This has never happened (at least to my knowledge), since removing all bacteria from a human being would be extremely difficult and also dangerous. And there is a proven relationship between the human microbiome and stress, but "extenuating circumstances" won't remove all bacteria from your body.

However you can look in the Internet for "germ-free animals", "gnotobiotic animal" or "axenic mice". Caesarean section in aseptic conditions is practiced (a fetus in normal conditions has no germs in it) and the "newborn" is immediately put in a sterilized enviroment. There is plenty of research with this kind of animals.

I hope my answer was useful for you! Cheers!


Do plants need O₂ to consume energy they've stored via sugar?

Plants need sugar not only for energy but also for synthesizing essential metabolites and building blocks including cellulose (used in cell wall), glycoproteins and 5-carbon sugars for nucleotides.

As already mentioned by canadianer, plants respire by oxidizing sugars. This happens mostly during the night. However photosynthesis also produces ATP and therefore plants are not strictly dependent on respiration for energy. Moreover the fixed carbon in the form of starch makes up an energy reserve (like fats and glycogen in animals).


Your premise is incorrect, the genetic code is NOT universal. There is a 'standard' genetic code, which is found among higher animals and plants and most bacteria, but there is a variety of other genetic codes found in the main genome of more obscure organisms. These are listed at: http://www.ncbi.nlm.nih.gov/Taxonomy/Utils/wprintgc.cgi .

There is also no mitochondrial genetic code but a variety of mitochondrial (and plastid) genetic codes. One feature of genomes with non-standard genetic codes is small size, so that the number of proteins influenced by a change from a common precursor genetic code would have been small.

In the case of mammalian mitochondria there are fewer tRNAs and these have non-standard anticodon-codon interactions. Thus rationalization of these genetic codes may have been due to pressure to reduce the size of the genome.


Population Genetics Using WGS: How do I know when I have enough individuals?

I think that many of the applications that you mention require wildly different numbers of individuals. It would help to know more about goals, questions, organism details, etc.
For example, for simple population statistic estimates, you can depend on the large number of sites in the genome to get an accurate estimates (such as Watterson) from a single individual, if you are working in a diploid organism, as you can use heterozygosity. See the first Neandertal genome paper for what you can do with one single not very good sequence.
For applications such as linkage maps, you will need a rather larger number of individuals, as you need to sample a large number of recombinations. However, "large" is relative, as a centimorgan-level resolution of the human genome was achieved with a mere 110 humans and ~6000 loci. For finer linkage analysis you may need more individuals; however, with WGS your loci will be much less limited.
For McDonald-Kreitman tests or such-like, it is possibly more important to have more individuals. But you don't need WGS of every individual, in principle you could just find the gene(s) of interest and Sanger it for every individual, which is in most cases still much cheaper.
Obviously each of these has its own power and precision added by more samples, more could be said of each. General resources can be found here and here and here and here, in case it is helpful.


Is this maritime plant a species of zostera?

It certainly looks like a Zostera species.  The ones that appear in the UK are Zostera angustifolia, Zostera noltii, and Zostera marina.  Its hard to tell exactly which species this one is without size information and knowing the conditions of the bay.  Z. marina has the broadest leaves at around 5 - 10 mm, whilst Z. angustifolia has leaves just 2 - 3 mm broad.  Is 40m around the mid-water mark?  If so I would hazard a guess this is Z. angustifolia.  Z. marina tends to stick to areas permanently covered by the sea (sub-littoral) whilst Z. noltii likes much more sheltered conditions than the middle of the bay, tending to stick to the upper shore.

Hope that helps!


What happens to the precursor protein's signal sequence after it is cleaved?

After cleavage, the signal sequence is generally thought to be degraded by intramembrane proteases (since it is embedded in the endoplasmic reticulum membrane). For at least some proteins, the signal sequence is further processed and released into the cytoplasm or ER lumen.

Martoglio B. 2003. Intramembrane proteolysis and post-targeting functions of signal peptides. Biochem Soc Trans 31:1243-1247

  When translocation continues, the signal sequence’s c-region appears in the ER lumen and becomes accessible to signal peptidase, which cleaves the signal sequence from the pre-protein. The latter is further translocated into the ER lumen, while the liberated signal peptide is usually not detected in assay systems, implying rapid degradation. In a cell-free in vitro system with ER membranes from canine pancreas, we reported several years ago that after cleavage by signal peptidase, the liberated signal peptide is transiently embedded in the lipid bilayer and undergoes further processing to be released from the membrane.

The activity of released signal sequences is not entirely known and only partially characterized for some proteins. The following review discusses some functions of signal peptides after cleavage:

Martoglio B, Dobberstein B. 1998. Signal sequences: more than just greasy peptides. Trends Cell Bio 8(10):410-415

The signal peptide of bovine preprolactin and HIV gp160 can bind calmodulin.

  …the signal sequence of bovine preprolactin, which consists of 30 amino acid residues, is cleaved by signal peptidase and then further processed by an unknown signal peptide peptidase (SPPase; Fig. 4) … This signal peptide fragment resides initially in the membrane and, after a chase period, is released into the cytosol. Once in the cytosol, the signal peptide fragment binds to calmodulin in a Ca2+-dependent manner. A signal peptide fragment derived from HIV-1 gp160 also binds to calmodulin when it is released into the cytosol … With their n-regions having the potential to form a basic amphiphilic α-helix and their hydrophobic C-terminal region, they are similar to other calmodulin-binding domains. Calmodulin is a small, acidic protein involved in the regulation of many cellular processes controlled by Ca2+-dependent signalling pathways. It is possible that binding of signal peptide fragments to calmodulin influences Ca2+/calmodulin-dependent cellular signal-transduction pathways. Further studies are required to elucidate the physiological consequences of interactions between signal peptide fragments and calmodulin.

The signal peptides of MHC class I proteins are presented to NK cells by MHC-I (with HLA-E alpha chain). This allows monitoring of MHC-I expression, which is often disrupted in virally infected or cancerous cells.

  Peptides presented by classical MHC class I molecules represent the broad spectrum of peptides generated by the proteasome. In contrast to this general use of peptides, only a very specific signal peptide fragment is presented by so-called nonclassical MHC class I molecules (HLA-E in human). These molecules monitor the presence of classical MHC class I molecules by presenting a signal peptide fragment derived from HLA-A, -B or -C to natural killer (NK) cells (Fig. 5b). NK cells destroy cells unable to activate inhibitory receptors specific for MHC class I molecules.

This book section discusses the function of signal peptides in some viruses:

Kapp K, Schrempf S, Lemberg MK, Dobberstein B. 2009. Post-targeting functions of signal peptides. In: Protein Transport into the Endoplasmic Reticulum, Zimmermann R.


What is an accessible book about plant evolution for a non-biologist?

I have Fossil Plants by Paul Kenrick and Paul Davis, published by The Natural History Museum in London.  It takes the reader through a well-researched but accessible illustrated history of the evolution of plantlife from the beginnings to now.  There are photos of many key fossils, and artist's renderings of what the landscapes of the past would have looked like.


How does a seed determine when to start germination?

Certain conditions are necessary for seed germination:

Moisture — seeds dry out during dispersal, but at germination the cells need to absorb water in order to rehydrate so that metabolic reactions can take place, which will eventually lead to the growth of the embryo tops and shoot. Furthermore, some seeds contain a hormone that inhibits germination and water is needed in order to wash it out of the seed. The water needed for these processes is absorbed by the micropyle.
Warmth —  many of the metabolic events of germination use enzymes, and these are sensitive to temperatures. Temperature will often be used as a trigger for germination.
Oxygen — many of the metabolic events that occur during germination use energy. This energy is produced by aerobic respiration.

Many metabolic processes take place at the start of germination, such as the synthesis  of giberrellin, this is a plant hormone that stimulates mitosis and cell division in the embryo. Other plant hormones include Abscisic acid (ABA), which regulates seed dormancy and germination. It has been found to stop germination once it has been placed in the soil, it causes the seed to enter a period of dormancy. This allows the seed to remain dormant until when the conditions are more favorable for the seed to grow.


Does age affect the frequency of flatus?

I do not have access to journals, but there is this paper claiming in its abstract that age DOES NOT play a role in flatus frequency.

Reference:  Furne JK, Levitt MD. 1996. Factors influencing frequency of flatus emission by healthy subjects. Digestive diseases and sciences 41: 1631–5.


Sample preparation for protein gels is not a complex task. Simply mix the appropriate amount of sample buffer with your sample and load it. For a 2x sample buffer use equal amounts of sample and buffer, for 5x sample buffer use 4 parts of sample and 1 part of buffer (for examle 40µl + 10µl). Heat the mixed samples for 5 minutes at 95°C, cool them immediately on ice and load an appropriate amount of it on the gel. How much is possible really depends on the type of gel you use - 20-30µl should usually be possible.

Do not load too much protein, otherwise you will not be able to seperate them appropriately. I usually use between 20-30µg of total protein per well or as little as 50ng for purified proteins (this depends on the antibodies as well).

Have a look on this webpage for some further information.

For sample buffers I usually use the following recipes. I prefer the 5x, because I can load more protein, if the preparation is not very good. I also prefer the use of DTT to Mercaptoethanol, as it is much less smelly. If you have no DTT (or prefer mercaptoethanol) it can be replaced by an equal amount (200mM in the 2x, 500mM in the 5x buffer). If you use DTT, you need to make aliquots of the buffer and store it at -20°C, a working aliquot can be kept at 4°C for two weeks or so.

2x sample buffer:

4% SDS
20% glycerol
100 mM Tris-Cl, pH 6.8
2 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye

5x sample buffer

10% SDS
50% glycerol
250 mM Tris-Cl, pH 6.8
5 mM EDTA (ethylene diamine tetraacetic acid)
200 mM DTT (dithiothreitol)
0.25 % (w/v) bromphenol blue dye


Why do plants produce so many hybrids as a kingdom?

Yes, it has very much to do with the poliploidy events. Specifically if you look at the grasses, most grasses that are diploid (eg., AA, BB), cannot hybridize, but in some rare events when they form polyploid (AAAA, BBBB), they can readily hybridize to form fertile progenies (AABB).


Do cows chew in a preferential chirality?

This study deals with the chewing direction of cows. It splits the chewing into three phases, the first jaw movement, the middle ones and the last one. It finds out that the first one is always in the opposite direction of the middle ones, that generally the middle ones are usually in the same direction and that seemimgly cows change chewing direction from one middle jaw movement period to another.


The evolution of dogs through domestication and artificial selection

According to Serpell, 1995 (http://books.google.co.uk/books?id=I8HU_3ycrrEC, page 8), wolf bones in association with human bones have been found from as early as the middle pleistocene (126,000–781,000 years ago). I think we're talking about more than a few centuries here :) It's still relatively little in comparison to naturally selected evolution, but that's probably the point he is trying to emphasize.


Bats observed hunting insect prey - any evidence of "handedness" (laterality) in circular flight pattern?

This article shows a lefthanded bias for climbing and eating, with one bat species:
Paolo Zucca, Alessandra Palladini, Luigi Baciadonna, Dino Scaravelli.
"Handedness in the echolocating Schreiber's Long-Fingered Bat (Miniopterus schreibersii)"
Behavioural Processes,
Volume 84, Issue 3,
2010,
Pages 693-695,
ISSN 0376-6357,
https://doi.org/10.1016/j.beproc.2010.04.006.

Paywalled - only the abstract is visible.

Found using Google Scholar with search terms: handedness, microchiroptera


The largest flying bird ever was probably Argentavis, which weighed about 70 kg, far smaller than a horse but still pretty impressive:

A duck scaled even to 70 kg wouldn't be able to fly since it wouldn't have the same relative wingspan.  A 1 kg duck has a wingspan less than 100 cm; volume (and weight) increase as the cube of dimensions, so a 70 kg duck would have maybe a 4-meter wingspan, whereas Argentavis was nearly double that (around 7 m).

The largest flying animal we know of was probably Quetzalcoatlus, or perhaps one of the other Azhdarchid pterosaurs, which were definitely horse-sized depending how you measure:

These pterosaurs were comfortably over 250 kg, which puts them into small-horse range, so something that is "horse-sized" could definitely fly.  However, these are very differently shaped and scaled from ducks, as you can see.

One important difference is probably that pterosaurs launched from the ground using their wing muscles -- quadrapedal launching -- whereas birds use their legs; heavier leg muscles needed to launch a big bird are wasted weight in flight, while heavier wing muscles needed to launch a big pterosaur remained functional in flight. That re-emphasizes that big things are not just scaled-up small things, but need to reshape their bodies to cope with their size; the square-cube law is just part of it.


Can humans distinguish light having the same color but different spectrum?

If by "same color in RGB space" you mean "activates human cones the same way" then the answer is no: color perception is based on the ratio that different cones are activated at. There is no difference between a spectrum that has a smooth distribution across wavelengths or one that is properly calibrated into three or more specific peaks.

This concept is why RGB monitors and TV screens work to produce just about every color (though there are of course limits to the spectrum that a RGB monitor can produce, but that is a technological limitation).


How do afferent mechanoreceptors work on the finger pads?

Short answer
Tactile grating stimuli with a higher line density (number of lines per surface area) and applied with an equal force result in a lower amount of pressure per unit of skin area under the grating, and hence smaller afferent responses.

Background
In the Discussion section of the linked article (Phillips et al, 1993) the authors explain on p. 838 (left column) that the reduction in the response of SA afferents (slowly adapting fibers) when grating density is increased is due to the higher proximity of neighboring areas of stimulation, i.e., the lines in the grating stimuli are more closely spaced. The authors reason that this leads to a reduction in the effective stimulus (i.e., compressive strain) at the receptor terminal due to the presence of adjacent stimulus elements that distributes, and hence reduces the skin loads per line.

Reference
- Phillips et al, J Neurosci; 12(3): 927-39


Problem with bacterial transformation with electroporation

I did try another transformation:

again with our electrocompetent cells
Cells form other lab
chemically competent cells I made

The good thing is that on chemically competent cells there is no weir colonies, however efficiency of transformation was very low, but still, I think it is ok - will confirm it in next day if I really got the right insert.

On the other hand my electroporation still did not clear out. I got colonies on both our cells and cells from other lab, however in much lower amount there. I will try to change the cuvettes and try to use different electroporator as this seems to be the only thing that could make problems - although I am still not convinced about that :)

Thank you for your help and I will report the progress so if somebody else will have that problem again he could maybe benefit from my findings.


From a computer science perspective, how is DNA compared for various purposes?

From a computer science perspective, there's nothing at all special about DNA. It's stored as a simple ASCII text file consisting of repetitions of 4-15 different letters.

DNA, the molecule, is a long chain of nearly identical smaller molecules (nucleotides) joined together. The nucleotides differ only in which of four possible bases (A,C,T/U or G) they have attached. Therefore, when representing a DNA sequence, we only need to represent the bases.
There are also the so-called "ambiguity codes" which represent different possibilities:

IUPAC Code   Meaning
  A            A
  C            C
  G            G
  T/U          T
  M            A or C
  R            A or G
  W            A or T
  S            C or G
  Y            C or T
  K            G or T
  V            A or C or G
  H            A or C or T
  D            A or G or T
  B            C or G or T
  N            G or A or T or C

The vast majority of sequences, however, won't use the ambiguity codes and will only have A,C,T,G and the occasional N.

The most common DNA sequence format is FASTA, which consists of one or more sequences each of which has a header (lines beginning with a >) and 60-character long sequences. This, for example, is an excerpt of human chromosome 17:

>chr17
AAGCTTCTCACCCTGTTCCTGCATAGATAATTGCATGACAATTGCCTTGT
CCCTGCTGAATGTGCTCTGGGGTCTCTGGGGTCTCACCCACGACCAACTC
CCTGGGCCTGGCACCAGGGAGCTTAACAAACATCTGTCCAGCGAATACCT
GCATCCCTAGAAGTGAAGCCACCGCCCAAAGACACGCCCATGTCCAGCTT
AACCTGCATCCCTAGAAGTGAAGGCACCGCCCAAAGACACGCCCATGTCC
AGCTTATTCTGCCCAGTTCCTCTCCAGAAAGGCTGCATGGTTGACACACA
GTGcctgcgacaaagctgaatgctatcatttaaaaactccttgctggttt
gagaggcagaaaatgatatctcatagttgctttactttgcatattttAAA
ATTGTGACTTTCATGGCATAAATAATACTGGTTTATTACAGAAGCACTAG
AAAATGCATGTGGACAAAAGTTGGGATTAGGAGagagaaatgaagacata

So, in conclusion, there's nothing special about DNA. If you're writing software that compares DNA sequences, you are writing software that compares ASCII text. You can hash it, salt it and anything else you might want to do.

The only thing you should be aware of is that minor variations are very rarely meaningful. The level of identity you will need will depend on the precise biological question being asked but as a general rule, a single nucleotide difference is as likely to be a sequencing error as a real difference. You will need to collaborate with biologists in order to set up the right threshold for whatever your project is looking at.


Antigen presentation by MHC will induce a cytotoxic response by the immune system, which is usually a good thing in the body since most cells can just divide and replicate again.  Neurons, however, are particularly ineffective at regenerating from such an attack, and are not easy to come by; they are also rather important!  Better not to risk it, eh?

That being said, neuronal expression of MHC is actually a pretty complex case, and this open-access article is a good start down the rabbit hole (see also here, here, and here if you have access).


Which is the tissue damaging agent in krokodil (street desomorphine)

Note: Don't click on the links, or even search for information, if you don't have a strong stomach

From what I've read, it's not necessarily 100% known, most likely because it's not easy to study (small, reclusive users who die quickly of a complex concoction) but the line everyone has quoted is:

  "They extract [the drug] and even though they believe that most of the oil and gasoline is gone, there is still remnants of it. You can imagine just injecting a little bit of it into your veins can cause a lot of damage… it eats you from the inside out".

That's from Dr. Frank LoVecchio in Phoenix, Arizona, who saw two cases within a week.  It's not hugely scientific, but it's not wrong.  Krokodil is never pure and highly toxic chemicals are thus injected into the veins.  If you want specifics, then gasoline, hydrochloric acid, phosphorous scraped off matchboxes, paint thinner, iodine, and cleaning oils.  Injecting any one of those should be enough to kill a repeated user.  Those substances rupture blood vessels, and the subsequent leakage creates gangrenous wounds like you see in the pictures.


Why should evolution not be equated with progress?

I'm glad you've asked the question as it is a common layman misunderstanding.

Dog vs Human

Your example comparing humans and dogs is actually very central to the logical flaw that yields many to equate evolution with progress.

There are several issues when you say

  humans do seem to be more advanced than dogs

Humans are not more evolved than dogs

Humans, dogs, jellyfish, oak tree, fungi, bacteria, .... we have all evolved during about 3.5 billion years. None of the extant lineages is more evolved than any other at least in terms of the number of years of evolution. Note, however, that what matters most when considering evolutionary time is the number of generations. Humans having a rather long generation time, it tends to make fewer generations. In this regard, one could expect a dog to have been through more generations than humans and could eventually be called more evolved but even there it is not that easy. See also Are we “more evolved” than present-day bacteria?

You are a human, be aware of your biases

As @Jamesqf rightly said in the comments, you did not feel like considering the dog's extraordinary sense of smell, better hearing, higher jumps, stronger jaws or protective fur. Not to mention, dogs can typically raise way more offsprings than humans can. Not to become personal but my 8 months old, 9 kg Cocker Spaniel runs 300 meters at the same time Usain Bolt runs 200 meters! You seem to have only considered things that make you human such as opposable thumbs and high cognitive abilities. Coming to cognitive abilities you will note that a puppy learns by association faster than a baby human. Dogs just plateau much quicker than humans.
Make sure that you understand that high cognitive abilities are not a goal or a direction of evolution. While it is hard to measure the evolution of intelligence for both a question of definition and question of measurement tools, it is very very likely that many lineages (incl. eventually the Homo lineage) have evolved toward reducing intelligence at some point (see this post).
You say humans could wipe out dogs from Earth however again it feels very human (and awkwardly combative and hostile) to consider the ability to kill as a measure of progress.

The illusion of considering two variables

You consider a correlation between two variables 1) how evolved a lineage is and 2) how advanced a lineage is. (As discussed in the first point, there is actually no variance in how evolved lineages are if we consider evolutionary time). You are determining those that are more evolved by how "advanced" you visualize the lineage. Your explanatory and response variables are therefore the same and you do not explain anything by saying 'humans are both more advanced and more evolved than dogs so evolution should equate progress'

Definition of progress

A big issue in your question is the definition of progress. For example, if you define progress as an increase of mean fitness (the concept of fitness in biology has nothing to do with bodybuilding, see here) over time, then yes evolution is in part to be equated with progress as increase in mean fitness over time is exactly what natural selection is doing (see the so-called Fundamental Theorem of Natural Selection).

Evolution ≠ Natural Selection

So, let's assume we define progress as an increase in mean fitness over time. As stated in the previous section, this is exactly what natural selection is doing. So, instead of saying Evolution should not be equated with progress, one could say Natural selection is to be equated with progress (as a reminder this assumes a very specific definition of progress)

You will note that I replace the term evolution with natural selection. It is often unclear to laymen but these two terms, while related, are different.

Evolution is a change of allele (loosely speaking, an allele is a variant of a gene) frequency over time. There are a number of mechanisms that can cause evolution, one of which is natural selection (which itself is caused by a fitness differential associated with genetic variance). But there is way more to evolution than just natural selection. Genetic drift, mutations, migration and other demographic elements are all important factors causing the evolution of populations.

You should have a look at Understanding Evolution by UC Berkeley. It is a very introductory online course on evolutionary biology that will teach you about the basic forces that cause evolution.


What is this creature I found on my house?

Well, your question ended up being closed... If I understand it correctly, you simply asked "what is this creature?" and, after that, you asked "what species is this?". That being the case, the question seems to be clear enough to me.

Therefore, let's see:

What is this creature?

It's a caterpillar of a moth from the Genus Orgyia.

What species is this?

The Wikipedia link above lists more than 40 species. Here is, for instance, Orgyia antiqua:

And Orgyia leucostigma:

But my guess is that your specimen is Orgyia australis (specially if you live here down under):

Adding your location will greatly improve the chances of defining the species inside that genus.

Conclusion

That's simply a caterpillar (larva) of a moth from the Genus Orgyia. Narrowing it down to the species depends on you adding more information to the question, specially geographic location.


Why does our body regulate metabolic processes using the thyroid hormone?

The answer is in special situations, where a trade-off has to be done between thermogenesis and energy saving. This applies to hibernation of animals as well as to critical illness in humans.

This kind of adaptation is referred to as TACITUS syndrome (thyroid allostasis in critical illness, tumours, uraemia and starvation), NTIS (non-thyroidal illness syndrome) or ESS (euthyroid sick syndrome). In this situation, total and free T3 are downregulated, and, in special cases, TSH and T4, too. See an open review article by Wajner and Maja, which is available from http://dx.doi.org/10.3389/fendo.2012.00008 , for details.


The range from mean to maximum of wolve's bite force is huge.

Is it really? According to this Wikipedia page, (Scully, C. (2003). Oxford Handbook of Applied Dental Sciences. p. 151) claims that human masticatory forces range from 70 N to 700 N. Also, (Kim et al., 2018) claims that domestic dogs have a bite force of (147-3417) N, so I don't think it's too implausible for wolves to have the value of (774-2255) N of wolves that @Olga_Swider claims. We see also, on Table 4 on p. 550 of (Eng et al., 2013), the estimated maximum bite force (MBF) spread over the $M^2$ area of the jaw. Eng claims that Gorillas and Chimpanzees have MBFs of 3200 N and 1800 N respectively. I think there's quite a large degree of control of masticatory muscles, which wouldn't make it too surprising that you can have a large range of forces.

  This range of wolves' bite forces could put them on par with big cats.

According to p. 621 of (Wroe et al., 2005), lions have a bite force of around 1768 N, while tigers have a bite force of 1525 N. So, it seems that wolves have a significantly smaller mean bite force than big cats. But bear in mind that while dogs and wolves might have a fairly similar jaw size, lions jaws are much larger so their bite force is spread over a much greater area. So exercise caution when comparing them. Similarly, note that PSI is a unit of pressure (force over area), while newtons are a unit of force.

  Why isn't there a maximum bite force for wolves?

Says who? Of course there's a maximum. Wolves can't make arbitrarily large forces with their mouths, that's physically impossible.


How many phosphates are in the 5' end of a DNA strand?

The DNA polymerase can only extend a primer and therefore almost all lifeforms have a primase (which is a type of RNA polymerase) that synthesizes RNA primers at the replication origins that the DNA polymerase can extend.

As you guessed, the 5' end would indeed have a triphosphate.

  Organism            Template Sequence        Primer Synthesized
Herpes simplex-1        3′-GPyPy                 pppPuPu
T4                      3′-TTG                   pppAC
T7                      3′-CTG                   pppAC
E. coli                 3′-GTC                   pppAG
S. aureus               3′-ATPy                  pppAPu
S. aureus               3′-ATPy                  pppAPu
A. aeolicus             3′-CCC, CCG, CGC         pppGG, pppGC, pppCG
B. stearothermophilus   3′-ATPy                  pppAPu
Human                   3′-PyNN                  pppPuNN
Calf                    3′-PyNN                  pppPuNN

  Initiation sites used by primase from different sources. Pu = purine, Py = pyrimidine, N = any base ppp = the triphosphate on the 5′-end of the primer. Those bases that are required but do not code for a base in the primer (“cryptic” nucleotides) are underlined and in bold.

  Kuchta and Stengel (2010)

In the final stages of replication, these RNA primers are removed by RNAseH and DNA polymerase I in bacteria and the gaps are filled by the latter (Cooper (2000) The Cell). In eukaryotes, the primer is removed by the action of Fen1 and Dna2 exonucleases and the gaps are filled by DNA polymerase δ (Burgers 2009).

In PCR, it is quite straightforward: the product will have whatever 5' modifications the primers have (usually none).


How can epigenetic changes be erased if they are inherited?

I have done a presentation in epigenetics and the main topic was imprinting.
This paper will answer all your questions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941233/
I am adding some glimpses from this  paper here
Mammals are diploid organisms whose cells possess two
matched sets of chromosomes, one inherited from the mother
and one from the father. Thus, mammals have two copies of
every gene. Normally both the maternal and paternal copy of
each gene has the same potential to be active in any cell.
Genomic imprinting is an epigenetic mechanism that changes
this potential because it restricts the expression of a gene to
one of the two parental chromosomes. It is a phenomenon
displayed by only a few hundred of the approximately 25,000
genes in our genome, the majority being expressed equally
when inherited from either parent. Genomic imprinting affects
both male and female offspring and is, therefore, a consequence
of parental inheritance, not of sex. As an example of
what is meant by this, an imprinted gene that is active on a
maternally inherited chromosome will be active on the maternal
chromosome and silent on the paternal chromosome in
all males and females.

Hope this help and please ask if you do not understand the paper.Thank you


Biphasic T wave caused by digitalis toxicity

Digitalis (which was by the way originally synthesized from Digitalis Purpurea) has two mechanisms of action:

The action by which digoxin improves contractility appears to be inhibition of the sarcolemmal Na$^+$K$^+$-ATPase "pump", normally responsible for maintaining transmembrane Na$^+$ and K$^+$ gradients
The major therapeutic electrical effect of digoxin occurs at the AV node, where it slows conduction velocity and increases refractoriness.

So it has a mechanical and an electrical mechanism. About the toxicity:

For example, in atrial and ventricular Purkinje fibers, a high dixogin concentration has three important actions that may lead to dangerous arrhythmias:

less negative resting potential

decreased action potential duration

enhanced automaticity

All quotes are from the book Pathophysiology of Heart Disease by Leonard S. Lilly, 5th edition.
So, I would assume one of the three (or a combination of them) is the reason for the biphasic T-wave. I hope someone more experienced can improve upon this answer.
This maybe has something to do with the relative refractory period ending during the T-wave.
Also, since the figure is from lead I, you can use that information for looking at where the net electrical axis is pointing at during the T-wave. Refer to the hexaxial system.


How much energy is required to blind someone?

Light can affect retina in many ways [1]:

photothermal mechanisms - exposure to intense flashes of less than 20 microseconds that cause a rise in temperature of at least 10 degrees Celsius [5];
photomechanical mechanisms - exposure to flashes shorter than 5 nanoseconds [5];
photochemical mechanisms - light is absorbed by a chromophore and leads to the formation of an electronically excited state of it, resulting in chemical transformations [5].

The retina is more susceptible to light induced degeneration at lower wavelengths [2, 8]. The damage degree also depends on intensity and exposure duration. 12 hours a day of more than 500 lux light, more than three consecutive days can affect rat retina [3]. 2 hours  exposure to white light of 3000 lux has lead to apoptosis in rats retina [4].

Sunlight irradiance is about 11 W/cm2 (ranges between 1.5 and 122 W/cm2) and causes damage when exposure time is tens of minutes or even less [5].

Light induces apoptosis by different mechanisms:

  Intense light triggers cell death in cones and rods by two distinct mechanisms: rapid, necrosis-like cell death occurs in cones; prolonged, apoptotic death is displayed by rods. However, the areas of cone and rod loss coincide, suggesting some interrelationship [6].

Cones and rods have different vulnerability [7].

References:

Youssef PN, Sheibani N, Albert DM. Retinal light toxicity. Eye (Lond). 2011 Jan;25(1):1-14. doi: 10.1038/eye.2010.149. PubMed PMID: 21178995.
Rozanowska, M. B. (2012), Light-Induced Damage to the Retina: Current Understanding of the Mechanisms and Unresolved Questions: A Symposium-in-Print. Photochemistry and Photobiology, 88: 1303–1308. doi: 10.1111/j.1751-1097.2012.01240.x
Jin X, Wu L, Zheng H, Mishima S. [Retinal light damage: I. The influences of light intensity and exposure duration at moderate and low intensities of cyclic light]. Yan Ke Xue Bao. 1998 Dec;14(4):215-9. PubMed PMID: 12579740.
Remé CE, Weller M, Szczyesny P, Munz K, Hafezi F, et al. Light-induced apoptosis in the rat retina in-vivo. In: Anderson RE, LaVail MM, Hollyfield JG, editors. Degenerative Diseases of the Retina. Plenum Press; New York: 1995. Via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831109/
Malgorzata Rozanowska, Bartosz Rozanowski, Michael Boulton. LIGHT-INDUCED DAMAGE to the RETINA (2009). Available from http://www.photobiology.info/Rozanowska.html (accessed 20.07.2014).
Cortina MS, Gordon WC, Lukiw WJ, Bazan NG. Light-induced photoreceptor damage triggers DNA repair: differential fate of rods and cones. Adv. Exp. Med. Biol. 2004;533:229-40. PubMed PMID: 15180269.
Okano K, Maeda A, Chen Y, Chauhan V, Tang J, Palczewska G, Sakai T, Tsuneoka H, Palczewski K, Maeda T. Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage. J. Neurochem. 2012 Apr;121(1):146-56. doi: 10.1111/j.1471-4159.2012.07647.x. PubMed PMID: 22220722.
Kuse Y, Ogawa K, Tsuruma K, Shimazawa M, Hara H. Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light. Sci Rep. 2014 Jun 9;4:5223. doi: 10.1038/srep05223. PubMed PMID: 24909301.


Rice left in water for several months - what biological reactions or growths would occur?

It is likely a volatile organic compound (VOC) that is released as a by-product of microbial metabolism, although microbes can also produce some inorganic compounds, such as hydrogen sulfide (rotten egg smell). It could be any of a number of compounds, depending on the microbial species and the environmental conditions. The only relevant paper I could find based on a cursory search was by Yanqiang et al. (2013) on volatile compounds released from the anaerobic digestion of food waste in general; based on the results, the odor likely consists of a complex mixture of gases, and may be especially rich in aromatic compounds. Whether it could have any negative health effects is challenging to prove, but you would likely want to avoid exposure.

I presume that your container is made of plastic or at least contains a silicone ring. You can remove odors from metal or glass by washing them, but porous substances like plastics, rubber and the like will absorb volatile compounds, rendering them largely inaccessible to solvents such as water, and will release them slowly over time, which you can perceive via olfaction as you have noticed. If you want to eliminate the odor faster, you will need to accelerate this outgassing process. The way this is usually done is by baking in an oven (optimally in a vacuum, although this is not necessary). The rate of outgassing grows exponentially with the temperature, so you should use the maximum temperature that the material in question can withstand.


That's a nice female Dolomedes tenebrosus - the upland Fishing Spider that lives in similar habitat to Wolf Spiders, and eats the same sort of foods.
The way it holds its long, stripey legs together (the front pair, anyway) is pretty standard for the Pisauridae, and the pattern on the body (while a bit variable in this species) is pretty distinctive.

https://bugguide.net/node/view/2011


Automatic cropping of collimated digital X-ray images

There is a software package ImageJ which can be used to what you are asking. Depending on your capability and the complexity of what you are doing you can either write a Macro in the program to crop images or you can extend the program in Java and write a custom plugin to do what you describe.

I used this program for years it is a very strong program.


Best data repository to publish a large 'plotly' table containing all annotations on a transcriptome?

Journals and services where you can submit your script and manuscript and get DOI:

PLOS One
F1000
Zenodo
CodeOcean


What is the name/type/species of this spider?

I presume it is Eratigena atrica, commonly called the giant house spider.

It belongs to      Agelenidae family.

  E. atrica is found in Europe, Central Asia and Northern Africa. It was unwittingly introduced to the Pacific Northwest of North America circa 1900 due to human activity and has strongly increased in numbers for the last century.

Reference: Wikipedia


Is it possible to have different genes in different parts of our body?

The general answer is that no, it's not possible to have different genes in different parts of the body.  There are two interesting classes of exceptions, but they are exceptions.

The first is that mutations can and do occur in cells during their growth.  Most of these are probably neutral - they occur in the vast wasteland of genetic junk in the chromosome, and nothing happens.  But some of them are harmful, and this is what puts cells on the pathway toward cancer.  Outright cancers, that we can detect, are the result of at least a half-dozen mutations occurring in the same cell lineage, that cumulatively allow the cells in that lineage to grow in uncontrolled manner, to avoid immune clearance, to encourage their own blood vessel growth, and so on.  (In fact, cancer cells generally have far more than a half-dozen mutations, because a route toward getting the mutations they need is to turn down DNA repair, allowing mutations to accumulate with minimal control.  For example, Genomic landscape of DNA repair genes in cancer, Genomic profiling of pediatric acute myeloid leukemia reveals a changing mutational landscape from disease diagnosis to relapse.)

The second set of exceptions is in the immune system.  Both B cells and T cells specifically modify their chromosomes during their development, making huge numbers (trillions) or new genes.  The catch is that these are all in the same region, the antibody or T cell receptor genes.  It's part of the mechanism by which the adaptive immune system "remembers" which pathogens it's interacted with in the past.  The wikipedia article on V(D)J recombination is a starting point.


Why eukaryotes have three different types of cytoskeleton filaments?

While eukaryotes contain tubulin-containing microtubles and actin filaments, prokaryotic homologues do exist.
For example FitZ protein, the most common bacterial Tubulin homologue[1], is involved in cell division. Genes for this protein are actually present in eukaryotic nuclear DNA and the protein facilitate the division of the mitrochrondria and chloroplast organelles which were created by endosymbiosis[2].

Similarly, MreB, functions as the most common prokaryotic analogue of actin.

Regarding IF filaments, certainly subsets such as nuclear lamins are uniquely found within Eukarya, however a paper published by Bafchi[4] has suggested that IF-like proteins are present within bacteria.

Bi, E., & Lutkenhaus, J. (1991). FtsZ ring structure associated with division in Escherichia coli. Nature, 354(6349), 161-164. doi:10.1038/354161a0
Margolin W. FTSZ AND THE DIVISION OF PROKARYOTIC CELLS AND ORGANELLES. Nature reviews Molecular cell biology. 2005;6(11):862-871. doi:10.1038/nrm1745.
Gunning, P. W., Ghoshdastider, U., Whitaker, S., Popp, D., & Robinson, R. C. (2015). The evolution of compositionally and functionally distinct actin filaments. Journal of Cell Science, 128(11), 2009-2019. doi:10.1242/jcs.165563
Bagchi S, Tomenius H, Belova LM, Ausmees N. Intermediate filament-like proteins in bacteria and a cytoskeletal function in Streptomyces. Molecular Microbiology. 2008;70(4):1037-1050. doi:10.1111/j.1365-2958.2008.06473.x.


What is the evolutionary explanation for bat's echolocation

The main reason for bats to "develop" their echolocation system was the avalability of an almost empty niche: Hunting insects at night. Birds are not able to hunt without light and here is where the bats come in. They are able to hunt at night and also to live and orientate in environments where they are protected over the day: Caves. Bats at night are also protected from predatory birds.

There is are a few interesting sources if you want to dive deeper into the stuff:

The evolution of flight and echolocation in bats: another leap in
the dark
Echolocation in bats
Evolutionary aspects of bat echolocation


Calculating fraction of protein unfolded from spectroscopy data

I've plotted the data for ease of answering, though it is not necessary if you know what to look for in the data.

As expected, the melting curves are sigmoidal with horizontal asymptotes at approximately 0.5 and 1. You should be able to see this in the raw data as well: the absorbances hover around 0.5 before rising rapidly and then plateauing around 1.

You want the fraction of unfolded protein as a function of absorbance, so you need to normalize this data to the range of [0,1]. There's a straightforward formula for this which, put into the terms of your question, would be:

$f = \frac{A_{222} - min(A_{222})}{max(A_{222}) - min(A_{222})}$

$f = \frac{A_{222} - 0.5}{1 - 0.5}$

$f = \frac{A_{222} - 0.5}{0.5} = 2(A_{222} - 0.5)$

Intuitively, you might think about it as follows: at low temperatures, when the protein is folded, absorbance is 0.5. Consider this a blank or baseline measurement which gives the absorbance of the solution when no protein is unfolded. Since you are only interested in the signal from unfolded protein, you can subtract this value (0.5) from the rest of the data.


Are there specific non-protein substances that pathogens release into their host?

Sticking my neck out (and expecting it to be bitten by a black swan) it appears that all the examples of toxins secreted by bacterial pathogens when they infect an animal host (exotoxins) are proteins.

However fungi secrete a variety of exotic (and often very nasty) small non-protein molecules (mycotoxins). It’s not clear from the question whether you would be interested in these systems as they differ somewhat from those involving bacteria. One difference from bacterial toxins is that fungal toxins not secreted inside an infected cell, but just into their environment. Thus, cercosporin is secreted onto the surface of plants on which Cercospora reside and may be taken up through lesions in the plant. However it is not clear whether the plant is the main target of such toxins, rather than bacterial ‘foes’. So the host/pathogen concept is less clear in this context.

A similarly ambiguous host/pathogen situation would appear to exists with toxins such as saxitoxin, the paralytic shellfish toxin secreted by certain marine algae and cyanobacteria.


Why don't we keep evolving until we are super-human?

Welcome to Biology.SE!

There are a many misunderstanding of what evolutionary processes are in your post and it is therefore quite hard to answer (hence the current two close votes I guess). You might want to read some introductory textbook on evolutionary biology or other online resources such as the "understanding evolution" project.

The most obvious misunderstanding is that evolution is NOT some kind of forever "improvement" process in a static environment. Evolution is something else! But I can't make a good overview of evolutionary processes in just one post.

  [why don't we live on] average of 300 years?

You may want to read about this post concerning the evolution of aging but it would probably be slightly too advanced but you would probably still get something out of the answers.

  Why don't we just keep evolving [..]?

Humans, definitely keep evolving. Nothing have stopped. We evolved as we have always and it won't stop until we get extinct! This post may for example help you to understand that evolution keep occurring today in humans.

When you say Humans (homo sapiens) have been on the earth for thousands of generations it sounds a bit like human have came to existence some time ago and have evolved since. It is a terribly misleading point of view, one of the reason is that one cannot date the existence of the first humans without making a very arbitrary decision about what a human is. A more correct way of looking at life on earth is that everything have come to existence about 3.5 billions years ago and everything have kept evolving since. Any single living thing on earth have been evolving for the exact same amount of time. Humans have evolved for 3.5 billions (even if we don't call earlier forms as humans) and unicellular algea have evolved for 3.5 billions years (even if we don't call earlier forms as algea).

Hope that helped!


How does taxonomy work? The case of the Avian Dinosaurs

There was a taxonomic revolution brought about by cladistics https://en.wikipedia.org/wiki/Cladistics. Willi Hennig wrote about it in 1950, but he was an East German, and his work did not gain traction in the West until it was translated into English in the late 1960s. Then it took a while to become consensus. Since then, all taxonomy is based on phylogenetic relationships. So for 100 years, we talked about "Reptiles" and knew what they were. Under phylogenetic taxonomy however, once we understood that birds were descended from theropod dinosaurs, nomenclatural rules require that birds ARE dinosaurs. This makes sense, because a Robin is more closely related to a Tyrannosaurus than a Tyrannosaurus is to an Iguanodon. Technically, taxonomy changes with the publication of phylogenies that make formal nomenclatural changes. Once a peer-reviewed paper is published, the names change. But sometimes phylogeny papers are sloppy, or wrong. So for something as major as Avian Dinosaurs, it would generally take more than just one sloppy paper to change consensus. Scientists now consider birds to be Dinosaurs. The public will continue thinking of Dinosaurs without birds. This is a difference between common names and scientific names. Birds are a subgroup of Dinosauria. Consensus depends on whether you are a scientist or not. Scientists now are at a consensus that Birds are derived from theropod dinosaurs, and therefore, ARE dinosaurs. The consensus of the public will lag behind.


What is a good source for info on disease frequency distribution among age groups?

You may need to study each disease individually or do a literature review.  The Online Mendelian Inheritance in Man website may be a good starting point http://www.omim.org/
The Centers for Disease Control and Prevention lists several diseases with a variety of different statistics here:  http://www.cdc.gov/DiseasesConditions/


What is the advantage of restriction enzymes cutting only at specific sites?

Such universal restriction enzymes would be very dangerous to leave lying around even if contained within a vacuole. Remember that bacteria are prokaryotes and have no nuclear membrane to protect their DNA.

The analogy would be having a burglar alarm capable of burning down the house in order to protect it against thieves.


The spider in question is actually Xysticus Cristatus, also known as the common crab spider.

From Wikipedia:

  The adult female reaches a length of 8mm and the smaller male 5mm. The colour varies from light cream, dark brown to greyish with a dark triangle on the carapace which ends in sharp, defined point. The abdomen has a broad middle band fringed by two darker rows of triangular marks which extends back to about two thirds of the carapace length from the posterior row of eyes. ... Active adults have been recorded from February to December, with a peak of male activity in May and June. ... The species has a Palearctic distribution, being found throughout Europe, including Iceland.

Arachnology.cz provides several photos of the species. The image below is a perfect match.

Copyright by Rudolf Macek; published at https://www.arachnology.cz/druh/xysticus-cristatus-800.html; page viewed in May 2019


Is the swimming pool water harmful to frogs who jump in? If so, how?

The chlorine concentration in pools is +- 0,5 mg/L.

+

  0.002 mg/L will fatally damage the sensitive skin on tadpoles, frogs, salamanders and other amphibians.

another source:

  Free chlorine (Cl2) is a greenish gas that is well known for its
  highly toxic properties as can be attested to by the thousands of
  soldiers that died and were severely injured from chlorine exposure
  during World War I. In water, chlorine is the most toxic substance
  that we will discuss. Ironically for the amphibian keeper, it is this
  toxic nature of chlorine and its ability to denature proteins, which
  makes its encounter inevitable. Chlorine is generally used as an
  antibacterial agent in municipal water supplies and may be present in
  concentrations of over 9 mg/1 in some tap water (measured in Houston,
  Texas as an example, although levels were generally lower). The
  concentration of chlorine in municipal water supplies can vary greatly
  from day to day, or even hour to hour, depending on conditions at the
  water treatment facilities. Concentrations as low as 0.0034 mg/1 have
  been noted to reduce reproduction in fathead minnows with 72 hour
  LC100 (lethal concentration for 100% kill) at 0.15 mg/1 (Arthur and
  Eaton,1971). LC50 (96 hour) for the shiners (Notemigonus chrysoleucas)
  was as low as 0.19 mg/1 (Esvelt et al., 1971). The concentrations
  found in municipal water supplies are many times greater than the
  minimum lethal concentrations for many aquatic life forms.

Thus, the well being of the frog in the water of the swimming pool depends on the time the frog spends in the water. Eventually, with extended exposure the chlorine concentration will exceed the one compatible will life and the frog will die. This time is multifactorial variable, thus cannot be assessed easily - the weight and the skin surface area and skin permeability will affect the frog survival in a great degree.


Parallels between pixelized image and the human retina

The pixels of the visual system are represented by the photoreceptors. Their shape is the following (adapted from "The Brain from Top to Bottom, MgGill University"):

There are about a 180 photoreceptors packed on 288 microns on the retina (see "What's the smallest size a human eye can see?") so about 1 pixel per 2 microns. The rods and cones are packed closely together on the retina, referred to as the retinal mosaic. This retinal mosaic is not unlike a photosensitive chip, as can be seen on the folllowing image (Developmetal Neurobiology lab, UCLA, Santa Barbara):

We do not visually perceive this mosaic, as the optics of the eye (e.g., light diffraction by the cornea and the lens, and distortions due to the relatively large pupil size) prevents optimal use of the photoreceptor density (the maximal resolution). Furthermore, especially outside the field of view (the foveal region), the output of many photoreceptors are funneled onto one single optic nerve fiber, thereby fusing the output of many photoreceptors (See the question "Why can we not see around our point of focus of our eyes?"). Lastly, the brain actively 'glues' any gaps in the visual field together. Most strikingly, the blind spot, which is the place where the optic nerve exits the eye is fairly large, is normally not visible to us: see the following picture (PNAS online content):

Hence, any gaps in the retinal image are in fact actively smoothened out by the brain.


How does a plant grow before photosynthesis is possible?

There are quite a few questions and thoughts in there, I'll try to cover them all:

First, to correct your initial word equation: During photosynthesis, a plant translates CO2 and water into O2 and carbon compounds using energy from light (photons).

You are correct to assume the C is further used for the growing process; it is used to make sugars which store energy in their bonds. That energy is then released when required to power other reactions, which is how a plant lives and grows. C is also incorporated into all the organic molecules in the plant.

Plants require several things to live: CO2, light, water and minerals. If any of those things is missing for a sustained period, growth will suffer. Most molecules in a plant require some carbon, which comes originally from CO2, and also an assortment of other elements which come from the mineral nutrients in the soil. So the plant is completely reliant on minerals.

Most plants, before a leaf is established or roots develop, grow using energy and nutrients stored in the endosperm and cotyledons of the seed. I whipped up a rough diagram below. Cotyledons are primitive leaves inside the seed. The endosperm is a starchy tissue used only for storage of nutrients and energy. The radicle is the juvenile root. The embryo is the baby plant.

When the seed germinates the embryo elongates, the endosperm depletes, the testa ruptures, and the cotyledons emerge from the seed. The cotyledons are green, and like leaves can photosynthesise, so as soon as they are in the light the plant is able to make carbon compounds. The radicle elongates at the same time, and becomes the root, so the plant is very quickly able to obtain fresh nutrients from the soil (or whatever it's growing in).

At all stages of a plant's life it is using both energy stored in carbon compounds (from CO2) and nutrients which it took up via its roots. At no point does the plant start to depend solely on the CO2 in the air for its growth.

You are right that the way in which plants acquire energy and nutrients prior to leaves and roots being established varies between plants. Above I outlined the way most plants use. But there are lots of variations. For example, orchids have very tiny seeds, some barely visible to the naked eye, like specks of dust. They have no endosperm or storage tissue, so they have to rely on a symbiotic mycorrhizal fungus to get carbon and nutrients. The fungus grows through the coat of the orchid seed, then provides everything the growing plant needs until it has its own leaves. Then the orchid repays the fungus by providing sugars.

There are lots of other examples, but we could go on all day!


Most painless method for killing insects

The terrestrial invertebrate taxon advisory group of the Association of Zoos and Aquariums recommends anesthetizing the insects with carbon dioxide and then placing them in a freezer to euthanize them.


Identify this large exotic bird spotted in Taipei, Taiwan

For me it looks like a Malayan Night Heron, Gorsachius melanolophus.

They seems to be common in this part of Asia, see the distribution.

It looks strange because he probably get scared.


How is it possible for only one in five children to have brown eyes when their parents both have brown eyes?

Possible...yes of course! The answer could stop there but I guess you want to ask how likely it is.

Here is a chart of probability of a given kid to have eyes of a certain color given the parents eyes color. (Note that the second column contain probabilites and not odds contrary to what the figure is stating).

The probability that $k$ kids out of $n$ have eyes of a color which appears with probability $p$ is given by the probability mass function of the binomial distribution $\binom{n}{k} p^k (1-p)^{n-k}$

Knowing that both parents have brown eyes (even for your oldest sister):

The probability that exactly one out of 5 offsprings have brown eyes (and the others have eyes of another color) is about 0.015 (3 out of 200).
The probability that exactly 3 offsprings have blue eyes (and the others have eyes of another color) is about 0.0021 (2 out of 1000)

You might want to calculate the probability of having $k$ or more kids that have eyes of a given color (a p.value) is obtained by summing probabilities. For example, the probability that 3 or more kids (out of 5) have blue eyes is  $\binom{5}{3} 0.0625^3 (1-0.0625)^{5-3} + \binom{5}{4} 0.0625^4 (1-0.0625)^{5-4} + \binom{5}{5}  0.0625^5  (1-0.0625)^{5-5} ≈ 0.0022$

Learn more about Stats

You'll probably want to learn a bit about statistics if some things are unclear. You might want to make sure you understand the concept of p.value and its interest and make sure you understand what a binomial distribution is. You may also want to understand the concept of multiple testing to avoid falling in simple pitfalls.


How long does it take a leech to attach?

Apparently, the leech won't wait for you to swallow it, but it'll attach in your aerodigestive tract as soon as it's in it. This case study of children who drank leech-infested water explains pretty well (and in a rather graphical way, in my opinion) what happened to them. I'll copy here just an excerpt (emphasis mine):

  A seven year old girl was brought from a remote village (Kamardin Karaiz) with four days history of cough with blood stained sputum after drinking water from a pond. She also developed pain in her throat and was unable to swallow except for liquids. [...]
  Her coagulation profile was with in normal limits however her hemoglobin level was 9 g/dl. [...]
  On direct laryngoscopy a leech was found attached to the right pyriform fossa with its one end in the glottis which was removed immediately. The patient made a smooth postoperative recovery. On recovery the patient had no dyspnea, stridor or dysphagia and was discharged the next day on oral antibiotics.

This article also reports a historical case of a leech attached into the throat of a Pashtun man in India. The leech was removed with no consequences.

In short, leech ingestion will probably result in having a leech sucking your blood from inside your throat. Although removing it will probably grant a full recovery, it doesn't seem a pleasant experience.


Can MHC class I be used for presenting peptides of extracellular origin by non-professional APCs?

when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria

Dendritic cells and probably neutrophils are professional APC, so this part of the question is a little confusing.

You're asking about cross-presentation, which is the process by which extracellular antigen can be presented to CD8 T cells on MHC class I.  Cross-presentation is mainly performed by certain sub-classes of dendritic cell. A number of other cell types have been shown to be capable of it, but it's not clear how important they are in vivo.

A decent review of cross-presentation is Understanding the Biology of Antigen Cross-Presentation for the Design of Vaccines Against Cancer.  A review of a related but somewhat different concept (MHC recycling) is Endocytic Recycling of MHC Class I Molecules in Non-professional Antigen Presenting and Dendritic Cells.


How is oxygen and carbon dioxide exchange mediated by hemoglobin?

Under conditions of high CO2 (in tissues such as muscle) and hence high acidity hemoglobin binds preferentially CO2, thereby mediating CO2 removal. Under conditions of low CO2 (high pH) and high O2 (conditions met in the lungs), it preferably binds O2, thereby releasing CO2. Hence, the specific characteristics of hemoglobin allow for CO2 uptake in the body, and O2 uptake and CO2 release in the lungs. Info from wikipedia on hemoglobin


They should be Red Imported Fireants.
https://en.wikipedia.org/wiki/Red_imported_fire_ant


After a long hunt it seems they are Dermanyssus gallinae. It appears I have a pigeon's nest somewhere near my building.

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


I cannot give a thorough answer right now (if I even find one) because I'm on my phone, but here are some papers that could inform the question in the meantime (or their abstracts at least!)
One element I have gathered so far is that the evolution of nervous systems likely involved not the evolution of wholly new molecules and structures, but the cooptation of existing structures for new purposes. Meaning the first neurotransmitters would have been pre-existing with some other purpose in early proto-neurons, not new molecules evolved expressly for the first synapses. One paper talks about neurotransmitters like dopamine being common across all life, including plants (no nervous systems there!). This does not answer which of these molecules would have been the first neurotransmitters however.
The abstract of this paper doesn't say much but the title is tantalizing:
https://link.springer.com/chapter/10.1007/978-3-319-20215-0_2
"New Trends and Perspectives in the Evolution of Neurotransmitters in Microbial, Plant, and Animal Cells"
This paper shows a unicellular eukaryote reacting to various neurotransmitters. If the full paper goes into the phylogeny some more it might be interesting:
https://sciprofiles.com/publication/view/0cc41fa28399e0e366d3199c3bcc48eb
"The Phylogenetic Background of Neurotransmitters in the Unicellular Organism Tetrahymena Pyriformis"
This paper's abstract says all I was saying about the development of neurons and synapses relying on pre-existing molecules and structures:
https://pubmed.ncbi.nlm.nih.gov/2830635/
"Evolution of Neurotransmitter Receptor Systems"
What I'm looking for to find how close science is to answering your question (or if it already has) is papers looking at the phylogenetic relationships of different neurotransmitters and related molecules. That might say a lot about which ones have been used as neurotransmitters the longest. I haven't found this yet but I'll try more tomorrow when I'm not on mobile.
ETA: will re-edit this comment later, but this paper answers your question I believe, or as well as any could at present at least:
https://cichlid.biosci.utexas.edu/sites/default/files/evoneuro/files/liebeskind_et_al_2017.pdf?m=1511200627
"Evolution of Animal Neural Systems"
This paper, which is available in full and is a review paper from 2017, looks at the evolution of every aspect of animal neural systems (i.e. nervous systems mediated by neurons, a concept the paper also defines because the line is apparently blurry). One interesting aspect of it is that while you point to Cnidarians as the most "primitive" nervous systems, the paper points out the latest evidence suggests Ctenophores are the earliest branch off the animal tree, meaning nervous systems either evolved convergently, or sponges lost their nervous systems secondarily, in which case Cnidarians would lose this special status.
The paper has a section about neurotransmitters, which says the following:

Several types of molecules are used as neurotransmitters; their evolutionary deployment in different synapse types across animals is fascinating and still poorly understood. Many are used widely in eukaryotes for intercellular communication, but some of the biogenic amines may be present in animals as a result of the late horizontal transfer of synthesis enzymes from bacteria(Iyer et al. 2004). For instance, epinephrine and norepinephrine are important neurotransmitters in vertebrates but not in protostomes (but see Bauknecht & Jekely 2017), whereas the opposite is true of octopamine and tyramine (Figure 4). Cnidarians make a set of neurotransmitters similar to those in vertebrates (Kass-Simon & Pierobon 2007), but Nematostella expresses most nonpeptide types in the endoderm near the pharynx and testes—only peptide transmitters are found in neurons(Oren et al. 2014)
Intriguingly, ctenophores seem to use a much more restricted set, as glutamate is the only well-validated neurotransmitter (Moroz et al. 2014). This is consistent with the theory that neurons arose independently in ctenophores and planulozoans because vertebrates and most protostomes use acetylcholine at the NMJ [neuromuscular junction I assume -my edit]. However, arthropods use glutamate at the NMJ, just as ctenophores do ( Jan & Jan 1976), and cnidarians probably use neuropeptides (Oren et al. 2014). Although sponges do not have true synapses, they use γ-aminobutyric acid (GABA), glutamate, and nitric oxide to coordinate contractions (Elliott & Leys 2010). Trichoplax individuals also lack synapses,but their secretory flask cells label for FMRFamide, suggesting a conserved role in transmission for this peptide class (Smith et al. 2014).

This gives at least a few names of neurotransmitters that are particularly conserved and candidates for neurotransmitters the common ancestor of neurons used (glutamate, acetylcholine; they may have been peptides, whatever that covers), and I think makes it clear that it is very much not known what those first neurotransmitters were.


In the video, "Inner Life of a Cell", what's the empty space between the molecules?

This is a common simplification of videos and textbook illustrations. In reality a cell is much more crowded and there is hardly any space between proteins. You can find a more realistic drawing here (I linked the pictures, because I am not sure about the license).

Regarding the cytosol:
Quoting wikipedia:

  The cytosol or cytoplasmic matrix is the liquid found inside cells.
  [...]
  Most of the cytosol is water, which makes up about 70% of the total volume of a typical cell
  [...]
  The amount of protein in cells is extremely high, and approaches 200 mg/ml, occupying about 20-30% of the volume of the cytosol


How do parasitic fungi sense optimal fruiting conditions from inside the host?

In model fungi, the G protein coupled receptor Gpr1 is known to sense sugars and upregulate a cAMP linked PKA pathway, while in pathogenic strains, it senses Methionine. This probably is the environmental cue that sets off fruiting. There is a recently published extensive review too: Heterotrimeric G protein signaling in filamentous fungi

Reference

Li, Liande, Sara J. Wright, Svetlana Krystofova, Gyungsoon Park, and Katherine A. Borkovich. “Heterotrimeric G Protein Signaling in Filamentous Fungi.” Annual Review of Microbiology 61, no. 1 (October 2007): 423–452.


Would I be correct in saying that the Bohr effect is ONLY related to the concentration of [H+] in the tissues.

I would say no. Because oxygen binding affinity is inversely related to both [1]:

high $[H^+]$ concentration and
$CO_2$ increase (which is can be a consequence of the first)

$CO_2$ is involved in the Bohr effect:

  The biological significance of the negative influence of the carbon dioxide pressure on the oxygen binding of blood is obviously very big. [...] During the bloods movement through the body the oxygen-pressure will decrease to a relatively low value, whereas at the same time the carbon dioxide-pressure rises. This will greatly support the oxygen release from the blood, resulting in an improved efficiency in oxygen usage [2].

References:

Wikipedia contributors, "Bohr effect," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Bohr_effect&oldid=618215597 (accessed August 4, 2014).
Chr. Bohr, K. Hasselbalch, and August Krogh. Concerning a Biologically Important Relationship - The Influence of the Carbon Dioxide Content of Blood on its Oxygen Binding. Available from http://www.udel.edu/chem/white/C342/Bohr%281904%29.html (accessed 04.08.2014)


I would definitely go for option A. If you are assuming that the staining in band 6 is all due to whatever you are measuring, there is no reason to think that the signal at the top of lane 1 is not meaningful.

That said, this type of measures is only semi-quantitative, so being too "picky" in how you choose your region probably won't really increase the precision of your result. If you want to get a quantitative measure I am afraid you will have to turn to some other technique.

Finally note that the area obviously means a lot if you are looking at total intensity of the bands, rather than average intensity.


Where does the number 67 in the nuclear protein/antigen Ki-67 come from? Why not 66 or 68?

From Wikipedia: "The name is derived from the city of origin (Kiel, Germany) and the number of the original clone in the 96-well plate".


What are good practices with reusing desalting columns

Regardless of what protocol you use, and what the advertised efficacy of that protocol might be, in any situation like this I think the important thing to consider is: what would happen if the material taken from a re-used column was contaminated by a previous application? Can you live with the consequences of such contamination?

If you are preparing DNA for further use (PCR and/or cloning and/or transformation) then you run the risk of propagating a contaminant through subsequent steps and getting into a real mess. I worked in a lab once where one postgrad ended up spending several weeks working with a cloned fragment that was actually derived from someone else's work in the same lab (although not due to re-use of a column as far as I remember).

If you are preparing protein samples then the risks are possibly reduced, but if the protein sample is going to be subjected to sensitive methods (blotting, MS) then again, could get messy.


Choice of Molecular markers to carry out molecular phylogenetics

The molecular markers need have an appropriate amount of divergence to resolve the phylogeny at the desired scale. If the markers are too conserved, there will not be enough characters differing between taxa. On the contrary, if the markers are too divergent, the sequences may be somewhat randomized, there may be misleading convergences between distant taxa...

Non-coding regions are usually less constrained than coding regions, so they can accumulate more mutations. This makes them more suitable for studies at small evolutionary scale.


Is the EC50 of an activating protein for an enzyme a good indicator for the binding affinity Kd?

You can certainly get massive differences between EC50 and affinity. This is especially true for cell-based assays and membrane protein systems.

The reason why is because the appropriate time scales to achieve binding equilibrium (hrs for nM affinity, days for picomolar, feptomolar affinity according to back of the envelope calculations) may be and likely will be different from the appropriate time scales of activation, endocytosis, degradation, etc. Furthermore, you can have avidity effects that would not be apparent in a dilute membrane assay compared to a cell's surface. It could very much be that the dominant terms in mass transport change depending on the geometry and antigen density and while I'm not entirely sure bout vesicles vs. emulsions it is true for cancer models. Theoretical analysis of antibody targeting of tumor spheroids: importance of dosage for penetration, and affinity for retention.

Case study number I: hGH:hGHR interactions have been extensively studied and high affinity hGH have been produced. However, none of the variants showed improved EC50. It turns out that the binding was primarily influenced by the off-rates which were so slow, that affecting those values did little to the kinetics of the system. Growth Hormone Binding Affinity for Its Receptor Surpasses the Requirements for Cellular Activity

Case study number II: CEA-antibodies have been affinity matured to have pM activity compared to the wild-type nM affinity. However, the antibody had minimal effect on tumor uptake. As CEA gets endocytosed on the order of 30 minutes, all of the antibody was simply getting endocytosed rather than acting as an inhibitor. Directed evolution of an anti-carcinoembryonic antigen scFv with a 4-day monovalent dissociation half-time at 37°C.

(edit)
I realized that this answer is more applicable to IC50s vs. the EC50 experiments described above. However, many of the points remains. The Km between a substrate and its enzyme is a thermodynamic property where as the EC50 also has dynamic factors that may influence its measurement.

I would also add that simply adjusting the pH 2 units may result in a 2 orders of magnitude change in activity.

(edit2)
A further point to make about enzymatic assays is that from an observation of Michaelis-Menten kinetics, the KM of the reaction isn't the KD of the enzyme but alternatively the effective binding constant.

Recall that:

If there is a non-trivial kcat comparable to the dissociation rate kr, the enzyme will have an effective half maximal concentration that is significantly higher than the Kd. There are multiple ways how your assay can result in the discrepancies that you're seeing. The first would your strategy in measuring your EC50. If one is an enzymatic readout and the other is a binding readout, you would naturally have very different results.  Alternatively, the enzyme in the detergent system may be catalytically more active than the vesicle system resulting in a higher effective KM. Again, the pH thing.

Finally, there is always that awkward moment when you realized that you might accidentally have measured a titration curve rather than a binding curve.


how to clone a gene fragment in two direction as sense and antisense in vector

Tour sequence's complementary is TAC CCC GGG AAA TTT ATT. Together they form a DNA strand. Now replicate this and then, after transcription of both the DNA you get the RNA sequence you wanted. Use it as sense or antisense.


Fruit Moonshine is quite desirable :)

Peel the bananas. Good workflow here:

http://www.moonshiners.club/banana-moonshine-recipe/

It takes considerable work especially in large quantities. Furthermore, check legality and read up on methanol poisoning.  Don't poison yourself!


How is green fluorescent protein distributed while inside an organism?

Distribution of GFP

When used as a reporter usually GFP is expressed by the cells themselves or attached to an antibody and injected. It ends up everywhere, is what I mean.

Localization of GFP

There are three solutions to the hidden-behind-tissue problem for fluorescence.

Use a functionally 2D sample (nematodes, mouse limbs, etc)
Sacrifice the organism(if it's not dead already) and use optical clearing
Cleverness

Of these cleverness is the most interesting. Types of cleverness include time-resolution imaging(Light scatters instantly but most fluorescent proteins take a few nanoseconds to relax) to separate fluorescence from backscatter. Excite a slice of the sample and look at it from a slight angle 3 ns later, and you should see a depth-map. Repeat.

You could also use optical tomography to essentially use computers and many cameras instead of time-delay imaging to solve for the 3d distribution of signal. Computed tomography is much cheaper, mostly because you don't need a nanosecond-scale laser + capture system(those are expensive).


How to compute the regression of individual fitness on individual phenotype

I am not sure I understood the question. Let me know if this helps.

Case: N=2, freq=0.5

Let's assume that the frequency of those who cooperate is 0.5. The slope of the regression line (which R.squared is equal to 1 as we have as many data point than degrees of freedom) is by definition $\frac{\Delta w}{\Delta p}$. You defined $\Delta p = 1$. What is $\Delta w$ then?

Well, given that one cooperate and the other defect (as indicated in the fact that the frequency of cooperators is 0.5), then one will have the payoff of a cooperator that is facing a defector and the other one will have the payoff of a defector facing a cooperator. The cooperator has a fitness of $w_0 + b$ and the defector has a fitness of $w_0 - c$. I think you may misread the payoff matrix. To know the fitness of someone with strategy $i$ when facing someone with strategy $j$, you look that payoff at row $i$ and column $j$.

Therefore, $\Delta w = (w_0 - c) - (w_0 + b) = - (b+c) = -b - c$, and so the slope is  $\frac{\Delta w}{\Delta p}=\frac{-b-c}{1} = - b -c$

Case: N>2, freq=0.5

In such case the slope of the regression will necessarily be lower than $-b-c$ because some cooperators will meet other cooperators, increasing their fitness (=highering the points on the right hand side of your graph) and some defectors will meet other defectors, decreasing their fitness (=lowering the points on the left hand side of your graph)

At equilibrium

The only stable equilibrium is when the frequency of cooperators is 0. In such case, there is no variance and we cannot even talk about regression.

Conclusion

The slope is not necessarily $-b-c$. It is $-b-c$ for the very special case where we have two individuals, one cooperate, the other one defects. In any other scenario the slope $s$ of the regression is lower. More specifically, the slope $s$ of the regression for any $N$ and for any $freq$ is $0 =< s < -( b+c)$


It's almost certainly a crustacean of the order Decapoda. The long antennae, fan-like tail and long legs are dead giveaways.

You said you it came from a water tank, so I assume it's a species of freshwater crayfish.

Type "crayfish" into Google images and you'll see lots of pictures, though yours appears to be more translucent.


Non-monotonic knock-out effects in prokaryotes

Here is an example in which the knockout of a non-essential gene in yeast (Saccharomyces cerevisiae) suppresses the lethal effects of a different knockout.

  Amy L. Kistler and Christine Guthrie (2001) Deletion of MUD2, the yeast homolog of U2AF65, can bypass the requirement for Sub2, an essential spliceosomal ATPase. Genes & Development 15:42-49

The SUB2 gene encodes a protein which is a component of the TREX complex required for nuclear mRNA export. Deletion of the SUB2 gene is lethal. The MUD2 gene encodes a non-essential protein involved in pre-mRNA splicing.

The authors show that -

  "...the essential requirement for the SUB2 ATPase can be bypassed by deletion of the nonessential splicing factor MUD2..."

Detailed information about these (and all other) Saccharomyces cerevisiae genes is freely available at the Saccharomyces Genome Database


All cells are susceptible to cold, but freezing is particularly difficult.  If the water in the cells freeze, it would usually burst the cells (water expands when it turns to ice) and tearing the cell membrane (totally killing it).

Some plants and animals have adapted to colder temperatures by putting antifreeze proteins in their cells.  A lot like adding antifreeze to the radiator of a car, this lowers the freezing temperature of the water in the cell.

So the answer is that some plants have adapted to colder climates with the help of additional genes.  There are other things that have to change too - the chemical reactions in the cell will go haywire when temperature changes too, so lots of genes must make adjustment for a fully cold adapted plant.


Try Campbell biology.....it covers almost all the topics under biology in a lucid way...also the book has packed quite a volume of info in it ranging from a beginner level to a fairly advanced level....excellent book also in matters of presentation & writing style so that one won't feel bored....

Pros:

Genetics ( both classical and modern)
Ecology (including ethology)
Evolutionary biology
Animal classification
Immunology

Cons:

Biochemistry ( it somewhat feels short)
Plant anatomy ( not adequately covered)
Plant classification ( same as above)

& the rest of the chapters are like animal physiology etc. they are mixed...like some
principles they have gone thoroughly...some others not...but it's acceptable as they have to cover everything in one book...

But of course it's my personal opinion...so before considering it I would rather recommend downloading the book in pdf format & have a look at it yourself...but I feel you won't be disappointed....


If I understand what you're talking about by "gnarl", they are usually caused by a bacterium like Agrobacterium tumescens infecting and creating a gall.

Update: Forgot, also in some cases caused by insects.


Meaning of "external demands" in a paper describing the gut-brain axis

From the context, it seems to refer to those demands outside of the human body. i.e. perceptions of the external world. Examples could include a perceived threat, diunal cycles, or stress about that public presentation you're giving later.

If you are about to be chased by a dangerous predator, a sudden urge to poop would probably impair your chances of survival. Luckily, when our sympathetic nervous system kicks in, our GI motility slows down, so our body can focus on surviving the external threat and live to poop another day.


Are vacuum centrifuges the same as normal centrifuges?

A "normal" centrifuge = piece of laboratory equipment, driven by a motor, which spins liquid samples at high speed to allow centripetal acceleration to separate substances of greater and lesser density.

Without further information regarding the method you read, a "vacuum" centrifuge might be a reference to one of the following:

Ultracentrifuge

a centrifuge optimized for spinning a rotor at very high speeds.

  The vacuum ultracentrifuge was invented by Edward Greydon Pickels in the Physics Department at the University of Virginia. It was his contribution of the vacuum which allowed a reduction in friction generated at high speeds. Vacuum systems also enabled the maintenance of constant temperature across the sample, eliminating convection currents that interfered with the interpretation of sedimentation results

Centrifugal evaporator

device used in chemical and biochemical laboratories for the efficient and gentle evaporation of solvents from many samples at the same time.

  The system works by lowering the pressure in the centrifuge system [via a vacuum pump] - as the pressure drops so does the boiling point of the solvent(s) in the system.

  The centrifugal force generated by spinning the centrifuge rotor creates a pressure gradient within the solvent contained in the tubes or vials, this means that the samples boil from the top down, helping to prevent "bumping".

"Vacuum Concentrators"

  Use a combination of centrifugal force, vacuum and heat to speed evaporation of multiple small samples. They offer maximum throughput required by biology, microbiology, biochemistry, pharmaceutical research and analytical chemistry laboratories

UPDATE: Based on updated info from the OP quoting the method of the paper, it sounds like they're most likely talking about using a centrifugal evaporator to remove solvent.


Earth's history: The Great Oxidation Event and the 'Boring Billion'

Your question probably arises from a misunderstanding regarding the 'flooding' metaphor. I would not assume that 'flooded Earth's atmosphere with oxygen' means a lot of oxygen in the first place ... the metaphor means that oxygen levels rose from basically absent to noticeable.

If you look at the history of oxygen in Earth's atmosphere you see a general trend of gradual increase with a 1GY lasting stationary phase (Holland (2006), picture taken from above linked Wikipedia article - red and green lines are upper and lower estimates, respectively):

After initial atmospheric oxygenation about 2.5 GYa, Earth's oxygen sinks (mainly the oceans, after that landmasses and the ozone layer) were filled and buffered atmospheric oxygen levels, keeping them low. Once those sinks were saturated (approx. 850 MYa), the atmosphere started to oxygenise rapidly.

The constant (or as discussed below: drop in) oxygen concentration is caused by these sinks. The oxygen that is produced by photosynthesis was just not available to Earth's organisms as it was not atmospheric.

As @GerardoFurtado points out in the comment, modalities of the stationary phase are still debated. A review by Lyons et al. (2014) presents evidence that after the initial increase in oxygen levels, a drop in atmospheric oxygen preceded the stationary phase (see their Fig. 1, blue boxes). This does not change much as the newly inferred stationary phase, though probably a more fluctuating stationary phase than suggested by Holland (2006), is still higher than before the great oxidation event and lower than at present.

The major conclusions remains the same: There is evidence that the seemingly slow evolution 2-1 GYa was probably caused by oxygen limitation and oxygen levels were buffered by oxygen sinks. The change of oxygen concentration was determined by both the rate of oxygen production and the rate with which oxygen is stored in those sinks; the interplay of those rates caused the oxygen concentration to remain constant, drop or occasionally even rise, i.e. fluctuated.


Evolution question on speciation? Really confusing!

The answer is C

Because it explicitly tells you the fly speciates faster than the tree (1my vs 10my). That means after the extinction event, all things being equal, the fly will speciate into more niches/species in the same amount of time. While other outcomes could occur, with the information given C is by far the most likely outcome.

This is no different than a physics question asking you which of two object will reach some arbitrary marker first give two different known velocities.


Short answer
It has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.

Background
First off all, there are many types of memories, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental.

Beneficial effects of loosing memories
Long-term memory is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that detect (anterior cingulate cortex) and resolve (dorsolateral and ventrolateral prefrontal cortex) mnemonic competition (Kuhl et al., 2007). The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones (Shea & Right, 1991).
Inherently volatile memory
Short-term working memory is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (which objects depicted here match the colors you just saw?). If all these memories would be retained, tasks dependent on working memory would not be possible. Sensory memory an ultra-short term memory that is kept only for very short amounts of time, allowing people to, e.g., track a light and make a symbol or letter out of it before the information is funneled to the short term-memory.
Neutral effects of loss of neural function: a side track off memory lane
However, forgetting may be simply another example of the use it or lose it principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the plasticity of the cortex. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated (Stronks et al, 2015). In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available per se. Hence, 'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever, barred a minority of studies that showed a slight benefit of being blind in auditory tasks (Stronks et al., 2015).
Pathological memory loss - not so good:
However, forgetting of memories may also be pathological; think of the impaired short-term memory of Alzheimer's patients, or amnesia due to stroke. Forgetting is not always beneficial.

References
- Kuhl et al., Nature Neurosci (2007); 10: 908-14
- Shea & Right, Res Quarterly Exercise Sport (1991); 62(3)
- Stronks et al., Brain Res (2015); 1624: 140–52


It's a good question and has confused me as well.

A standard definition of cDNA is that it is a double stranded (ds) product of mature mRNA. I suppose it is possible to get a nascent RNA strand copied into cDNA, but I've never heard of that being done.

Because cDNA is dsDNA, the original strand is made from your mRNA as the complementary strand, but then you dispose of the RNA and make the second strand to get a stable, reproducable molecule. The total dsDNA molecule is what we refer to as cDNA (not a single strand of this material).

consider this simplified DNA molecule:

ATG-INTRON-CTCTAG

TAC-INTRON-GAGATC

this could be transcribed into the following mRNA (corresponding to Met-INTRON-Leu-Stop):

AUG-INTRON-CUCUAG

before nuclear export the intron is removed, making mature mRNA:

AUGCUCUAG

you make cDNA from this:

ATGCTCTAG

TACGAGATC

So, you have both a coding and a complementary strand in your cDNA.

As for directionality on the chromosome, genes can be in either direction (meaning that they can use either strand as the coding strand), but remember that the forces that contribute to transcription are just locally determined (assembly of transcription factors, etc) and pay no heed to what direction they're going or strand they are on relative to any other gene. The strands are labeled as positive and negative, but that's just a reference for orientation. A good place to browse the human (or other species) genome is the NIH's map viewer. Click on a chromosome to see the genes mapped to it. Note the column labeled 'O' is for orientation.


E. coli and other bacteria metabolize tryptophan into odoriferous skatole and other indole compounds.

If you're culturing these organisms in medium that contains tryptophan, that may be what you're smelling.


Can salt-water frogs survive in normal water (A well)?

According to Wikipedia the Crab-eating frog is the only amphibian that can survive in sea water. However Wikipedia also suggests that it can only survive brief excursions into the sea.
There are no such things as sea frogs.
Even the Crab-eating frog doesn't live in the sea though. Its natural habitat is mangrove swamps.

The crab-eating frog (Fejervarya cancrivora), is a frog native to south-eastern Asia including Taiwan, China, the Philippines and more rarely as far west as Orissa in India. It inhabits mangrove swamps and marshes and is the only known modern amphibian which can tolerate brief excursions into sea water.
This frog can tolerate marine environments (immersion in sea water for brief periods or brackish water for extended periods) by increasing urea production and retention, and by remaining slightly hyperosmotic within urea and sodium flux. Adults can survive in salt water with salinity as high as 2.8%, and tadpoles can survive salinities as high as 3.9%.

https://en.wikipedia.org/wiki/Crab-eating_frog


It reminds me of silverfish, a common wingless house insect.


DNA is any piece of DNA. Genome is a very specific piece (or pieces) of DNA: all of the DNA contained inside one cell, or organelle, or virus particle, from a specific species.

For a species with a single chromosome, like the bacterium, E. coli, then the bacterial genome is equivalent to the cell's chromosome. Same for a virus. For a metazoan, like C. elegans, which has six chromosomes, the nuclear genome is one copy of all the chromosomes and the mitochondrial genome is one copy of the mitochondrial chromosome.

So DNA is a general term, while genome is a specific term that can be used most clearly with a modifier to specify the species you are referring to (e.g., the human genome, or the duckbill platypus genome, etc.).


What is this type of diagram called and how to interpret?

They used a stain that marks tyrosine hydroyxylase (most likely using an antibody to TH, followed by a secondary antibody tagged to an enzyme that then produces a dark precipitate in the presence of the proper precursor).

The dark regions are where more antibody bound, so you can infer this is where TH is highest. It's very difficult using these techniques to take anything quantitative from this, but you can use the technique to identify regions and possibly compare between them, given you have an appropriate control region.