynaceae, the family to which A. blanchetti belongs; they have epipetalous stamens, that is the stamens are "adnate" i.e. fused with the petal.) This is the male part of the flower; the anthers have the pollen grains which the plant is trying to get transferred to another flower.
Above the knife is the style.  This part of the female structure is a hollow tube which runs from the openings in the stigma (the out of focus green blob) down to the ovary (not in photo). The central part of the fourth photo is presumably the ovary (missing its style). The ovary contain the ovules which will become seeds after fertilization from pollen which sticks to the stigma and grows a tube down the style.


Is there any source for raw data of SNP genotype frequency?

You might be able to get some raw data on SNP frequency by batch querying the dbSNP database.  I have not used it myself, though.


When designing primers how important is the GC clamp?

It's hard to provide an objective answer. If you have a decent length and good complexity, even a single terminal 3' G or C would do. Of course, one has to take into account the primer's overall GC:AT ratio and things like annealing temperature.

Here's a link to diverse opinions on the topic and it has this nugget (which I subscribe to when possible):

  FWIW, my preferred offerings to the PCR gods are primers with a single
  G or C 3', FWIW. Seems to keep 'em happy most phases of the moon.


Were there any vertebrates with 6 or more limbs?

I've not read it but this SE question Why don't mammals have more than 4 limbs?
though not a duplicate (it asks about mammals not all vertebrates) may have some elements in its answers pertinent to your question.

And the question Why are there no vertebrates with more than four limbs? has been asked in Quora where it has 7 answers you may find useful.

Also this discussion thread Why can insects have 6+ limbs, but mammals only have 4? in reddit.

  Does paleontology has any evidence of a vertebrate that had 3 (or more) sets of bilaterally symmetric limbs or lobe-based fins?

You sent me far down the rabbit hole with this one, for reasons that escape me my instant response was 'yes the Coelacanth' but as you correctly point out that has only 4 paired fins.

As seen from The origin of tetrapods our limbs came from fins, Coelacanth is a good example of the likely early beginnings of Tetrapod limbs, they occasionally use them to 'walk' on the seabed.

The image provided in this National Geographic article Coelacanth Rediscovered gives a much clearer picture of it's 'limb' structures.

Latimeria chalumnae, the coelacanth (SEE-lee-uh-kanth), thought extinct until a biologist identified one off the coast of South Africa in 1939.

I've trawled Google for early chordates looking for examples of more than two pairs of fins & haven't been able to find any, it seems the earliest paired fins appeared in (or shortly before) Ostracoderms & from there continued in an unbroken line to the tetrapods & our limbs.

Paired fins don't appear to have developed in chordates before then or to have ever developed into more than two pairs.

So to the best of my knowledge it appears that the answer to your question is no.

Other links.
Yunnanozoon
Myllokunmingia
Haikouichthys
Evolution of fish


Why are humans and almost every species on earth symmetrical?

[If we are talking about animals, there is a number of types of body symmetry: asymmetry, radial, bilateral, spiral, rotational, glide and metameric symmetries. Bilateral and radial are the two basic types, which served as main classificatory character for animal mega-systematics in the past.]

It's assumed that body symmetry is associated with general environmental gradients.

Animals with (elements of) radial symmetry have one dorso-ventral axis which echos only one environmental gradient: substrate/water column, depth etc. Besides this polarity, resources/signals/danger may come from any direction. Imagine a Hydra polyp with its foot attached to a waterweed and its tentacles surrounding the mouth on the opposite end and expecting the victim to come from any side.

Body of bilateral animals possesses the same dorso-ventral axis and yet another polarity, orthogonal to it: the anterior-posterior axis. This axis is conjugated with the gradient created by locomotion: the anterior margin of the body is likely to encounter something new first. This principle lies in the basis of cephalization: most bilaterial animals have more or less shaped "head".

Evolutionary changes in body symmetry are thus thought to be associated with changes in life-style, e.g.:

there is a hypothesis that cnidarians were originally bilateral (and many of them still show some degree bilaterality), but lost it after becoming sedentary.
non-walkers echinoderms originated from fully bilateral animals and later acquired their famed pentameric radial symmetry (were they originally fully sedentary like modern stalked sea lilies?). This symmetry, however was again distorted towards secondary bilaterality (not matching the original plane of symmetry) in endobenthic forms: sand dollars and some holothurians.
worms like nematodes or priapulids are dwellers of viscous media, similar in all directions: dorso-ventral gradient of environment in this case is absent or weak. Though the original bilateral symmetry is very clear in their body plans, signs of radial symmetry prevail in some organ systems, including the general vermiform appearance. Thus, nematodes combine triradial (head sensilla, pharynx), biradial (musculature) and bilateral (nervous system, genitalia, tail) symmetries.


This phenomena has elements of what,  in the UK, are termed Phoenix Trees, however this term, and the term Phoenix Regeneration, is more often used when describing characteristics of ancient and veteran trees.

The principles that underlie what the photo shows is that new growth on trees will always grow strongest where there is the most light available, and so in this case as the trunk has become bent towards the canopies, and the shade, of neighbouring trees this branch has become the part of the tree to encounter the most available light.

It is possible to find many trees in a woodland that may show elements of this phenomena; your photo is of a tree that is on the more extreme end of the spectrum for a tree that is still standing. It has developed a different 'dominant' stem to the one it 'started' with.

It is probably not now possible to discover what has happened in the past to cause this tree to bend over in this way; it could have been perhaps a heavy build up of snow or ice at a particularly vulnerable point in its growth, or more likely one or more other trees, or a part of another tree perhaps falling in such a way to knock into it and stay in that position long enough for this tree to adopt this shape in its trunk. If this was the case it may be that the tree/s that fell into it has since been cleared, or decayed away if it was a dead tree or branch.

Often trees that are completely blown over can remain alive because enough roots remain in the soil for it to survive. When this happens the branches on the trunk start to grow upwards into the new space and light that has been created by the tree itself falling. Over time the result is a tree where the main trunk is lying on the ground but the canopy is now a series of branches at right angles heading straight up.

The name for a tree that continues to live and grow after it has fallen over is a "Phoenix tree", named after the mythical bird that regenerates itself after catching on fire; it rises from the ashes.

This term is often applied to old trees, but it could, and does, also be used to describe any tree that has fallen over but continued to grow.

References can be found in Natural England's excellent publication on Veteran and Ancient Tree management
http://publications.naturalengland.org.uk/publication/75035

For example in Chapter 2 "What are Veteran Trees and why are they important?" Section 2.3.4.6 (page 21) of Veteran Trees: A guide to good management

Old trees may fall over completely and then re-grow or collapse and layer well away
from the original base. This is characteristic of lime, willow, alder, black poplar, medlar
and bird cherry but can occur in any species. A particularly notable example is the
Tortworth Chestnut.

The term phoenix regeneration has been applied to trees that have fallen over, or
split apart, and successfully continued growing.


Does cow urine have medicinal properties?

Interesting question anomdsgf. There are substances present in Bos taurus urine that promote antimicrobial activity. Studies like this and this have shown how the urine can inhibit the growth of certain bacterial strains.

However, with all that said, Bos taurus urine could still contain other harmful bacteria that are not inhibited simply because it was excreted out of a cows urethra and could cause infections. Read more on possible harmful effects here.


Can Taq polymerase be used instead of polymerase Vent exo (-)?

I haven't done ARMS PCR myself, so my answer is based on theory and there might be other practical factors I overlooked.

The characteristic feature of the Vent exo(-) polymerase is the lack of exonuclease activity compared to the regular Vent polymerase. ARMS uses the fact that a mismatch at the 3' position prevents primer extension. For this to work it is important to use a polymerase without exonuclease activity, as such a polymerase could "repair" the mismatch and the whole method would not work. Taq polymerase also doesn't have any exonuclease activity, so in theory you should be able to use it for this experiment.

The primers don't have to be changed for different polymerases, the polymerase buffer though is different and I wouldn't recommend using the wrong one.


To diagnose osteomyelitis of vertebral column in chronic kidney failure

Osteomyelitis can be diagnosed with the following imaging techniques [1]:

first of all: radiography to view the anatomy of the bone
the sonography can be used to diagnose fluid collections, periosteal involvement. It is also the most useful procedure for kidney assessment [2].
CT is also useful to detect early osseous erosion, but is less sensitive when it comes to bone infection
MRI is the most sensitive and specific for osteomyelitis
Nuclear imaging can be used to identify multifocal osseous involvement.

References:

Carlos Pineda et al., Radiographic Imaging in Osteomyelitis: The Role of Plain Radiography, Computed Tomography, Ultrasonography, Magnetic Resonance Imaging, and Scintigraphy
American College of Radiology, Renal failure


How was gene therapy able to cure diseases through the transformation of actively dividing cells?

Short answer
Both dividing and non-dividing cells can permanently be modified with gene therapy by using vectors that incorporate their payload in the host's chromosomal DNA

Background
Vector-based gene therapy can be applied by using vectors, such as modified retroviruses or adenoviruses, that incorporate their payload in the host's chromosome.

Whether the transformed cells are replicating yes or no, the parent as well as any possible daughter cells will carry the new DNA. For example, immunodeficiency has been treated successfully with gene therapy, but the first trials resulted in blood-bone cancers, because the stem cells started to proliferate uncontrollably, hence dividing cells definitely can be permanently transformed. In fact, when germ line cells are transformed in this way, even the offspring of the host will inherit it.

Sources
- American Medical Association
- Learn Genetics
- Utah University


So does U there mean unique?

No. The name of the Viral Protein U comes from the names of the Open Read Frames (ORFs) of the Visna lentivirus, termed by Sonigo et al (1985).

According to the paper that actually named the Vpu (Strebel, Klimkait and Martin, 1988):

  In this study, we show that another small (81 codons) HIV-1 ORF, designated vpu ["U", see (2)] encodes a 16-kD protein that is expressed in vitro and in vivo. Mutagenesis of vpu in an infectious molecular clone of HIV-1 results in the synthesis of particles with altered replicative capacity.

If you look at that reference number 2, you will find a paper named Nucleotide Sequence of the Visna Lentivirus: Relationship to the AIDS Virus, from Sonigo et al. (1985).

In that paper you will find several ORFs, named F, Q, R, U3, U5 etc. Why are they named like that is another question, but it seems to me that they are just letters of the alphabet, with no meaning. Vpu was named because of U3. By the way, HIV also has a Vpr, because of the ORF R.

Sources:

Strebel, K., Klimkait, T. and Martin, M. (1988). A novel gene of HIV-1, vpu, and its 16-kilodalton product. Science, 241(4870), pp.1221-1223.
SONIGO, P., ALIZON, M., STASKUS, K., KLATZMANN, D., COLE, S., DANOS, O., RETZEL, E., TIOLLAIS, P., HAASE, A. and WAINHOBSON, S. (1985). Nucleotide sequence of the visna lentivirus: relationship to the AIDS virus. Cell, 42(1), pp.369-382.


How was Restriction Site of EcoRI sequenced?

The first determination of a recognition site for a restriction endonulease was reported in:

  Kelly & Smith (1970) A restriction enzyme from Hemophilus influenzae II. Base sequence of the recognition site. J Mol. Biol. 51: 393-409

The enzyme was then called endonuclease R, but is now known as HindII (or HincII).

The method used was to cut DNA with the enzyme and then remove the exposed terminal phosphates with alkaline phosphatase. These ends could then be labelled with 32P using polynucleotide kinase and γ-labelled ATP.

The end-labelled DNA was then treated with nucleases in three different ways to release mononucleotides, dinucleotides, and a mixture enriched for trinucleotides. In each case the labelled products were identified by their behaviour in 2D thin-layer chromatography, and were  further characterised for their total base composition after digestion to mononucleotides where appropriate.

The deduced site was/is

5'----GTY RAC----3'
3'----CAR YTG----5'

Thus the labelled mononucleotides were found to be A and G (purine=R), the dinucleotides were found to be GA and AA and so on.

The EcoRI sequence was determined by essentially the same methodology and was reported by

  Hedgpeth et al (1972) DNA nucleotide sequence restricted by the RI endonuclease. Proc. Natl. Acad. Sci USA 69:3448 - 3452

Addendum:

Although Sanger sequencing (the plus-minus method) may have been developed through the 1970s, it really didn't catch on until the early 80s. So for example the first complete plasmid sequence to be determined was pBR322 in 1979:

  Sutcliffe (1979) Complete nucleotide sequence of the Escherichia coli plasmid pBR322. CSH Symp. Quant. Biol. 43: 77 - 90

  "I have determined the 4362-nucleotide-pair sequence of the plasmid cloning vector pBR322 using the DNA-sequencing technique of Maxam and Gilbert (1977). The DNA structure has several interesting features that lead to testable predictions."

The standard sequencing method in use at that time was chemical sequencing using the Maxam-Gilbert methodology. When I started a postdoc in the USA in 1979 M-G sequencing was the standard method. Sanger sequencing really only took off following the development of the M13 mp vectors (and later the pUC plasmids) by J Messing in the early 80s. And what a relief it was: M-G sequencing was extremely laborious, as anyone who ever did it will testify.


Have there been attempts to identify Chomsky's "language mutation" in humans?

The anthropologist Svante Pääbo is more recently famous for trying to track down the 'language gene'.  There isn't a lot of reference to Chomsky in his work as I've noticed, but it is to me the same intriguing idea.

That being that the chimpanzee and the bonobo have 99+% identical to human genome sequences and we also have data from human variations as well from a few thousand individuals.  Using this data you could try to evaluate a small list of differences which might have led to the inborn trait human beings have to acquire language.

Pääbo's work focused on FOXP2, which leads to language disorders in humans when it is damaged in human beings.  On the other hand its also known that primates can learn to speak rather well if they are trained their entire lives by the right people.  They can even reflect on abstract ideas such as life after death.  This is a typical result when looking for a single gene that causes something- it rarely leads to a conclusive result as a phenotype like verbality, or even height or body mass is the result of the action and fine tuning of many genes acting in concert.

That is, if you introduced human FoxP2 into transgenic chimps its unlikely that they would be as verbal as human beings.  This current reference for instance talks about how important the slower development rate for human children is.  This is one of the most unusual thing about human beings - it takes 1/3 to 1/5 of the human lifetime before we are fully mature.  This phenotype is incredibly unlikely to be the result of FoxP2 alone, or any single gene.

There has been recent work published (2012) where the unique human FOXP2 gene was put into transgenic mice.  They seem to have different sort of personality tendencies and are said to vocalize differently - brain activity profiles are also different.  Kinda exciting, but not the Secret of NIMH yet....


What determines if an allele is dominant or recessive?

Dominance is seldom complete. Owing to effects like co-dominance, incomplete dominance, collaborative (additive) effects of polygenes, our classical concept of dominance doesn't work. Having said that, there are certain ways in which a gene, if showing complete dominance can be analysed from the molecular level.

In an individual heterozygous for a certain trait, the following possibilities exist:

Both the alleles, though different, code for a protein (which might be an enzyme or a regulatory protein) which is functional and is indistinguishable atleast in terms of its functions. In this case, no matter if the person is heterozygous or homozygous for either allele, the concerned protein will be in sufficient amounts and will always be functional. These alleles can be treated as the same allele while performing Mendelian analysis though their products might differ slightly, leading to formation of two (or more) functionally similar Alloenzymes (as opposed to Isozymes which are similar enzymes produced by genes at different loci).
Haplosufficiency. In this case, one of the two alleles codes for a functional protein and the other either codes for a non-functional protein (or does not code at all). But, even in heterozygous condition where only one allele producing functional protein is present, the amount of protein produced is sufficient to show the phenotype and hence, even in heterozygous individuals, enough protein is coded for by the single functional allele exhibiting the normal phenotype. If the two non-functional alleles are present as a homozygous pair, no functional protein is synthesised and hence the phenotype is not shown (i.e a different phenotype is shown). Here, the functional allele is Haplosufficient (able to produce enough protein in heterozygous condition) and is called the dominant since it expresses its phenotype both in heterozygous and homozygous conditions. this is pretty common.
Complete Haploinsufficiency. Here again one allele codes for a functional protein while the other does not. But this time, if the functional allele is present in heterozygous condition, then the amount of the protein produced is not at all sufficient and hence the phenotype is not exhibited. Here the non-functional allele is said to be dominant because heterozygous phenotype resembles the phenotype of homozygous non-functional allele (where no protein is synthesized) since the functional allele is completely haploinsufficient (unable to produce enough protein in heterozygous condition). This method is pretty rare.(e.g rare autosomal dominant dyskeratosis congenita)

If there is partial haplosufficiency /partial haploinsufficiency, the phenomenon of incomplete dominance can be explained. (heterozygous individual produces protein not sufficient for a full-blown phenotype but just a partial expression of the phenotype)

Here, "functional" refers to being actually "functional" as in case of flower colour (anthocyanin synthesis) or just performing certain kind of a conversion leading to a particular effect on thephenotype.


It's a Japanese Beetle Popillia japonica - they are invasive in most of North America and some of Europe now.

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

They are spreading rapidly west in the United States and many areas are reporting the largest numbers ever observed, for example:
http://www.wisconsinrapidstribune.com/story/life/2017/07/19/japanese-beetles-invade-central-wisconsin/490140001/

http://www.omaha.com/living/japanese-beetle-swarms-are-worse-than-ever-this-year-and/article_77257d36-6c28-11e7-839a-877ff3c8538b.html

For control around your plants, it is recommended to manually remove them; brushing or placing them in water with some dish soap works well. They tend to congregate with other individuals of the species, so if you take them off your plants that will tend to limit the numbers that join them. However, they likely do the most damage to gardens etc as larvae, and there doesn't seem to be a good, specific way to control them at that stage.


It is a longhorn beetle, family Cerambycidae. Two of the "eight legs" are antennae. It looks a lot like the one pictured here: https://hiveminer.com/Tags/cerambycidae%2Cfrance


Can a gene-expression or epigenetic 'user-history' be found in the body?

First Paragraph - let's debunk what was poorly phrased

Many sentences you wrote are quite misleading. You should have a look at an introduction to molecular genetic to have a better understanding such as what you can find on Khan Academy. In short:

  the double helix DNA strands are the building blocks of an organism

This sentence is very opinion based. as a matter of proof, one could for example replace the term double helix DNA by "cells" (or other terms) and many would still be satisfied with the sentence.

  Genes are chunks of DNA telling the body what to do.

A gene is a part of DNA which contains regions coding for proteins. There are many sequences which are not coding for any proteins that are essential for the individual survival (such as regulatory sequences or sequence coding for rRNA for examples).

  Genes naturally switch on and off.

The regulation of gene expression is actually much more continuous than just on/off. Also, regulation of protein concentration can occur at different levels and not only by regulating gene expression.

  DNA is essentially stored in Chromosomes.

This sounds like chromosomes are boxes in which one can find DNA. In reality, DNA is a type of molecule which can be found under different forms. In humans (and other eukaryotes) most of the DNA (but not all) is present in the form of chromosomes.

Second Paragraph - What is epigenetics?

  External and environmental factors can influence the expression of genes,

This is correct

  and the information stored in the DNA

This is wrong. Environmental factors do not affect the sequence of base pairs of the DNA. It only regulate its expression. Such regulation of expression can last for a long time and even be transmitted to the offspring. The term epigenetics is loosely defined. In short epigenetics refers to the set of mechanisms that affect gene expression at short and long term. The classic mechanism of interet in epigenetics in the methylation of histone tails (quickly speaking, histones are proteic structures around which DNA is wrapped).

Your question

  Does the body store a history of these expressions? Do the chromosomes (or some other part) of an older organism store a 'user-history' of which genes where previously activated when the organism was younger? eg, can you tell which genes where active when a person was 12, from the cells of an 80 year old?

As explained above, some of the molecular mechanisms yielding to changes in gene expression can have long term consequences on gene expression (which can even be inherited). But there is not data bank (or other centralized or not source of information) that specifically record the expression of each gene at any one time in the history of the cell life.


I normally use 1-2 ul (depending on whether my gut tells me I have a lot of DNA, or a little that day) in a 70 ml 1% gel (which is probably 60-65 ml after boiling in the microwave). I have no trouble whatsoever seeing ladders and DNA samples of down to 100 ug in wells not much bigger than about 4 mm.

Here are the factors that you can manipulate to alter the brightness:

Amount of EtBr. More is brighter. (However, you already use a lot - using less may even be better because it would reduce background while still saturating the DNA with EtBr)
Amount of DNA. More is brighter. To avoid guesswork, use a ladder and consult the instructions in its manual or spec sheet. They usually have an example picture of a gel, and say exactly how they obtained it.
You messed up. Do other people in the lab get good gels? Ask them to do the protocol with you.
Sample preparation. Are you using a loading dye in the correct amount? Is the DNA diffusing out of the wells? Are you spilling a lot of it when you load?
Band width. Obviously if you load the same amount of DNA in a well 4 times as wide, it will be 4 times fainter.
Strength of UV light. Many illuminators have a knob to adjust the intensity, people turn it down to avoid damaging DNA when gel-purifying restriction fragments. You can also play with intensity, gamma and exposure in a geldoc machine.
Quality of EtBr. I've never actually had this happen, but your stock may be bad for some reason. Ask another lab for a ul or two to easily control for this.
Quality of DNA. Obviously, your sample must actually have DNA in it, and not be degraded. You can check amount and purity easily with a spectrophotometer, but it will not tell you if the DNA has been digested into its component nucleotides (that is usually checked with a gel).
Amount of gel. The crucial variable is obviously not total amount of EtBr, but concentration. Less gel, brighter bands - but you seem to be using a standard gel amount.
Quality of gel. Again, never had this happen, but try making the gel with someone else's reagents.

I can see that you have a ladder in the middle, so at least some DNA is definitely there.

Also, keep in mind that off-the-shelf cameras are not good at imaging the EtBr fluorescence, because the wavelength is a bit unusual. The nice pictures you see in papers are taken with a specialized geldoc machine or a camera with an appropriate filter.


What are all the possible developmental stages an insect can be in?

This process is refereed to as Metamorphosis, is a biological process by which an animal physically develops. Furthermore, Animals can be divided into species that undergo complete metamorphosis ("holometaboly"), incomplete metamorphosis ("hemimetaboly"), or no metamorphosis ("ametaboly").
Otherwise there is the process known as Holometabolism, which more specifically pertains to insect development. This process defines almost all the types of insect development.
Others include: Ametabolism and Hemimetabolism.


According to Smith et al., 1978, bacterial ribosomes don't necessarily bind directly to the membrane, but through the nascent chain, in which case nothing is truly attaching to anything..


Prostaglandin F2-alpha production in men

As I know:

One of the most important chemical mediators are prostaglandins that in vivo act on different cell receptors and have different effects on the body. Prostaglandins are twenty-carbon lipid molecules and structurally similar to cholesterol. Prostaglandins have different types, such as F2, E2 alpha, PGI2, and so on.

A phospholipase enzyme converts phospholipids of cell membranes into arachidonic acid. The arachidonic acid within the cyclooxygenase enzyme or Cox (both type 1 and 2) can be converted to prostaglandins.

PGF2alpha has functions in uterus contraction and bronchoconstriction, so I think both uterus and lung cells produce it.

I have no special information about production of PGF2alpha in men.