How can the following data regarding flower phenotypes be explained?

Because it seems you might be studying for a test, I will try to not answer directly but show the beginning of a chain of logic that might be more useful.

Let's review the very plain evidence. blue crossed against other colors leads to 3:1 ratios of blue:other. So it seems that blue is dominant in those cases. But when you cross those colors against each other, you get silly nonsense, a 3:1.2:1 ratio or something.

So, based on the linked answers, you are justified in thinking that genetics determines flower color, just because of the simple Mendelian pattern of the first 2 crosses. But things don't work for a straightforward monogenic trait in the pinkxwhite cross.

Let's now analyze your explanation. You say: "I was thinking blue (BB) was the dominant epistatic flower color allele—BB or Bb would give blue regardless of the other color allele, and bb would allow the expression of color dictated by the other gene..."

But look at the parents and offspring of the third cross. You say blue is dominant- but it is in fact expressed in the offspring of non-blue parents! So blue can't both be dominant and be the "controlling" epistatic gene. So now: let's consider some other similar possibilities:

1) blue = dominant and is controlled by another locus (recessive or dominant?)

2) blue = recessive and controls another locus (recessive or dominant?)

Do any of those hypotheses match the data?

A final observation: I find it always helps to add up all the combinations of phenotypes (if possible; for example the ratio of (blue+white) : pink, etc.) to see if anything looks like a familiar ratio.

I hope that is useful (and not too late to be helpful in studying, if that is your goal).


What is the name of this plant I found in a park?

I think this is Lysichiton americanus,  skunk cabbage. It has these large, rolled-up leaves and grows in wet habitats as you describe. In Europe, it is an invasive species, but in America it is native. I am not 100% sure, because I don't know if there are any similar species in the US.

EDIT
As Anongoodnurse pointed out, I was right to be unsure. This is Eastern skunk cabbage, Symplocarpus foetides. This species occurs in the Eastern parts of the USA.


Performing PCR on samples whose DNA concentration is nul

Nope, you could get amplification from samples that are orders of magnitude below the nanodrop detection limit (~2 ng/uL). To compare: most manuals for polymerases recommend 1 ng of plasmid template, and will probably work with much less, especially if you use a few more cycles.

But if you expected to see something on the nanodrop, and you get nothing, something else might be completely wrong.


Hardy Weinberg Equilibrium after 5 Generations

You are almost correct, but with a few modifications/comments.

The calculations in Q1 are independent of HWE, and are just calculating the current allele frequencies in the population based on genotype frequencies (i.e. would be the same irrespectively of if the population is in HWE or not).
In Q2 it is unclear if the questions is asking for genotype frequencies or allele frequencies. Your answer of genotype frequencies of $p^2=0.42$ ($a^+a^+$), $q^2 =0.12$ ($a^-a^-$) and $2pq =0.46$ ($a^+a^-$) is correct if you assume the allele frequencies from Q1 and HWE. However, your allele frequencies are incorrect and should be $p = 0.42 + 0.46/2 = 0.65$ and $q = 0.12 + 0.46/2 = 0.35$, i.e. the same as in Q1. Remember that the allele frequencies shouldn't change under HWE.
Yes frequencies should not change in Q3. This is the textbook definition of HWE, i.e. that allele and genotype frequencies remain constant between generations in the absence of evolutionary forces (i.e. under the HWE).


Is it true to say that the more an organism is smaller, the faster it's going through evolution?

I think that you are talking about what are sometimes called "rates of evolution", see also https://www.thenakedscientists.com/articles/questions/do-smaller-organisms-evolve-faster. That wiki is a collection of info of interest mostly to specialists, but the blog post may be helpful.

The short answer is that there is a strong negative correlation between mass of an individual organism and rate of evolution, in terms of years or whatever. But there is not necessarily a causal relationship there.

People can argue that there is such a causal relationship, because the life cycles of small organisms are shorter, and more generations means more mutations, which means more evolution is possible. In the classic example, E. coli reproduces every 30 minutes under good conditions, whereas humans reproduce every 30 years. This is sometimes true but not always.

Alternately, there are bacteria such as Micrococcus that are smaller than E. coli but divide more slowly, and by this same logic must therefore be evolving more slowly than the larger bacteria. So there's a lot of variation.

As another counterexample, bacterial cells can form spores that undergo stasis for tens of thousands of years, then wake up under better conditions and go about their life. During that time, elephants are evolving much faster than the bacterial spores- even though outside of that time the bacteria are dramatically faster.

Another confounding issue is that the different groups you name are of dramatically different ages. Bacteria are probably ~4 billion years old, and have had tons of time to diversify. Even if they had the same evolutionary rate as elephants, you would still expect more species in bacteria than you would in flowering plants, which are ~200 million years old. So measuring evolutionary rate in terms of "number of species" is quite misleading.

Yet another issue is that evolution may not happen at a constant rate. This is a normal assumption people make because it makes life simpler, but there is a certain amount of data that suggests that a lot of large evolutionary changes happen very quickly, and then there are periods of relative stasis; this is sometimes called "punctuated equilibrium" or "saltation". An example of this is the so-called Cambrian Explosion. So even though one group A may have gone through 1/2 the generations of group B in a unit of time, it may have gone through 10X the "evolution" in terms of changes to body shape/other characters.

So, it's complicated, and there's a large field of research in evolutionary biology that is trying to answer these kinds of questions. Your assumption is broadly correct in terms of agreement with the data, but it's not clear that smallness per se is what makes evolution happen more quickly.


What is the mechanism of labeling a DNA molecule with deuterated water?

I would assume that the labeling occurs in the reduction of NTPs to form dNTPS.

This process (catalyzed by ribonucleotide reductase) involves protonating the hydroxyl group on the 2' carbon, allowing it to leave as water, and then adding a hydride to the newly formed carbocation. The two hydrogen atoms (the proton and the hydride) come from two thiols on the enzyme, which in the process are oxidized to form a disulfide bond.

The crux is that, in the presence of heavy water, the two thiols would rapidly exchange their hydrogen for deuterium. That means that the hydride that gets added to the carbocation would be a deuterium, and the resulting dNTP would be deuterium labeled.

This is the only step that I can imagine the labeling working for, as a carbon-hydrogen bond is formed (which doesn't exchange rapidly with the solvent) using the hydrogen from a sulfer-hydrogen bond (which does exchange rapidly with the solvent).


We called those "Indian strawberries". They are also known as Mock Strawberry (Duchesnea indica). Survivalists are pretty familiar with this plant.

They are a lot like strawberries in appearance, but the berry is rounder, not pointed, and held upright (they point up) on the stem, not pending. Though the berries are edible, they don't have much flavor at all. The leaves are also similar, and the flower is yellow, not white. The fruit's seeds are the same color as the fruit. They flower late spring and throughout summer. Your specimen looks like it was nibbled on at some point. The inside of this berry is white and kind of spongy and dry (especially compared to the real thing, i.e. wild strawberries.) The stalk it's on is hairy (as it should be) but damaged, and only one part of the leaflet is visible in your photograph.

They're in the Rose family, but there's some discussion about what genus they really belong to; may be more similar to Potentilla.

See also http://www.sierrapotomac.org/W_Needham/IndianStrawberry_080617.htm


What are the effects of caffeine on the mammalian circulatory system?

I can't speak to the causes of hypotension, but you are indeed correct, caffeine is a stimulant. As a stimulant, there is a well documented acute period of hypertension that lasts for up to 4 hours. Interestingly, there is no causal link established between caffiene consumption and chronic hypertension leading to cardiovascular disease (see here and here).

Having said that, caffeine is also a diuretic, which could cause someone who is already fairly dehydrated to exacerbate that state. It's possible to faint from a result of severe dehydration but I think it would have to be pretty severe.

It's possible someone is prone to fainting for non-medical, purely physiological reasons, such as standing for long periods, standing up too quickly, hypoglycemia, or some other predisposition.


Why are there no known photosynthetic archaea?

There are photosynthetic archaea (such as Halobacterium) but the mechanism is different. They use rhodopsin-like ion pumps (bacteriorhodopsin and halorhodopsin) to move ions against the gradient and produce ATP via chemiosmosis (like mitochondria).


Minor differences in morphology of a snake: Why designate it a different species?

Short explanation

According to the papers I could find, Dendrelaphis ashoki and D. girii aren't as closely related as you suggest: D. ashoki appears to be closely related to D. pictus, a Southeast Asian snake species, while D. girii appears to be closely related to D. bifrenalis, a Sri Lankan/South Indian snake species. They were distinguished from their sister species largely on the basis of morphological differences and geographical isolation.

How do we know D. ashoki is a distinct species?

The key to this answer is in Vogel and van Rooijen, 2011a, the scientific article in which Dendrelaphis ashoki was first described. Before their work, these snakes were thought to belong to the species Dendrelaphis pictus. To test whether this was in fact the case, they compared 9 individuals of D. ashoki with 34 individuals of D. pictus, and found statistically significant ($p < 0.05$) differences in five morphological characters: SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal diameter of the eye), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent). Here's the statistical analyses they ran:

  The south Indian form that has previously been referred to as D. pictus (e.g., Wall, 1921; Smith, 1943; Whitaker and Captain, 2004) differs from Indochinese D. pictus in the characters SUBC ($F_{1,25} = 17.7, P = 0.0003$), TAIL ($F_{1,25} = 30.0, P = 0.00003$), EYED ($F_{1,35} = 22.5, P = 0.00003$), SUBL (Mann-Whitney U, $Z = −4.6, N=40, P < 0.00001$) and STRIPE1 ($\chi^2_1 = 42, P < 0.00001$).

They also compared the 9 individuals of D. ashoki with 48 individuals of D. proarchos, and found statistically significant ($p < 0.05$) differences in five morphological characters: VENT (number of ventrals), SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal eye diameter), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent).

  [The south Indian form] differs from D. proarchos in VENT ($F_{1,49} = 24.1, P = 0.00001$), SUBC ($F_{1,28} = 13.7, P=0.001$), TAIL ($F_{1,28} = 40.1, P < 0.00001$), EYED ($F_{1,47} = 16.8, P=0.0001$), SUBL (Mann-Whitney U, $Z = −4.7, N=52, P < 0.00001$), and STRIPE1 ($\chi^2_1 = 53.0, P < 0.00001$).

The authors didn't rely just on morphological evidence: they note that D. ashoki, which is found in the Western Ghats, is also geographically isolated from other populations of D. pictus, which are found in Northeast India, Myanmar and South East Asia. Therefore, they concluded (emphasis mine):

  The distinct morphology and coloration as well as strong geographic isolation of the population from the Western Ghats imply a unique evolutionary history that does not allow application of either the name D. pictus or the name D. proarchos. Consequently, we describe this form, previously referred to as D. pictus, as a new species, D. ashoki sp. nov., endemic to the Western Ghats.

How do we know that D. girii is a distinct species?

For this information, we need to look up another paper published that same year,  Vogel and van Rooijen, 2011b. Interestingly, the authors don't compare this snake with D. ashoki at all, but with Dendrelaphis bifrenalis:

  Due to their double loreal shield, D. girii sp. nov. and D. bifrenalis occupy a unique position within the genus. A congeneric species with a double loreal shield has been described in the past, namely Dendrelaphis biloreatus (Wall, 1908). However, the presence of a double loreal in D. biloreatus appears to be based either on an anomalous specimen or on a misjudgement (Vogel & Van Rooijen, 2011b). Furthermore, D. biloreatus differs from D. girii sp. nov. and D. bifrenalis in its number of dorsal scale rows (13) and its number of ventral scales (190-199).

  There are several differences between Dendrelaphis girii sp. nov and D. bifrenalis. The most obvious one is the light ventrolateral line, which is present in D. bifrenalis and missing or very faint in
  Dendrelaphis girii sp. nov. (see Fig. 3, 4).

  The postocular stripe is much broader in D. bifrenalis. In D. bifrenalis there are black oblique bars in the neck region of some, but not all specimens (8 specimens out of 12 in our data) (see Fig. 3-5). This pattern is not sex related. It is absent in D. girii sp. nov. For Dendrelaphis girii sp. nov. we had only 1 male, so it is not possible to compare the sexual dimorphism in this character. The snout of Dendrelaphis girii sp. nov. is much broader than that of D. bifrenalis. Dendrelaphis girii sp. nov. has, on average, fewer subcaudals and more ventrals than D. bifrenalis, but the ranges broadly overlap.


Is there a timeline for the frequency of evolution of any species?

There can be multiple changes at the DNA level generation after generation, however most of these changes are insignificant (doesn't contribute for any specific character). But rarely, there can be a significant trait/change gained by an individual because of such changes in DNA level. Unfortunately such changes gets 'lost', unless it is fixed in the population (i.e., the gained individual should be successful in breeding and passing the trait/change to large number of progenies. Those progenies should further continue to pass on the trait till about every one (or most of them) in the population has those trait/change). Only such changes contribute for the species development (continuous accumulation of such changes, over time will result in the novel population that is very different from the original population).

Most of the timelines that we know are reconstructed from the DNA/protein sequences. Usually, DNA or protein sequences from the closely related species will be compared and looking at the differences they have, using suitable models, ancestral state of those sequences are determined. Once the sequence for the last common ancestor is known, mutational rate per unit time can be used to estimate the evolutionary time for those species.

A simple example would be the blue eye color in humans: it occurred about 10,000 years ago and it is still not fixed in the population.


Not with bench centrifuges.
Bacteria have cell wall and are rather small. This gives the cell wall alot of strength. I am not even sure that ultra centrifuges would work.

What you will likely get is a cell pellet. If you want DNA, pellet the cell and either go for direct PCR or sequencing. Or use a DNA extraction kit to obtain the DNA you want.


Author statements (Readers) in biological nomenclature

As @C_Z_ mentions, the double author citation is due to a naming revision. In your case, 'Panzer' has revised the name given by 'L' (Linneus). It can for instance be due to an assignment to a new genus or a change in rank status (e.g. going from subspecies to species).

Note that author citations differ between botany and zoology, where changes in authorship are usually not recognized in zoology (as long as there is a proper and complete species description in the first place), while the botanical code allows for multiple author citations. From Wikipedia: Author citation (botany):

  ... in contrast to the situation in zoology, where no authorship change is recognized within family-group, genus-group, and species-group names, thus a change from subspecies to species, or subgenus to genus, is not associated with any change in cited authorship

So under the Zoological code, the old author name is kept when a species is reassinged to a new genus, e.g. when Seriola gracilis (Lowe, 1843) --> Cubiceps gracilis (Lowe, 1843). On the other hand, the Botanical code allows for multiple and sequential revisions, so you can have situations as "Dummy species (L.) Thom. emend. Müll.".


It does appear to be a young spider, and seems consistent with a young Steatoda of some sort, so "False Widow" sounds OK.

Edit:  I just did a quick Google search and pulled up a useful paper (link below) that pretty clearly indicates that this is almost certainly a young Steatoda nobilis, one of the 'False Widows'.  See the top left - image A

Dugon, M.M., et al. 2017. Occurrence, reproductive rate and identification of the non-native noble false widow spider Steatoda nobilis (Thorell, 1875) in Ireland. In Biology and Environment: Proceedings of the Royal Irish Academy 117(2):77-89


What is the point of having evolved two nostrils?

There are two aspects to your question.

First, organisms have some kind of symmetry. The field of evolutionary developmental biology has some theories on why our anatomy is the way that it is.  So, we have two eyes, two halves of our nose and two nostrils, one "tube" that becomes the path from our mouth to anus, etc. Our nostrils are just part of that symmetry. It may be evolutionary advantageous to keep two nostrils so that an animal can tell what direction a smell is coming from.

Second, we see that evolution has provided a path to having just one nostril.  Blowholes in toothed whales are just one nostril.  The other nostril does not have an opening to the outside of the whale.  It would be interesting to explore the split between baleen (two nostrils) and toothed whales (one nostril).  This evolutionary divergence may have been caused by differences in communication styles or the different blowholes may have caused a difference in communications http://www.whoi.edu/science/B/people/kamaral/marinemammalacoustics.html .


Are Triceratops and Eotriceratops similar enough to be considered as the same genus?

Taxonomists have wide leeway over assigning higher taxa. The publication process in which Eotriceratops was described as a new genus made it a new genus. However, given a different set of reviewers, they may have rejected the new generic description, and suggested that the author put it into Triceratops. The process is somewhat arbitrary, and there are some random elements to higher taxon assignment. But it is the system we use. If somebody were to write a paper to synonomize Eotriceratops with Triceratops, and that paper were accepted, then Eotriceratops would cease to be a valid name. Its all about publication precedence. Gregory  Paul may have good reason for his suggestion, but it must be published before a change is made.


Who gives a newly discovered microbe its name?

I sthere any reason for your question to be specific to microbes? Whether a microbe or multi-cellular organism is found, the problem is the same. Who name it?

  Who name it?

Whoever discovered it. Of course, discovering a new species is not as easy as just taking a picture. One has to provide a very thorough description of the species morphology and eventually argue that it should be considered as a new species and not just as a subspecies or something else. See here for discussion on the definition of a species.

  How does the discoverer name it?

If the new species is considered part of an already existing genus, then the author has to keep the genus name. The species name the author chooses is mainly to up himself / herself. Consider for example Macrocarpaea dies-viridis (dies-viridis means "green day") was named like this because the researchers were listening to Greenday when they found it!


Why DNA needs histones to be packaged and ordered?

Sort of like having one of these:

instead of this:

Surely you could simply wrap DNA up in a coil, but to do it in a neat fashion that allows you to package and repackage sections as needed, it's a lot better to have some dedicated machinery.

It is also difficult to organize DNA without a supporting structure because the negative charge of the DNA polymer repels other parts of the molecule, whereas histones are rich in positive charges.

As Galen mentioned in comments, histones both pack DNA into a smaller space (human DNA from one cell would be about the height of an adult if it was all in a straight line) and contribute to gene regulation. Modifications of histones control whether the DNA around that histone can be accessed by transcription machinery and therefore whether those genes will be expressed.


Hela live cell confocal laser scanning - reccommendations for good fluorophore that will show good movement

MitoSOX looks pretty cool. I've never used it myself, but I'm sure you could see some cool mitochondrial dynamics going on. Its a bit pricey though, but all dyes are going to be.

Even at only 8 hours you should probably be able to see a few divisions, which would be cool with hoechst.


Is mammalian vision processed as a sequence of frames?

Short answer: no, there is no fixed frame rate or frame-based processing in mammalian vision.

Photons arriving at the photoreceptors at the back of the human retina interact with photo-sensitive pigments called opsins, and modulate their release of the neurotransmitter glutamate . The level of glutamate released from a photoreceptor then changes the membrane potential of the other neurons in the retina connected to the photoreceptor (bipolar cells, for instance). Signals are processed within the retina, then passed through retinal ganglion cells (RGCs), along the optic nerve, through sub-cortical structures and in to visual cortex.

This process occurs continuously, but all of the elements along the way have intrinsic time constants and other temporal constraints (number of photons required for opsin activation; recovery rate of the opsins in the photoreceptors; membrane time constants and refractory periods of neurons; synaptic delays; etc.). Persistence of vision (the effect underlying the perception of a movie as a continuous stream rather than a series of distinct frames) probably relies on the conjunction of many of these time constants.

Concretely, a flashed visual stimulus produces a response in (primate) visual cortex after around 30–50 ms (Maunsell and Gibson 1992). You can recognise and subsequently recall a lot of detail from a sequence of images flashed at around 100–150 ms per image [citation needed]. These are still not hard and fast definitions of the "speed" of vision.

Since we only learnt to produce movies as sequences of distinct frames, it's tempting to guesstimate the speed of human vision in those terms. Biology, as always, is more complicated.

As far as the "spinning rims" issue goes, there are many aspects of cortical and subcortical activity that tend towards oscillatory activity. In a system with an intrinsic frequency (for example, the neurons in the thalamocortical loop between LGN and primary visual cortex), providing an oscillatory stimulus can synchronise the system to the stimulus.

Many of the intrinsic time-constants I described above could result in a tendency to oscillate at some intrinsic frequency, and then be subject to phase locking due to a periodic stimulus close to that frequency.


Creating expression template from PCR: What annealing temperature to use?

It seems the answer, which may be context specific, is to use an annealing temperature about 5 degrees below the entire oligo melting temperature.  I did not get any bands at lower temperatures.


This appears to be an anemone, with the pedal disc towards the camera. I can't offer a positive ID, but would hazard a guess at genus Actinia.

Anemones sting, and the stings of anemones range from completely harmless to humans to highly toxic. In the absence of a positive ID, I would avoid poking it.


The score is the log odds ratio, times 100, that the ORF that you input is a coding region. For example, if Glimmer thinks the log odds are 10 to 1 that your region is coding, then your score will be 10x100 = 10000. Log odds of 10:1 imply more than a million to one certainty.


What are good sources of free-to-use images and diagrams

I'm guessing the videos are for a flipped/online course and posted on YouTube or Coursera?  I've done this. Biology is hard -- perhaps because I am picky and really want good images.

I used Wikimedia.com to search for many free images. I also contacted the publishers of the free online version of Molecular Biology of the Cell and asked if I could use up to 20 for my free online course, and they agreed.

My university was also able to work out an agreement with the textbook publisher to use 200 of the textbook images for the Coursera course as long as they were credited, and a link to purchasing the textbook was available on the site. They want to keep my university happy as our students buy a truckload of books every year.

I've also gotten somewhat decent at using a drawing tablet and powerpoint image (boxes, circles) manipulation to make some of my own cell processes and chromosomes and such.

Lastly, OpenStaxCollege.org has a wonderful collection of free textbooks for students, and they make their images available to faculty as free powerpoints. They aren't usually "good" enough to satisfy me, but definitely check them out.


Cloning problem. Digestion test at the end of the cloning is always negative

Even minute amounts of undigested vector will contaminate your transformation. You could PCR amplify your insert from the pJet cloning plasmid and then digest the PCR product with BamHI and HindIII. In order to get rid of the pJet template either gel purify the digested insert, digest pJet with some times which cuts it multiple times (less preferable) or put everything on a column and hope that pJet is diluted enough (less time consuming but a bit risky).

The other thing you could exploit is that pJet is ampicillin resistant while your target vector is also Zeocin resistant. If you add Zeocin to your E. Coli it will kill a pJet positive clones while sparing the pSecTag positive clones.

Your insert is fairly small so using a bit more DNA than usual won't hurt.

If you can post some pictures of your gels this might be helpful as well.


My answer assumes you are asking about in-vivo effects of cytokine responsiveness.

It has to do with the regulation of the differentiation process. Cytokine responsiveness depends on other factors like cell-cell signaling. To be sure that the differentiation occurs in the right place, the progenitor cells need a signal feedback from the surrounding context (the actual tissue where the cells will differentiate). If the feedback matches, they differentiate.

Stem cells on the contrary, are physically distant from that context, so they lack all the feebacks needed and do not respond to cytokines stimulation as the progenitors do.

Here's some literature about it:

Developmental changes in progenitor cell responsiveness to cytokines.
Mechanisms regulating lineage diversity during mammalian cerebral cortical neurogenesis and gliogenesis.
Signal transduction pathways involved in the lineage-differentiation of NSCs: can the knowledge gained from blood be used in the brain?
Enhanced responsiveness of committed macrophage precursors to macrophage-type colony-stimulating factor (CSF-1) induced in vitro by interferons alpha + beta 1.

However, note that the whole process is still largely unclear and it may vary for different cell types, so consider my answer as a generalization of the concept.


Reasons why people say that AIDS/HIV doesn't exist

I think no one can really deny the existence of HIV or AIDS, just a search on google scholar will show >1,500,000 hits for each of those terms, and ask (hopefully any) doctor and they will say it does, though AIDS denialists do debate whether HIV causes AIDS. This paper explains the process of HIV causing AIDS. Further, AIDS denialists have not offered up well supported alternatives as to how AIDS arises without HIV being involved.

I think however that there is more debate fuelled by conspiracy theorists as to how the disease came about. This article from TIME magazine on conspiracy theories is a short piece about it, there are two main conspiracy theories:

1) The west invented the disease to "decimate the African population."

2) The US government invented the disease in the 70's and injected gay men to stop the spread of homosexuality.

You should read this section on the critical response to the film House of Numbers, it seems to be thought that the film was driven by funding wishing to promote conspiracy theory and interviews were edited in such a way as to help portray that message.

Caution, the following is my own personal opinion ;)

  To most these seem like pretty outlandish claims and most people do ignore them - apart from anything, placing blame on someone won't stop the continuing spread of this horrendously devastating disease so the conspiracies are quite pointless. I personally think these conspiracies are driven by the uneducated, the scared, and those who want to "bring down the man & corporate/capitalist western society led by a powerful minority" etc..

Back to the science: The people who discovered the disease (Dr. Robert Gallo of the National Cancer Institute and Dr. Luc Montagnier of the Pasteur Institute in Paris) along with the majority of the scientific community say:

  "the virus jumped from monkeys to humans some time during the 1930s"

Molecular analysis of the genetic sequence for the virus supports the theory that the jump from apes to humans was around 1920-1930. Some other studies support the jump being made around this time though some estimate it to be a little earlier, this is due to estimated rates of mutation being used to calibrate molecular clocks.

I recommend taking a look at AIDStruth.org and more specifically start with this page (thanks for the link @MattDMo) if you have watched House of Numbers.


What is the scientific name of this butterfly?

With the information given, I have to say I think it's a Spangle, Papilio protenor, of the swallowtail family, probably a male.

It also is listed on the butterflies of Taiwan.

See pictures for comparison:

........................Male...............................................female............................................................................


Is it possible for two brown-eyed parents to have blue-eyed child?

Possible, yes but probable, no. (I assume that the history of the parental family as you mention is important)

Let us first consider HERC2 (H=brown, h=blue) and OCA2 (O=brown, o=blue) as per the names mentioned in the reference you cite, to be completely unlinked, such that they are independently assorted. Since the father's lineage has no history of the recessive phenotype(blue), and the genes segregate independently (our assumption), we can conclude that the father is homozygous for the dominant allele in both the genes(HHOO). In this scenario, it is very unlikely to get blue eyed children, but is still possible in the following two ways:-

The father's lineage does have a recessive gene (which probably entered his family gene pool due to non-consanguineous mates carrying a heterozygous phenotype in either of the gene pair HERC2 or OCA2), and has evaded expression by pure chance or because the recessive gene carrier entered into the family very close to the father,i.e. probably just one or two generations above the father(so that not enough generations have passed to allow the homozygous recessive trait to develop). In each of these cases, one or both the gene loci in the father might be heterozygous(HhOO or HHOo or HhOo) and coupled with the mother's heterozygous genotype(a good guess considering the history of many recessive phenotypes), might produce a blue-eyed child due to homozygosity in any one of the gene.
There is a mutation in the germinal cells of the father which creates a non-functional mutant allele and thus can give a blue-eyed child with a heterozygous mother.
But in either case, considering independent assortment, the chances are very bleak.

But if we also take into account the linkage of the two genes, then the probability rises significantly. Now there is a good chance that the father's lineage might contain a heterozygous (or homozygous recessive) allele pair on a single chromosome, which due to their tight linkage, might pass on without any recombinations and therefore might evade phenotypic expression more efficiently(although, since a dominant allele in both the genes is required for the dominant phenotype, the extra evasion efficiency due to linkage is less). As given at the end of your reference, suppose there is one chromosome in the parental ancestry that carries both the recessive genes. If they are linked, the chances of brown eyed parents to have blue eyed children decreases (and the chance of being heterozygous also decreases) thus making it more likely that the father's lineage could have a recessive allele in spite of there being no significant expression in his family history. Therefore, more tightly they are linked, greater is the probability that the father is heterozygous. Linkage does not significantly lessen the possibility for the father to have a blue-eyed child since the mother does contain a recessive linked- phenotypic pair in all probability. (Actually, the probability is also based on which combinations are linked, but the possibility of there being a heterozygous allele remains positive with most combinations).This again gives some chance for brown eyed parents with the history you mention, to have a blue eyed child.

In any case, there is a chance but the probabilities depend a lot on the linkage, the linked combinations, and the actual genotypes of the parents but there is always a possibility.

ADDITION

Just to add a bit of information, the kind of recessive epistasis we described here, where the homozygous recessive (at the hypostatic,HERC2, loci) phenotype resembles the phenotype for the recessive condition at the modifier pair (OAC1), is only a part of the story. Actually, certain polygenic influences further complicate the situation by introducing a variety of phenotypes.


Lethal genes evolve simply because of random deleterious mutations and absence of strong selection.

Recessive lethal genes

Random mutations can make a gene product non-functional or reduce its activity. However, in diploid organisms the other fully-functional copy of the gene can compensate for the non-functional allele.

Sometimes both the alleles can carry different mutations which can lead to complementation; this would not affect the gene activity. Also see:  Explain allelic complementation at molecular level. Let's not consider this case here.

So, the fitness of the heterozygotes would not be affected and they will continue to propagate. However, if both the alleles are affected then it would lead to lethality (or lets say reduced fitness). This can happen if two heterozygotes (with the same deleterious mutation) mate and give rise to a homozygote (with both the alleles affected). Since siblings (or other close kins) are genetically related, there is a good likelihood that both of them may be carrying a copy of a non-functional allele and homozygous offspring born out of such a mating may have reduced fitness.

Dominant lethal genes

There are some cases of dominant lethal alleles. Examples include the mutated genes responsible for Huntington's disease (or similar poly-Q disorders). Other examples include a mutant allele of a proto-oncogene that leads to its hyperactivity (and therefore cancer).

Dominant lethal alleles persist in the population primarily because of their late onset. In such cases an individual with such an allele would have already mated and produced offspring before the disease kills them.

Other reasons for the persistence of lethal genes

Another possibility (applicable to the case of cancer) is that the mutations are not in the germ cells and were acquired by somatic cells because of some external agent. These mutations would not be transmitted to the next generation.

Sometimes, the deleterious nature of the allele can exert its effect only under certain conditions. Let's say someone has a mutation that causes reduced immunity. Such a person would survive well if they remain in a sterile environment. In general, we can say that there is no strong selective pressure against the mutation.

Sometimes the reduced fitness because of a mutation under a certain condition can be overwhelmed by an increased fitness caused by it under some other condition. A very well known example is that of the haemoglobin allele that causes sickle-cell anaemia. However, the RBCs in the individuals affected by this disease are resistant to infection by the malarial parasite. The mortality due to malaria is much higher than that due to sickle cell anaemia. Therefore, in regions where malaria has high incidence (like Africa) this allele is positively selected.


How can I improve efficiency of Ecoli transformation?

The plasmid is quite big which might explain why it is difficult to transform bacteria (is it a lentiviral vector?).
If you could give additional details you might have a chance to have improved answers to your question.

Hello, I suggest you follow this protocol:

At step 7 instead of this "Add 250-1,000 μl LB or SOC media (without antibiotic) to the bacteria and grow in 37°C shaking incubator for 45 min. "

Do this " Add 250 μl LB or SOC media (without antibiotic) to the bacteria and grow in 30°C shaking incubator for 2 hours. Do not shake too hard, gentle motion might be fine (500 rpm).

At step 9 instead of this "Incubate plates at 37°C overnight."

Try to incubate at 30°C. I would even suggest to try to grow them at lower (25°C, or 16°C) temperature if you can prepare a second plate.
It will take much longer than overnight to grow the cultures, probably more 48 hours (might be 72 hours at 16°C).

Hope that helps good luck!


What are the obstacles to "refitting" the human body's metabolism?

Yes, you got it right. The theory you're referring to is called the thrifty gene hypothesis. There have been several attempts at "rigging" metabolism to reduce the amount of surplus calories stored as fat, as you suggest, and some of them have gone all the way to approved drugs.

One strategy is to block intestinal absorption of nutrients, so that excess food is simply excreted. Perhaps the most well known example is Orlistat, a prescription drug that prevents fat absorption by inhibiting lipases secreted by the pancreas. This has been proven (somewhat) effective in clinical trials, but also causes gastrointestinal problems like oily stool. Most drugs of this type, preventing the gut from doing normal digestion, will probably have this limitation.

There are also ideas about increasing metabolism of absorbed nutrients to "burn" more calories. Generally, utilization of nutrients in the body does not happen on its own; it is a consequence of activating other energy-demanding processes, like muscle contraction, brain activity, immune system function, and so on. And any attempt to increase metabolism, regardless of mechanism, will end up generating more heat. So in order to increase metabolism, it is necessary to turn on some heat-generating function (other than exercise :) Some research groups are experimenting with increasing energy expenditure in brown fat (a type of fat that normally oxidized nutrients to generate heat) to burn off excess nutrients. This is still a long way from medical use though.


Why would taking antibiotics increase stamina and energy?

I have never heard about this phenomenon from my patients or professors at the Medical School, but this is a possible mechanism that comes to my mind.

One of the classification for antibiotics takes consideration the effect on bacteria. Two possible effects are either stopping the proliferation (and letting the immune system to kill those that are currently present in the body) or killing bacteria directly.

The second approach is obviously more effective but has one big disadvantage: massive death of bacteria leads to the massive release of their toxins that are normally trapped within they bodies (so-called endotoxins). The symptoms you describe as "impossible fatigue" match exactly the symptoms of bacterial intoxication -- and this can increase upon the antibiotics intake.

Depending upon the bioavailability and pharmacokinetics some antibiotics might not kill all bacteria "on the first run" and the symptoms of intoxication recur several times with decreasing severity of manifestations.


Based on the species description in Speybroeck et al. 2016 and pattern of stripes (one central stripe with stripes on each side), and the lack of a distinct neck, the specimen in the top left appears to be an Eastern slow worm (Anguis colchica). That species is known to occur in Tbilisi.
Based on the species description in Speybroeck et al. 2016 a smooth snake (Coronella austriaca), also known from Tbilisi. The reddish color, two rows of dark spots, and the markings on the head are typical of this species. Also it can be seen that the anal scales are divided, which is a characteristic of this species.
Cited
Speybroeck et al. 2016. Field Guide to the Amphibians and Reptiles of Britain and Europe. Bloomsbury Natural History (publ).


What are these bugs skittering about the kitchen sink?

Those are springtails, order Collembola. Looks like they are in the family Entomobryidae. They are completely harmless. They don't bite, or spread disease. They often find their way into potted plants in people's homes. I'm not surprised that they are in your sink. Their small size makes them subject to desiccation.
https://en.wikipedia.org/wiki/Springtail https://en.wikipedia.org/wiki/Entomobryidae


Yes there are!

I think it would make more intuitive sense to you if you would have switched the words chimps and humans in your question:

  Are there genetic similarity between chimps and pigs that don't exist in humans?

Then, you would directly answer, of course, there are genes concerning bipedalism, brain (FoxP2 for example), digestive track (adult production of lactase for example) and so, and so… which are different in humans but might not have much reasons to be so different between pigs and chimps. Those mutations occured on the human lineage after the split between human and chimps.

To answer your question:

  Are there genetic similarity between humans and pigs that don't exist in chimps?

Yes. Most of these difference are due to mutations that occurred in the chimps lineage after the split of the original lineage into human lineage and chimps lineage.

The following are improbable but would also allow to explain such similarities:

Genetic admixture or introgression between human and pig after humans and chimps lineages splitted.
Convergent evolution.

Maybe pigs and human got the same beneficial mutation that never appeared in the chimps lineages.
Maybe pigs and human, due to the fact that today live in cold climates evolved the sequence ATTCGCTGA which cause them to produce a more efficient shivering!


Amazingly, yes.

See High level gene expression in mammalian cells by a nuclear T7-phage RNA polymerase. The authors recognize that the T7 RNA polymerase tends to work only in the cytoplasm thus is unable to transcribe genes in the nucleus. To remedy this limitation, the T7 polymerase was fused to a nuclear location signal peptide to localize the polymerase correctly.

Promega sells a T7 expression system for RNAi production.


How does DNA codon (5`-3`) convert to mRNA?

Your reasoning is correct and the table is wrong. The mRNA will have the same base sequence as the sense DNA strand (with T replaced by U).


How does blood reach skin cells and other closely packed cells?

The skin is highly vascularized up to the epidermis, with dense vessels right at the top of the dermis (your picture omits these, but you will find them in better diagrams like this one). The epidermis itself gets substantial oxygenation from the outside air (see Stücker et al, for example), though the very outermost layers are not metabolically active ("dead") and do not require oxygen.
As a gas, oxygen moves quite well through tissue, and cells can get sufficient oxygen from sources up to a few hundred micrometers away. No need to be in direct contact with blood cells (and typically no tissues of the body are in direct contact, besides vascular endothelial cells that line all blood vessels). Many small animals have no need for a circulatory system because their entire body is close enough to the outside for gas diffusion.

Stücker, M., Struk, A., Altmeyer, P., Herde, M., Baumgärtl, H., & Lübbers, D. W. (2002). The cutaneous uptake of atmospheric oxygen contributes significantly to the oxygen supply of human dermis and epidermis. The Journal of physiology, 538(3), 985-994.


How can you stabilize enzymes in pellets made from microcrystalline cellulose?

As you can probably guess from my comment, there are a lot of factors to take into account when thinking about protein stability. Here's what I would recommend you do.

First, make sure your extract is in a neutral buffer, like PBS, HEPES, or something similar. This is a fairly standard procedure when working with proteins. Next, since this is a kidney extract, there are likely to be gobs of proteases around, so I would strongly recommend adding broad-spectrum protease inhibitors, and keeping the extract as cold as possible to inhibit any enzyme activity. I would also add BSA at 10 mg/ml, both to stabilize the proteins and keep them from precipitating while in solution, and to lessen the chances that any proteases present will attack your enzyme of interest.

Once you have your solution stabilized, I would aliquot it and lyophilize it. Proteases are most active in solution, so once dried you'll reduce their activity even more. You can now add the inert ingredients (microcrystalline cellulose, etc.), mix thoroughly, press your tablets, and add the enteric coating. Finally, once everything is prepared, I would store the final product at as cold a temperature as is convenient. Again, this will inhibit any enzyme activity and prevent degradation.

I don't know if you have a functional assay to determine activity of the enzyme of interest, but if you don't I'd highly recommend developing one if at all possible. This way, you can test the activity of the fresh preparation of extract and compare it to various stages of processing into tablets, especially the finished goods, to ensure that you haven't lost much activity. I would also test random tablets throughout the year to make sure they haven't lost activity in storage, otherwise you won't be able to compare your experimental results.


As far as I can tell from the paper you linked to (Damiana et al) it is possible but inefficient:

  Naturally, we tried to translate ssDNA, but as previously described
  elsewhere, direct DNA translation was not really efficient in absence
  of antibiotics such as neomycin [5] and [6]. It seemed that the
  elongation phase was the limiting step in the direct translation of
  single-stranded DNA. Whether direct participation of DNA in protein
  synthesis could play any role in vivo must be excluded, although such
  a role could be attractive for modelling the evolution of the earliest
  forms of life.


Is this an eastern hemlock (Tsuga canadensis) seedling?

No, this is not a Tsuga canadensis seedling.

A hemlock seedling should look something like this:

http://www.uky.edu/hort/propagation-canadian-hemlock


Is there a reason why human eyesight and plants make use of the same wavelength of light?

Good question.

If you look at the spectral energy distribution in the accepted answer here, we see that photons with wavelengths less than ~300 nm are absorbed by species such as ozone. Much beyond 750 infrared radiation is largely absorbed by species such as water and carbon dioxide. Therefore the vast majority of solar photons reaching the surface have wavelengths that lie between these two extremes.

Therefore, I would suggest that surface organisms will have adapted to use these wavelengths of light whether it be used in photoreceptors or in photosynthesis since these are the wavelengths available; i.e., organisms have adapted to use these wavelengths of light, rather than these wavelengths being special per se (although in the specific case of photosynthesis there is a photon energy sweet spot).

For example this study suggests that some fungi might actually be able to utilize ionizing radiation in metabolism. This suggests that hypothetical organisms on a world bathed in ionizing radiation may evolve mechanisms to utilize this energy.


A quick google image search reveals that, indeed, Texas has quite lush forests. Remember that the state is extremely large (as compared to the Northeastern states, for example), and encompasses a huge variety of terrain, climates, rainfall amounts, etc. While the stereotypical view of Texas is rugged, dusty terrain:

From: http://texasmountaintrail.blogspot.com/2013/12/big-bend-landscape.html

The eastern part of the state borders Louisiana, and is definitely not dusty and dry:

From: https://www.flickr.com/photos/horwath/2488138213/

Rainfall varies across the state from east to west:

From: http://www.worldatlas.com/webimage/countrys/namerica/usstates/weathermaps/txprecip.htm

There are many different reasons why trees are not very likely to grow in certain regions, and these may vary from place to place. There may not be enough precipitation to support trees that are not adapted to a drier environment, while some species of grass could survive just fine. Temperature changes could be too severe between summer and winter (grasses just go dormant or die during harsh winters, and regrow in the spring). Fire is a big issue, as well - prairies often burn, and while grasses can regrow quite quickly, a tree that doesn't mature for 20 years may not make it between fires. Grasslands also have very deep, tightly-intertwined root networks, with some reaching 15 feet (~5m) or more below the surface:

(Click image for higher-resolution PDF)From: http://www.conservationresearchinstitute.org/educational-offerings.html

Tree species that survive the other challenges may not be able to penetrate deeply enough to adequately take root, sustain itself, and not fall over. Also, speaking of which, grasslands tend to be susceptible to tornadoes as well, and while grasses just bend before the wind, trees get uprooted or break. So, while any one or two of these issues may be overcome by a particular tree species, when added together it translates into a very inhospitable environment for trees.


In most species, females are pregnant as often as they can be. Since the availability of sex is rarely a limiting factor, it seems likely that female bonobos are as "always" pregnant as other chimps and socially living primates. The actual rate of pregnancy will be hormonally limited by things such as reduced fertility during lactation and so on.


There is variance in egg shape; sea-birds often use a more pear or conical shaped egg to prevent it from rolling off the cliff (where they nest) if it is disturbed. Some reptiles lay very spherical eggs (some turtles) whereas some reptiles lay very elongated ones (see black pine snake eggs).
I imagine that we don't see square eggs because they would be difficult to shape and difficult to lay. Shape may also influence strength.
Google your question (like I did after writing the above) and it will come up with this article which pretty much says what I just did. Here are some of the author's key points...

"If eggs were rectangular little boxes, they would be very strong on the corners, but very weak in the middle of the straight walls."
"The strongest shape of all is a ball, or sphere. But if you were to push or gently nudge a spherical egg, it would roll away downhill, never to be seen again."
"So one reason that eggs have an asymmetric tapered oval shape is that if you nudge them, they'll come back to you. They'll sweep out a circle around the pointed end, and come to a stop with the pointed end facing uphill. In fact, the eggs of birds that have their nests on cliffs are more oval than the eggs of birds that nest on the ground. This means the 'more-oval' eggs of these cliff-nesting birds will roll in a very tight little circle, and be less likely to roll out of the nest — and off the cliff."
"Another reason for eggs to be egg-shaped is that they fit together quite snugly in the nest, with only small air spaces between them. "
"Yet another reason that eggs are tapered is so that they can get pushed out of the hen."


Are Protocadherin Gamma Cluster transcripts considered separate genes?

I would say they are considered different genes because each isoform is under the control of its own promoter.


Affinity Column of membrane bound receptors

This is a classic reference where Stanley Cohen and Graham Carpenter used an affinity column made out of the epidermal growth factor (EGF), and used it to purify the EGF receptor: JBC 1980


If the question is related to exposure to radiation in a Nuclear submarine then the answer is valid for radiation exposure irrespective of the place.

As you are aware there are many effects of radiation. Some of them are.

  Nausea and vomiting
  Diarrhea
  Skin burns (skin reddening)
  Weakness
  Lethargy and fatigue
  Loss of appetite (anorexia)
  Fainting
  Dehydration
  Inflammation of tissues (swelling, redness or tenderness)
  Hemorrhages under the skin
  Bleeding from your nose, gums or mouth
  Anemia
  Hair loss (usually from just the scalp)
  Decrease in platelets (reference)

Of course there is no safe quantity of radiation that has been quantified (reference) and there are personal anecdotes by submarine officers about first hand problems they faced due to radiation (reference). However, since this is a career you chose, you can be happy that the amount of radiation that you would be exposed to has decreased over the years (reference). Since you are interested in the biological aspect of what happens in your body due to radiation, I quote

  When cells -- and what lies within them -- get exposed to radiation,
  components of DNA and critical proteins within the cell get all jazzed
  up (ionized), meaning that the electrons with our atoms get kicked
  out, causing the DNA strands to break and the proteins to cramp up
  (denature).

  Ionizing Radiation:

  Leads to the production of free radicals
  Breaks critical chemical bonds
  Leads to changes in cellular structure within irradiated cells
  Damages vital molecules, such as DNA, RNA, and other regulatory
  proteins

  Because our cells are mostly water, this ionizing radiation breaking
  H$_2$0 down is harmful to free radicals (H$^+$ and OH$^-$). While cells are
  damaged by free radicals all the time, they normally repair
  themselves, keeping the body healthy. However, high doses of radiation
  can damage the cell's ability to repair itself, and then all hell
  breaks loose.

  This shakes things up all over the body.

  Let's do a head-to-toe walk-through to investigate how high doses of
  radiation can damage the human body.

  BRAIN: Nerve cells (neurons) and brain blood vessels can die, leading to seizures.

  EYES: Radiation exposure increases the risk of cataracts.

  THYROID: When a nuclear reactor malfunctions, radioactive iodine (I-131) can be released into the atmosphere (this is one of the
  particles that hangs out in a "radioactive plume"). The thyroid is
  very sensitive to the effects of I-131 (in fact, I-131's affinity for
  the thyroid is used therapeutically to specifically attract radiation
  to the thyroid in order to treat thyroid cancer and overactive
  thyroid). When a healthy thyroid is exposed to I-131, it can lead to
  decreased thyroid function and, over time, thyroid cancer.

  LUNGS: When you breathe in invisible nuclear fallout particles, it can lead to lung cancer down the road.

  HEART: High doses of radiation can damage the cells in the blood vessels that feed the heart, reducing cardiac function.

  GI TRACT: Sensitive cells in the intestinal lining can be damaged, leading to nausea, bloody vomiting, and bloody diarrhea.

  REPRODUCTIVE ORGANS: Rapidly dividing cells (eggs and sperm) in the ovaries and testes can die, leading to sterility.

  SKIN: Rapidly dividing skin cells can be damaged, leading to skin lesions and burn.

  LYMPHATIC SYSTEM: Rapidly dividing lymphatic cells die and damaged bone marrow may have trouble replenishing these immune-boosting cells,
  increasing the risk of infection (reference).

Many jobs have occupational diseases connected with it so I would say don't worry about it too much, enjoy your job and keep your fingers off the firing mechanism.


Depends what you consider an organ. Typically though it's the cells which require the most metabolic activity which have the shortest life span. The kidney is the most of the major internal organs with up to 36 hours with liver coming second at up to 16 hours.


Yes you could think of an individual as having both(1).  A good place to start looking at "newer" diabetes other than the classic 1 and 2 is latent autoimmune diabetes (LADA).  Though, I don't know if one would say you had no insulin production.  It would seem as though patients exhibit some characteristics of both types(2), and indeed there maybe a continuum possible(3) between ether "pure" type on each extreme.

(1) The type 2 diabetes-associated variant in TCF7L2 is associated with latent autoimmune diabetes in adult Europeans and the gene effect is modified by obesity: a meta-analysis and an individual study. Diabetologia. 2012 Mar;55(3):689-93. doi: 10.1007/s00125-011-2378-z. Epub 2011 Nov 23.

(2) Latent autoimmune diabetes (LADA) is perched between type 1 and type 2: evidence from adults in one region of Spain. Diabetes/Metabolism Research and Reviews 2013; 1520-7560.

(3) Latent autoimmune diabetes in adults: evidences for diabetes spectrum?.Chin Med J 2013;126:783-788


Why do crows sit on treetops even when it is cold?

Birds (crows inclusive) have better heat conservation adaptations as compared to humans. Some of these are (but not limited to):

-Hollow tubes in feathers which provide insulation reducing heat loss.

-Reduction of appendage length especially in species that dwell in cold regions.

So conditions we perceive as cold are relatively warm for birds.

  My first guess was that it isn't cold enough.

From this question on biology.se I can say it could be warm for them as it addresses birds surviving at -40C. Plus some of the answers and comments on the same question cover a couple of adaptations that birds exhibit to strive in such conditions.

edit: links that provide additional information on the same

-http://toughlittlebirds.com/2012/12/26/how-do-birds-keep-warm/
-https://beyondpenguins.ehe.osu.edu/issue/arctic-and-anarctic-birds/how-do-birds-stay-warm
-http://birding.about.com/od/birdingbasics/a/howbirdskeepwarm.htm
-http://gardenwalkgardentalk.com/2013/02/19/how-do-birds-keep-warm-in-winter/


How can I calculate Shannon-Wiener diversity index in caves with different kind of habitats and different sampling methods?

You could account for this in your statistical analysis. I'm assuming that  you will collect terrestrial fauna the same way in every cave, and if there is a stream in a cave aquatic fauna will be collected in some standardized way as well. I'll also assume you'll have some other explanatory variables that you think may explain diversity, richness, or abundance. These could include cave temperature, length, depth, etc.

Calculate the Shannon-Weiner index for each cave using all species and abundances, whether they came from an aquatic or terrestrial sample. Then for you statistical model include whether a stream was present in a cave or not using a binary variable along with your other explanatory variables.

index ~ f(temperature, length, depth, stream)

In this example temperature, length, and depth are all continuous variables. Stream will be a binary variable (either 0 or 1, 1 meaning a stream was present). This will give you a measure of how much a stream contributes to diversity.


Why does a coconut have exactly three "holes"?

The three "holes" are the result of the 3 carpels in coconut flowers, and three carpels is typical of the family Arecaceae (Palms). The "holes" are actually germination pores, where one is usually functional and the other two are plugged. The new coconunt shoot will emerge from the functional, open, germination pore.

For further info and pictures, see this webpage or the paper Morphological and anatomical studies of the coconut (Smit 1970, link to pdf), which holds a wealth of information.


How many areas are there in Brodmann map?

I am no expert on the topic, but according to an article published on the centenary of his study, it states that the microscopical structure and classification of these areas are in parallel to the evolutionary distinction between old and new cortical subdivisions. So as and when new subdivisions are deduced (based on its function, cytoarchitecture or the structure and organisation of cells) the map can be extended to include them. There was no upper limit to the number of divisions set in any article I read so it would be nice if you could provide some reference to where it says that the extension can be done to 54. If you are interested, you could have a look at the map published by Constantin von Economo in 1925.


What happens to the nitrogen when an oxygen machine delivers only oxygen?

The nitrogen is returned to the air around the machine.  See Wikipedia's article on the oxygen concentrator for details about how the machine separates the nitrogen and oxygen.


What are the classical adaptations of amphibians?

"Amphibian" means "living both in water and on land" (see here). Here is a small list of classic adaptations in amphibians:

Eyes and nostril are positioned to poke out of the water while the rest of the body is immersed
Ears don't let any water gets in
Skin is very thin and allow direct gazeous and water exchange
Paws are webbed to move into water
Larvae of most amphibian species start their life in the water


Which components grow in size but not in number and which grow in number but not in size?

We navigated through this question with Fenil in comments, I'll resume the answer here:

Osteocytes

We know from this page that "osteocytes have an average half life of 25 years, they do not divide" and that "when osteoblasts become trapped in the matrix that they secrete, they become osteocytes. Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi".

We can thus conclude that bone cells don't grow in numbers, but in size by their cytoplasmic extensions.

Hair follicles

Well, we draw the conclusion that hair follicles grow in number and not in size based on the following common sense observations:

We don't get to see tiny hair follicles in babies and giant ones in adults;
If they don't grow in size, either they grow in number or they become less and less dense as the skin surface grows with age. If the latter, we should see the same hair number in babies and in adults, whichever their height is, and this is obviously not the case.

So, they grow in number.

The answer is $A$.


Does self replicating RNA occur in nature?

They probably existed in the beginning of life (on Earth or somewhere else). But any free RNA now would be almost immediately devoured by bacteria or other organisms.

Bacteria are ubiquitous. That's one of the first things you learn in a microbiology course. We do this experiment a few times: open up a Petri dish far from a Bunsen burner, and in a few days you can see how many bacteria and/or fungus colonies have grown in the Agar. Any good microbiology book will show you this. I have none right now with me, but have just found a few links by  searching for "bacteria are ubiquitous" on Google: Understanding Bacteria, The Purple Phototrophic Bacteria, Bacteria in Agrobiology: Plant Probiotics and Public Health and Infectious Diseases.

As for the science studying the origin of life, I recommend The Fifth Miracle: The Search for the Origin and Meaning of Life, by Paul Davies.


One example that I am aware of where an animal transgene was put into a plant was to produce the ZMapp, a chimeric, monoclonal antibody against the Ebola virus.

This is a wikipedia article on ZMapp, that gives you an idea of the process.

Other than this, I am not all that familiar with plant transgenics, other than Round Up resistance genes that were transfected from soil bacteria that developed a resistance to the active chemical in Round Up.

Hopefully other answers can provide you with more details, but these are the two examples that I know off the top of my head.


Optical Density is synonymous with absorbance which is based on the principle of absorption of light. The machine that is used to measure absorbance is called a spectrophotometer. Spectrometer does not indicate that light absorbance is being measured. A spectrometer can measure any spectrum; for e.g. Mass Spectrometer measures the spectrum of molecular mass (to be precice mass per charge).

Cell density can be also measured by the level of light scattering; turbidimeters or nephelometers are used for these kind of measurements.

PS: You should pay more attention in your class :P


What are the effects of buffer on genomic DNA shearing by sonication?

Could you use a spun column to exchange the buffer? Some sort of gel filtration column; equilibrate column in TE; add your DNA sample, spin through excluded DNA. TKMC components will be included in the column and thus retained.

Update
Have a look at this paper, and references therein. Apparently magnesium ions influence the flexibility of DNA. Clearly if the shape of your DNA in the two buffers is different this would impact upon the effects of shearing forces.


I will alter this answer in response to the poster's comments.
Looking at:
https://genent.cals.ncsu.edu/bug-bytes/circulatory-system/
The diagram doesn't show the digestive system - so no anus.
I see that there is expected to be an ostium (hole) near the end of the heart.
Think about where in the heart the many valves are located, then look at the segments of the abdomen and work out what happens with the heart when the abdomen extends or contracts, which you can see in bees.
What is more interesting in all the diagrams is the decision about whether the heart pumps just to the head, or also through pipes to the ventral region.


Setting up the binomial distribution:
For generation F1 each parent (F0) has a 50% chance of contribution the chromosome (under your simplified model), i.e. p=0.5, n=46 for the binomial distribution. I assume that when you say the 'normal' range you are looking for the mean +- 1 standard deviation? For p=0.5, n=46: mean=23 with standard deviation=3.39116 which helps define: Pr(20≤X≤26)=0.698. So in about 70% of cases a child will inherit 20-26 of their chromosomes from one parent.
For generation F2 each grandparent has a 25% probability of contributing a chromosome so we use p=0.25, n=46 which gives: mean = 11.5, standard deviation=2.93684 Pr(9≤X≤14)=0.6936. So in about 70% of cases a grandparent will have contributed 9-14 chromosomes.


Is the DNA different in each type of cell? What DNA is passed to offspring?

Most cells in a human body contain a complete set of the genome, which is two sets of 23 chromosomes. Having two of each chromosome is called diploidy.

Within an individual human the DNA is approximately identical in every cell. Different cells are produced by differential use of that DNA: certain genes are more (or less) highly expressed etc. You can read more about that here.

You inherit one copy of each chromosome from each parent. Gametes (eggs and sperm) are a bit different from regular cells because they contain one copy of each chromosome; they are haploid. These gametes fuse to make the complete set of 23 pairs in the offspring. There are some exceptions such as cytoplasmic DNA and sex chromosomes.


Determination of animal and vegetal pole

Do you have any reason to doubt this statement? The wikipedia article says pretty much the same thing. When reading the folllowing, don't forget that one can talk about such poles at different stages of development.

  The animal pole consists of small cells that divide rapidly, in contrast with the vegetal pole below it. In some cases, the animal pole is thought to differentiate into the later embryo itself, forming the three primary germ layers and participating in gastrulation. [..] The vegetal pole contains large yolky cells that divide very slowly, in contrast with the animal pole above it. [..] The animal hemisphere is dark brown, and the vegetal hemisphere is only weakly pigmented.

and it comes with the following picture


Insect making continuous sound in summers

These are Cicadas, of the superfamily Cicadoidea of the order Hemiptera.

These sounds are made by the males to attract mates. There are a lot of species, each making there own specific sound to attract the right mate. However, to the human ear, these sounds don't sound different. Cicadas are also able to produce other sounds, in distress or during courtship and mating, but the continuous sound during night and day is to attract mates.


Is it possible to deduce facts about a person's parents just by studying his/her genome?

Not the kind of complex phenotype that you describe (because nobody knows for example if/how "being abusive" is written in the genome), but yes, some things can be determined.

The easiest is through sex chromosomes.

For example: if you look at the X chromosome of a man, you can tell for sure that it comes from his mother (because the Y can only come from the father, quite logically) so any allele that you see there is also part of the mother's genome - but since she has a second copy, maybe it does not translate into a phenotype.

Sometimes you can even guess the phenotype of one of the parents: if you study a woman's X chromosomes and see that both have alleles that cause color-blindness (encoded on this chromosome) it means that the only X chromosome of the father has this allele, so the father is probably color-blind.

See: https://ghr.nlm.nih.gov/condition/color-vision-deficiency


Why some tissues like small intestine epithelium are able to be replaced so often, yet they are not one of the most common cancers?

The human prostate has two main epithelial cell types, basal and luminal, as well as a minor population of neuroendocrine cells. Primary prostate cancer nearly always has a luminal phenotype characterized by atypical glands, strong androgen receptor (AR) signaling, and an absence of basal cells .                  Intestinal epithelium. The intestinal epithelium is the single cell layer that form the luminal surface (lining) of both the small and large intestine (colon) of the gastrointestinal tract.


There are about 100 (Purves, 2001) to 400 (Zozulya et al., 2001) functional olfactory receptors in man. While the total tally of olfactory receptor genes exceeds 1000, more than half of them are inactive pseudogenes. The combined activity of the expressed functional receptors accounts for the number of distinct odors that can be discriminated by the human olfactory system, which is estimated to be about 10,000 (Purves, 2001).

Different receptors are sensitive to subsets of chemicals that define a “tuning curve.” Depending on the particular olfactory receptor molecules they contain, some olfactory receptor neurons exhibit marked selectivity to particular chemical stimuli, whereas others are activated by a number of different odorant molecules. In addition, olfactory receptor neurons can exhibit different thresholds for a particular odorant. How these olfactory responses encode a specific odorant is a complex issue that is unlikely to be explained at the level of the primary neurons (Purves, 2001).

So in a way, the answer to your question is yes, as there are approximately 100 to 400 olfactory receptors. Just like the photoreceptors in the visual system, each sensory neuron in the olfactory epithelium in the nose expresses only a single receptor gene (Kimball). In the visual system for color vision there are just three (red, green and blue cones - RGB) types of sensory neurons, so it's a bit more complicated in olfaction.

References
- Purves et al, Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Zozulya et al., Genome Biol (2001); 2(6): research0018.1–0018.12

Sources
- Kimball's Biology Pages


Why do insects avoid being on their back?

Welcome to Biology.SE

Insects don't "like" being on their back because they can't get back on their legs and they therefore get stuck somewhere where they can gently wait for death to come.

Not all insects are unable to switch back on their legs but some can't do that (or can hardly do that). The reasons for which many insects are not able to get back on their legs (while mammals for example usually can do that) is that they have a exoskeleton. Their exoskeleton limits drastically their movements.


What happens when we re-start a PCR reaction?

The polymerase used in PCR is extremely stable at room temperature. I would expect you to be able to continue your PCR reaction from the cycle it was stopped at without too much trouble. However, it is important to not over cycle your product. This will produce non-specific products. If a clean result is imperative, take a 1-5ul sample from your original reaction to use as a template in a new reaction.


How should "the human genome" be interpreted?

Certainly individuals have unique genomes. The human genome sequencing project used DNA from a handful of volunteers, and the reference human genome that resulted from this project can be thought of as an "average" genome for those individuals. Where sequences differed between the individuals, a representative consensus sequence was chosen. Hence, the sequence of a gene from a given individual may not perfectly match the reference genome, although mostly the differences are small: genetic difference between humans is estimated to be around 0.1 --- 0.4%, which means a few million base pairs in total.

As DNA sequencing is nowadays orders of magnitude cheaper, genomes for larger number of individuals are being sequenced; see for example the 1000 genomes project.


In It’s Not Just Conflict That Motivates Killing of Orangutans by Davis et al. (2013), the authors identify number of conflict and non-conflict reasons reported in the study why orangutans were killed in a certain part of Indonesia:

Conflict reasons:

pest
fear/self-defence
paid or forced to kill
orangutans interrupted logging or forestry operations

Non-conflict reasons:

traditional medicine
food
to sell or keep young as pets
hobby/sport hunting
for other trade of animals or meat
killed accidentally or opportunistically while hunting other animals

The results from this survey are depicted in this graph:

Obviously in this case they were not attacked for food. The impression I got from the article makes me think it was probably motivated by people viewing them as pests or as a threat/danger. It is almost certainly more of a social reason than a biological reason. However, in the absence of specific evidence, it is probably not helpful to speculate why this occurred.


Appears to be a ciliate protist called Vorticella.

 Image source: Wikimedia (Author: Frank fox, 2010)
Vorticella always stood out to me because of their long, narrow stalk they use for anchoring with ciliate-lined bell-shaped oral end.

 Image source: MicrobeWiki (originally from Haw River Program)
Fun fact from Wikipedia:

The stalk is made up of the spasmoneme [also called "myoneme" above], a contractile organelle, with rigid rod filaments, batonnets, surrounding it. The coiled spasmoneme and batonnets serve as a molecular spring, so that Vorticella can contract. The cell body can move hundreds of micrometers in milliseconds. The spasmoneme is said to have higher specific power than the engine of the average car.

You likely mistook this for the more-commonly known rotifer due to the beating cilia at the oral end and tendency to anchor down, which are also both characteristics seen in rotifers. See this SE post about rotifers I wrote a while back which includes some nice animations.
Also, you can quickly differentiate Vorticella (which are typically free-living) from closely-related and morphologically-similar Carchesium, which are colonial.
See this video ("Vorticella - Under the Microscope) by Nick Moore) for various videos and some more info.


What is the eye muscle status when you stare at distant view through a glass wall?

In the situation you describe, the eye would be focused on the distant mountain.  This would mean that the lens would be stretched and thin in order to minimize the focussing power of the eye.  Therefore the ciliary muscles would be relaxed.

When you are looking out of the window, it is possible to make a conscious decision to focus on the window pane itself (thus adjusting the focus to be more powerful as the ciliary muscles contract), however then the distant object will be out of focus and uncomfortable to look at.

This is because the light rays reflecting from the mountain are barely affected by the pane of glass, hence its transparency.


It's a sycamore fig (Ficus sycomorus)- a type of Mediterranean fig.

For details: see this wiki page


What is the meaning of "leukemic cell recovery" in an abstract?

TL;DR: Yes, it's just percentage of cells that survived. With the caveat that the assay doesn't give information on how much the number of cells is influenced by survival, dying, or growth rate.
"Recovery" in this context means "cells found after X amount of culture time". Generally speaking, recovery often refers to putting something in a program/dish/liquid/organism and seeing how much is still left after some processing/treatment/culture. For example, if I give a 1-year-old child 10 porcellain plates to play with, I might be interested in what percentage I can recover after 2h of play time. Of course in the context of cell culture, that percentage can be above 100% if the cells multiplied in the meantime.
As the methods of the article describe, the culture assay consists of first growing a single layer of stromal cells (HS-5 cells) on a culture plate for 24h. These cells provide support for the actual cells of interest. The researchers then spread 5.0 × 105 viable T-ALL lymphoblasts isolated from a patient sample on the stromal cell layer. They do this twice* for each sample, in one case collecting the cells after 1h (which isn't usually enough time for human cells to do anything), in the other case collecting them after 72h of culture (which is enough for healthy cells to grow substantially). Then they use flow cytometry to quantify how many T-ALL cells are now in the culture after that time has elapsed.
This helpful graphic is from the paper. The word "cells" in the formula refers to T-ALL cells.

The percentage of recovered T-ALL cells (RTC) was calculated by:

Essentially, what the authors here studied is whether the likelihood of a T-ALL patient to relapse might be related to the ability of their cancerous cells to survive or grow in a culture dish coated with stromal cells.
The quote from your colleague would mean that the T cells were surviving/growing less or dying more if they were transduced with the receptor.
*rather, four times. Twice for 1h and twice for 72h collection. At least this is what "in duplicate" implies.


Why does the slope of parent-offspring regression equals the heritability in the narrow sense?

Well, I think I found the very simple mistake I made…

Looking again in my equations, I realize that (for some reason) $cor = 2 \cdot \frac{\sigma_A^2}{\sigma}$

And looking at this website, I see that the slope of the parent-offspring regression is $\frac{h_N^2}{2} = slope$

Here was my mistake!


Sequencing the genomes of polyploid organisms

Take a look at the strategies used to sequence the wheat genome. Wheat is hexaploid. The project is described at http://www.wheatgenome.org/.

For early work on the maize genome, we employed methyl filtration in order to reduce genome complexity and size - transposons are filtered out and genes + promoters and such remain. The gene sequences are different from the two genomes, so says the theory, and those can be distinguished. See http://www.ncbi.nlm.nih.gov/pubmed/10545948 for the reference.


Is it Theoretically Possible to Create a Male clone from the donor Cell of a Female?

So, i want to know if the sex of the resulting clone is determined by
  the sex of the donor animal.

Generally yes for mammals and birds. In animals where the sex is determined by sex chromosomes, the sex of the clone will be dependent by the sex of the donor.

In animals (ie turtles and crocodiles) where the sex is determined by external factors (ie temperature), then the sex of clones will not be dependent on its donor.

  would it be theoretically possible to create a male clone where a
  single woman contributes both the egg and somatic cells used in the
  cloning process?

Short answer is No.

Sex in mammals and thus humans is dependent on presence or absence of the Y chromosome. If the Y Chromosome is present, the mammal is male. If absent the mammal is female.  So a woman does not have the Y chromosome. Hence it is not possible to create a male from her genetic material.

Longer answer... anything is possible. A woman does not have a Y chromosome, so if you added a Y chromosome to one of her ES cells and then used those cells to form the inner cell mass of a blastocyst, then yes you can get a male.


Correlation between genome size and mutation rate?

Bradwell et al. report RNA viruses with the smallest genome may have particularly high mutation rates. A particular bug was shown to have about 1.4 x $10^{-4}$ substitutions per nucleotide per round of copying (high for viruses generally) and the authors suggest this is to optimize adaptibility. Correlation Between Mutation Rate and Genome Size in Riboviruses: Mutation Rate of Bacteriophage $Q \beta$, Genetics, vol.195 no. 1 243-51 (2013).

Cuevas et al. report a phage with 1.0 x $10^{-6}$ mutations per base per round of copying (m/b/r), which conforms (they state) to Drake's rule of 0.003 mutations per genome per round of copying in DNA-based microorganisms. They indicate that DNA-based microorganisms range between $10^{-10}$ to $10^{-6}$ m/b/r. They state that RNA viruses vary between $10^{-6}$ and $10^{-4}$ m/b/r, consistent with the result above. Point Mutation Rate of Bacteriophage $\Phi X174,$ Genetics, vol. 183 no 2 (2009).

Drake's paper often-cited paper (one of them) is available at this link.
He has a remarkable graph on p. 7163 of this paper in which based on his observation of seven microorganisms with a wide range of genome size (bp) he plots the log of the mutation rate per base pair against the log of genome size (bp). The resulting (fitted) line has a slope of roughly negative one.

In a nutshell, Drake shows that over a wide range of genome size, as the genome size climbs exponentially the mutations per base per round of copying drops exponentially. This relationship is roughly log-log linear.

In his discussion he says that the factors influencing mutation rates (in either direction) are so general that they seem to have imposed a small range of variation of mutation rate per genome in microbes that have a large range in genome size and mutation rate per base pair.

As for more complex organisms, I have read very little. There is a recent review article in Nature about a report that a hypothesized inverse correlation between genome size and mutation rates in certain plants (angiosperms) is untrue. Genome size is positively correlated with genome size. Plants with the larger genomes have higher mutation rates than those with smaller than average genomes. I don't have access to this pay-walled article or the methods involved so I am quoting the abstract. Tasci, Nature Reviews Genetics 13, 148 (March 2012).

As usual an expert in this area could correct/expand these few details I've found but it's an interesting question. Drake's paper gives a remarkable result.

As for the question about correlation coefficient, I think that Drake's graph suggests a strong correlation between linearized functions over a certain range.
I suppose we could attach a number to that...


Why are so many species reproducing late this year?

It's hard to say without more information, but one substantial possibility is that you are mistaken that species are reproducing late - that's a problem with anecdotal rather than scientific data!
Additionally, species you mention like the common coot can attempt multiple broods where the season is long enough. Wikipedia specifically mentions Britain:

Eurasian coots normally only have a single brood each year but in some areas such as Britain they will sometimes attempt a second brood

The same could be true for species of frogs/toads and fish, so without knowing specific species it can't be known whether these are species reproducing again or species reproducing late.


Do mitochondria contain the genes to specify themselves?

The answer is a bit more complicated than that. Mitochondria contain their own genome called mitochondrial DNA (mtDNA), encoding 13 proteins that are part of respiratory complexes I, III, IV, and V, 22 transfer RNAs (tRNAs), and two ribosomal RNAs (rRNAs). The separate tRNAs and rRNAs are necessary because the mitochondrial genome uses a slightly different genetic code than the nuclear genome.

So, the mitochondria contain nearly all of the genes necessary to construct the respiratory chain, as well as the machinery to translate the mRNA into protein. However, it does not contain any of the genes necessary to actually replicate the mtDNA (DNA polymerases, etc.) or construct the mitochondrion itself - synthesize the components of the different membranes, arrange the membranes in their required conformation, chaperones to assemble the complexes of the respiratory chain, etc. - these are all encoded in the nuclear DNA.


What Evidence Do We Have For the First Mammal?

Obviously, it's impossible to point to "the" earliest mammal; dividing lines are pretty much arbitrary. However, a reasonable representative of a very early mammal or very late mammaliaform is Arboroharamiya jenkinsi, described in A new arboreal haramiyid shows the diversity of crown mammals in the Jurassic period, from roughly 155-160 million years ago.  That shows a number of fossils, including this quite nice one:

The supplementary information shows some cranial features, including this:

A related species from roughly the same time period, Haramiyavia clemmenseni, had CT scanning done on this fossil mandible:

yielding images like this:

Similarly, the euharamiyidans were either very early mammals or very mammal-like cynodonts, which are known from a number of quite nice fossils including these three (described in Three new Jurassic euharamiyidan species reinforce early divergence of mammals):


Are there any known mutual symbiotic relationships that has more than two agents?

I think what you are asking for is "Multiple Mutualism". Normally,

Most of the known cases of multiple mutualism involve relationships in
which two of the partners are at the same organizational level—usually
two bacteria that might be interacting directly—but are both essential
for the survival of the host
— Entente cordiale: Multiple symbiosis illustrates the intricate interconnectivity of nature -Philip Hunter

For example, the glassy-winged sharpshooter (Homalodisca coagulata) primarily feeds on xylem-fluid which is low on organic nutrients…so it depends on 2 bacteria, Baumannia cicadellinicola and Sulcia muelleri. The sharpshooter provides these with raw carbon skeletons present in the xylem fluid, and those bacteria in return synthesizes vitamins, essential amino acids, etc. For more detailed study, see Wu et al, 2006.
However, there are also examples of three-way mutualistic symbioses in which all the partners are at different organizational levels. One known case involving a virus, a bacterium and an insect, see Moran NA, Degnan PH, Santos SR, Dunbar HE, Ochman H (2005) The players in a mutualistic symbiosis: insects, bacteria, viruses, and virulence genes. Proc Natl Acad Sci USA 102: 16919–16926
Anyway, the essence as stated by Andreas Brune, Professor of Biogeochemistry at the Max Planck Institute for Terrestrial Microbiology in Marburg, Germany:

Multiple symbiosis is probably more widespread than we think, especially in view of the symbiotic systems involving different organizational levels, for example between bacterium, nematode and insect, or bacterium, protozoan and insect.


Depends completely on how good ultrasound you are producing.

Will they interpret your signal as an obstacle ?

Not really until you produce signals exactly calculated for the distance and speed of bat from obstacle. Here something known as dopler effect will come into play which will make bats understand probably thats not their sound. Otherwise every bat would have made a noise to divert another bat.

Is just making sound good for dislocating

Well, till this date we don't know what humans are speaking from their sound waves what you can guess for bat for what they did just speak. If you listen closely to bat sound you will find amplitude variation at non-constant duration.

Here is a detail of what else bats use . Its harmonics that takes sleep of physicists.


How are haplotype blocks different from genes?

Haplotype blocks may cover more than just one gene.

While positions within a gene are also in high linkage disequilbrium (or well correlated) with each other, this phenomena of high LD may extend beyond the gene body and overlap with the next gene.  A good visual representation of this comes from Jeffreys et al. in the figure below:

Red means more LD, black means zero LD.  Each point in the heatmap is essentially a pairwise correlation between two points in the genome.  Therefore regions of red represent regions of high LD or haplotype blocks.  Going from left to right we can see that each gene appears to be in its own block of high LD.  However, the genes PSMB9 and TAP1 appear to be in the same block.  Other examples exist as well, a great source is this review.


Difference between bacterial chlorophylls

From A search in Pubchem database, in substances for bacterioviridin, it seems just another synonym for bacteriochlorophyll-C.

.

The incomplete page do not show any image-entry. From another entry about bacteriochlorophyll-C, I've took the following image:

Bacteriochlorophyll-C; which is being told same as Bacterioviridin

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From similar search on same website for bacteriopurpurin, it shows,

Bacteriopurpurin

is a Xanthophyll compound; with another similar entry Bacteriopurpurin

It is also being called Hydroxyspirilloxanthin

....................................

Another search reslult, Bacteriopurpurin 18,

shows this photo:

Which is clearly a porphyrin-type compound (With smaller 4 pyrrole-type rings) with nitrogen (N) atoms.

......................................

......................................

Though you have not mentioned in the original question, another such old term is Chlorobium-chlorophyll. When searched ;  there i could found one entry in the PubChem database, about chlorobium chlorophyll; which tells; it is same as bacteriochlorophyll-D, though the incomplete page does not display any structure.

From some other entry about bacteriochlorophyll-d; the structure given here:

Bacteriochlorophyll-D, which is being told same as chlorobium chlorophyll. Look this has a little bit different structure from bacteriochlorophyll-C (bacterioviridin according to pubchem) , because chlorophyll-D (this) is lacking a methyl group at left hand middle side of the photo.

................................................

However, I cannot ensure they are free from nomenclatural conflicts. IMO it is better to use modern terms like bacteriochlorophyll-a, b, c, d, e, f and g.

................................................

  Reference: The PubChem Project by NCBI

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N.B. :

To quickly find differences among some main types of chlorophylls and bacteriochlorophylls; I've attached the following diagram. Most of the pictures are taken from PubChem; two I couldn't found in Pubchem, so I took them from a PMC articles. All are linked below the diagram.

Comparisons among some chlorophylls and bacteriochlorophylls.

Sources:

Chlorophyll-A : PubChem, Wikipedia .
Chlorophyll-B : PubChem, Wikipedia .
Chlorophyll-C1 : Pubchem (PubChem also tells as "Chlorophyllide C1") .
Chlorophyll-C2 : Pubchem (PubChem also tells as "Chlorophyllide C2") .
Chlorophyll-C (C1, C2, etc): Wikipedia .
Chlorophyll-D : PubChem, Wikipedia  .
Chlorophyll-E: No records seen.
Chlorophyll-F: PubChem .
Chlorophyll-F ' : PubChem .
Bacteriochlorophyll-A :  PubChem .
Bacteriochlorophyll-B : PubChem .
Bacteriochlorophyll-C : PubChem (Bacterioviridin) .
Bacteriochlorophyll-D : PubChem (Chlorobium chlorophyll) .
Bacteriochlorophyll-EF : A PMC article  * .
Bacteriochlorophyll-FF : same PMC article  * .
Bacteriochlorophyll-G : PubChem .

The PMC Article * : Bacteriochlorophyll f: properties of chlorosomes containing the “forbidden chlorophyll”, by Vogl, Tank, Orf, Blankenship, Bryant.

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How can I calculate alpha helix content from molar ellipticity?

You can use the information at this site, especially section 3. (https://www.photophysics.com/resources/tutorials/circular-dichroism-cd-spectroscopy)

Notice the different CD spectra for alpha-helix, beta-sheets and random coil. If your protein is measured at 222nm you need to compare your measured values to the the spectra at 222nm, this will allow you to guestimate the secondary structure of the protein, but if you want to be accurate, you will need to measure at several wavelengths to determine the distribution of alpha helix, beta-sheet and random coil. This is because all three contribute to the measure spectra and as such you need several measurements to figure out the relative contributions of each secondary structure.


Ercc1-/-DAT-Cre means the mice with Cre recombinase mediated conditional knockout of Ercc1 in the DA neurons. DAT-Cre is the mouse strain that expresses Cre recombinase from the promoter of Dopamine transporter.

  Cre-recombinase:loxP (Cre-loxP) system was used to generate mutants
  with targeted deletion in dopamine transporter (DAT)-expressing
  neurons. Specificity of Cre recombinase activity was validated using a
  lacZ reporter that confirmed expression in DA neurons of the SNpc and
  not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Figure S1).

From supplementary information:

  Conditional mutants were generated using the Cre-recombinase:loxP
  (Cre-loxP) system and crossing a strain carrying an Ercc1 allele
  flanked by loxP sites (Ercc1fl/fl), with a strain expressing the Cre
  recombinase under the control of the specific Dopamine Transporter
  (DAT) promoter (Zhuang et al., 2005). We validated the specificity of
  Cre recombinase activity by generating DAT-Cre+ROSA26-lacZ reporter
  (Soriano, 1999), which confirmed expression in DA neurons of the SNpc
  and not in other cell types, such as serotonergic neurons of the Raphe
  nucleus (Supp. fig. 1)


Elevated levels of thyroid hormone in the blood is called thyrotoxicosis. If this is due to a hyperfunction of the thyroid gland, it is known as hyperthyroidism. In common parlance, these terms are often interchanged.

Although a simple google search would tell you more, I add some detail here.

Hyperthyroid can have various causes. There can be a functional cancerous/ non-cancerous mass in the thyroid gland producing the hormone. Or as in graves disease which is an autoimmune condition where antibodies mimic to stimulate the thyroid gland to hyperfunction.

Non hyperthyroid causes of thyrotoxicosis include inflammation of thyroid or thyroiditis, where preformed hormone is released. It can also occur sometimes in a condition called struma ovarii where the tumor in the ovary turns into a thyroid like mass producing the hormone. Another possible case is an iatrogenic one where the the problem is due to the patient taking exogenous thyroid hormone.

Thyrotoxicosis is not fatal and can be controlled by drugs. Symptoms include cardiac problems, high BMR, ocular changes (bulging eyes), diarrhea and many more.
A special case of Graves disease called thyroid storm is a medical emergency and can be fatal.

Heres the medscape link for further reference. http://emedicine.medscape.com/article/121865-overview