The best review I can find is the one by Wang and Dai 2010, conveniently titled starting with "Concise review".
From the beginning of the abstract:

The human OCT4 gene can generate at least three transcripts (OCT4A, OCT4B, and OCT4B1) and four protein isoforms (OCT4A, OCT4B‐190, OCT4B‐265, and OCT4B‐164) by alternative splicing and alternative translation initiation

and from later on, in the introduction:

It is well established that OCT4 gene (official symbol POU5F1, also known as OCT3, OCT3/4, OTF3, and OTF4) functions as a master regulator in maintaining the properties of pluripotency and self‐renewal of ES cells

I take from this review that OCT4, OCT3, OCT3/4, whatever you want to call it, all refer to the same gene. However, this gene does have splice and translation variants. It seems that when talking about these variants, you will see them differentiated using A/B/B1. An older paper and some that cite it, Takeda et al, 1992, refers to the splice variants as OCT-3A and OCT-3B. If not noted, you can expect that the paper is considering them all together regardless of whether they call it OCT3 or OCT4.
I did find one thesis that treats Oct3 and Oct4 as separate proteins, renaming them from the A/B terminology, but they cite only the Takeda paper for this, which does not do the same. It seems more likely to me to be a mistake.

Takeda, J., Seino, S., & Bell, G. I. (1992). Human Oct3 gene family: cDNA sequences, alternative splicing, gene organization, chromosomal location, and expression at low levels in adult tissues. Nucleic acids research, 20(17), 4613-4620.
Wang, X., & Dai, J. (2010). Concise review: isoforms of OCT4 contribute to the confusing diversity in stem cell biology. Stem cells, 28(5), 885-893.


Are there animals that have evolved a resistance to human activity or encroachment?

Note: This is an answer to the last line of your question.
A classical example of animals adapting to the influence of humans on their environment is the adaption of the Peppered Moth.
Here is a brief summary:
The peppered moth was originally a mostly unpigmented animal (<1800). During the industrial revolution in the southern parts of the UK a lot of coal was burned. This led to soot blackening the countryside. Soon afterwards, a fully pigmented variety was first observed. Only a hundred years later, in 1895, this pigmented variety almost completely displaced the unpigmented variety.
It has been shown that the pigmentation is under strong selective pressure as birds hunt these moths. Since birds rely on their visual system to detect their prey, the variety that blends in with its environment (=camouflage) has a selective advantage over the variety that stands out.
As pointed out by Tim in the comments, since the 1970s there has been a rapid reversal with unpigmented animals being more abundant. As far as I understand, it is accepted that this reversal is due to a decrease in human induced air pollution leading to less sooty barks on trees which makes the unpigmented variety harder to prey upon.
Addendum: genetic basis of adaption
In a beautiful recent study, the causal mutation for the pigmented, or melanic, variety was identified: A ~9kb transposon insertion in the first intron of the gene cortex. The authors calculate that this mutation happened in the year 1819, a few years after the industrial revolution was in full swing. The interpretation is that due to sooty tree bark this mutation, causing pigmented moth, was under strong selection.


Why aren't native predators in Australia able to handle the mice problem?

The mice aren't invading Australia, they are invading the wheat producing zones, where the tractors are leveling the land and putting on pesticides. The local frog, amphibian and snake populations downstream of the farmer's fields is strongly affected by the farmland, and so are the birds of prey, if they weather the pesticide use, they have to hide in dense trees, hollow logs, caves, and old barns, which are very lacking in Australian farmland.
If the government enforced laws for field edge habitats for local ecology, then there would be less mice.
Have a look at the map of wheat producing areas.
Rodent Outbreaks: Ecology and Impacts pages 225-238
PDF Google book
The map of mice infestations:

From pestsmart.org.au, though no longer available.

and a map of Australian climate:

wikimedia


What test to apply to detect genomic signatures of selection?

I am assuming in this answer that you do not have any information about what environment is affecting the selection pressure so that methods like Bayenv2 can't be used.

The standard algorithms are:

Lewontin-Krakauer test
fdist
BayeScan
FLK
PCAdapt

Whitlock and Lotterhos 2014 showed that most often FLK and Bayenv2 perform better than the the three others. A number of articles (Meirmans 2012, Bierne et al 2013, De Mita et al 2013 and Fourcade et al 2013) have also shown that fdist and BayeScan suffer from high false positive rate. I would therefore recommend to go with FLK but I am probably not good enough to give very good advice.

Note that you should learn a bit about how these algorithms work and not using them blindly.


There are many other methods that are used for transfecting cells in culture. These include:

Cationic lipid mediated (as mentioned by user137)
Calcium Phosphate mediated transfection
Biolistic methods
Electroporation

Newer techniques include optical transfection (using lasers to bore a hole through membrane) and impalefection (using nanotubes). Wikipedia page on transfection nicely summarizes these techniques.

Induced pluripotent stem cells can be cultured from a patient, transformed using the plasmid and transplanted back to the tissue where it can replace the old cells with "corrected" cells.

There is another somewhat recent technique called in-vivo electroporation using which Nucleic Acid can be delivered directly in to the desired tissue.

However, to fix a mutation or introduce a transgene, just transfection is not enough; you have to make sure that the desired gene is inserted in the chromosome at the right location. Faulty gene can be replaced by the transfected functional gene via homologous recombination(HR), but rates of recombination are generally very low. Targeted gene insertion methods using genome editing tools such as Zinc-Finger Nuclease (ZFN), TALEN, and Crispr-Cas can increase this rate by introducing a break in the DNA at that region; this causes DNA repair systems to "repair" the break using HR.
There is another type of DNA repair system called NHEJ (Non-Homologous End Joining), and this is not what we are interested in. NHEJ can, in fact cause mutation through indels. Presence of the transfected DNA would shift the preference towards HR, however it has also been shown that different stages of cell cycle have different preference towards HR and NHEJ (cant find the reference as of now but I am sure about it because I was thinking at some point of time, to work on this).

Having said that, I would add that it is essential to screen the cells to see if the gene is incorporated or not. If some optimal protocol is devised then one can proceed to in-vivo electroporation.


The chloroplast, having multiple circular copies of its chromosome and its own tRNA and ribosome genes more resembles the bacterial systems it is descended from.  See @A.Kennard comment

Polysomes being found in bacteria frequently are single mRNA to which are attached multiple ribosomes.  This paper shows that chloroplast polysomes were observed in the mid 1960s by centrifugal sedimentation.


Human ancestor reproduction after chromosome fusion

Strangely enough we actually do have an answer for that.

There are a several examples of individuals who are born with two chromosomes fused together in all their cells.

We even have a few examples where these fused chromosome is in a diploid state, ie all instances of that chromosome are fused in the individual. Such individuals come from families in small isolated villages that are very inbred.

Chromosome number does not prevent fertility but it does reduce it in heterozygous state as it is now harder to get correct chromosome distribution during meiosis and thus fewer functional gametes are made. However in terms of function, as all genes are present in a somatic cell in the correct number, function is usually normal and the individual is alive.

If the population is inbred, it is possible to get an egg and a sperm that carry the same fused chromosome to meet. In which case you get a diploid individual with fused chromosomes. Fertility is now restored. And in an inbred population, a homozygote individual for the fused chromosome can meet another similar individual, and have offspring who are fully fertile.

AS you can imagine, over time there is a selection pressure for the population to separate. The homozygous state (be it fused or unfused chromosome) is more fertile that the heterozygous state.

So to put it short, chromosome fusion does not kill a cell. All gene are still present. However in the heterozygous state, where both fused and unfused chromosomes are present, fertility is dramatically reduced BUT is none zero. Fertility is restored in a homozygous state when an individual is diploid for either fused or unfused chromosomes. In small isolated populations, inbreeding allows for the emergence of diploid individuals which can reproduce with each other

http://genetics.thetech.org/original_news/news124


Why do some bacteria have an asymmetric replication?

The replication fork itself is always asymmetric. This is true for all organisms and is due to the fact that DNA polymerases can only add nucleic acids to the 3'-OH end of DNA. This leads to different mechanisms for the replication of the so called leading and lagging strands. You can find more details on wikipedia https://en.wikipedia.org/wiki/DNA_replication

Most Bacteria have circular chromosomes that they usually replicate using two replication forks. Both forks start from the origin of replication and progress in opposite directions to meet at the replication terminus which is opposite to the replication origin on the circular chromosome. Each replication fork replicates about half of the chromosome. We talk about the left replicore and the right replicore. I assume that your teacher was referring not asymmetry in the replication fork itself, but to asymmetry in the size of the replicores. In B. subtilis the left replicore is 196 kb longer than the right replicore (J Bacteriol. 1993 Feb; 175(3): 741–749.). I do not know whether there is any evolutionary explanation for this, but mechanistically it is caused by the fact that the terminus of replication is not placed opposite to the origin of replication on the circular chromosome.


Is there a fundamental reason that plants cannot fix their own nitrogen?

That is an interesting question. But rises some line of thought by analogy, e.g. why people won't evolve to produce their own ATP without mitochondria? (I mean of course Eukaryotas in general). I don't see any reason why multicellular organism cannot incorporate bacterial functionality either as happened with mitochondria, or as just separate cell type, that will provide desirable enzymatic reactions.

The answer, no matter how unsatisfactory, might be simple: because it so happened. We definitely can create experimental conditions lacking N-fixing bacteria as well as varying amounts of nitrates, nitrites etc. And then produce and screen line of mutants for ability to fix nitrogen without symbiotic partners.


How do fungi react to being grown in a tissue culture?

Generally, fungi are cultured on agar with a food source such as malt extract. One way to do this is to clone a mushroom from the fruitbody of a mushroom or from colonized substrate (e.g. rotting wood). Another approach is to germinate spores.

The fungus will grow as vegetative mycelia until it runs out of food. At that time, some species will grow tiny fruitbodies or sporulate before entering a more dormant phase, dying out. Unless refrigerated, standard agar plates dehydrate. Also, fungi may take on different textures: wispy, bumpy, root-like (rhizomorphic), leathery, powdery, and may darken or change color as they age.

Some cultures start to adapt their metabolism to the media after a large number of transfers (based on observation and discussed in Stamets' "The Mushroom Cultivator".) at this point, cultures may also start to grow more slowly.

The mycelia can be transferred from one plate to another or to another media (substrate) such as a log, 'fortified sawdust' (sawdust with ~30% w/w wheat bran), or pasteurized compost. With the appropriate nutrition and environmental stimuli (CO2 levels, temperature, moisture, light, etc), the mycelia will fruit, creating mushrooms - generally after fully colonizing the substrate.

Here is a figure of 35 agar plates with 16 different fungal cultures that I isolated from the wild (soil, wood, mushrooms, as described in Allison et. al, 2009; LeBauer, 2010), and have transferred from a mature culture (about a 2 months old) to a new plate, which are about two weeks old in this picture. Parent cultures are in the first and third row, with children below (they are genetic clones; instead of counting generations, I count number of transfers.

You can also find cultures of fungi (Yeast) in unfiltered beer.

I have used many techniques to isolate and culture fungi (Isikhuemhen and LeBauer, 2004; LeBauer, 2010) but I would recommend the books "The Mushroom Cultivator" and "Growing Gourmet and Medicinal Mushrooms" by Paul Stamets for more information on sterile culture techniques used in mushroom cultivation.


Time required for RNA precipitation in ethanol

As far as I know this has never been thoroughly analyzed for RNA, but there is an excellent paper on the precipitation of DNA and the usual conditions in BRL Focus by Zeugin (see below for the paper). Since DNA and RNA are pretty much the same (except for one OH-Group) and the conditions used for precipitation are also similar, I think we can use this for a very close estimate.

Interestingly neither the time nor the temperature of a precipitation have a great influence on the outcome - they change the yield only by a few percent. If you look on figure 2 from the paper mentioned, you see the following:

This subfigure shows that the recovery is almost not influenced by the temperature, but only by the conconcentration of the DNA (or RNA). Depending on how much RNA you expect (how much cells did you use for the isolation) I would add a co-precipitation agent when you have only very small amounts on RNA. Glycogen works very well here. Otherwise I wouldn't worry.

This figure shows that the incubation time has only an influence on the percentage of the recovery when then time is too short. If you incubate for an hour, you are on the safe side.

Reference:

Ethanol Precipitation of DNA.


I'd first try translating it and looking to see if there are big regions that jump out at you that do not have stop codons in them.  I normally use this tool for quick and dirty translations, it gives you all 6 reading frames.  Also, you could just try BLASTXing your sequence if it is short enough.  BLASTX translates your DNA in all 6 reading frames and will search the protein database for matching proteins.  Most anything will have a hit in there, and if you get a hit it will show you the DNA sequence and reading frame that got translated.  If your sequence is too big, break it down into smaller chunks until BLASTX works.  One of your chunks will have your gene in it, and it will get a protein hit.  You'll also need to break it up if you have two genes in one chunk, but you only get results for one of them because its longer and gives better hits.


Synaptic pruning and selective elimination during adolescence

An answer to this question could potentially be found in "Understanding Adolescent Brain Development and Its Implications for the Clinician"

  Thanks to research by Jay
  Giedd and colleagues at the National Institute of Mental Health, it has become
  clear that, during the adolescent years, the organization and functioning of the
  brain go through complex changes. Importantly, these changes seem to be unique
  to the adolescent years and not simply the trailing remnants of childhood brain
  development.

Changes in frontal lobes during adolescence

  Frontal lobe gray-matter volumes,
  which represent dense concentrations of neurons and their parts, increase
  throughout childhood and do not reach their peak until approximately the age of
  11 (girls) or 12 (boys), at which point they decline throughout the second decade
  of life and into young adulthood.

So why might frontal lobe gray-matter volumes go up during childhood and down
during adolescence?

  Recent data suggested that, during childhood, neurons in the
  frontal lobes are allowed to overgrow and form far too many points of communication,
  or synapses, with other neurons. As a result, gray-matter volumes
  increase. As childhood draws to a close and adolescence begins, the brain
  switches from overproduction mode to selection mode. Early in the second
  decade of life, the brain stops overproducing synapses in the frontal lobes and
  puts the synapses that exist on the chopping block. Hundreds of billions of points
  of communication will be sacrificed through the teenage years. Only those that
  form meaningful, useful points of contact will be kept. Guided by a teenager’s
  experiences, the frontal lobes are shaped and molded into a configuration that
  will carry the individual, for better or worse, through the adult years. As this
  pruning process unfolds, gray-matter volumes decrease.

Changes in other parts of the cortex (specifically temporal lobes)

  The temporal lobes, which are critical for memory formation as well as processing
  auditory information and seeing detailed patterns and shapes, do not reach
  their maximum levels of gray matter until the age of 16 to 17, at which point they
  plateau. The temporal lobes contain the hippocampus, a structure that is central
  to creating an autobiographical record of what one does and what one learns.

Sources:

White, Aaron M. "Understanding Adolescent Brain Development and Its Implications for the Clinician." Division of Medical Psychology, Department of Psychiatry, Duke University Medical Center, Box 3374, Durham, NC 27710, USA, 2009. Web. 7 Feb. 2016.
Steinberg, Laurence. "A Social Neuroscience Perspective on Adolescent Risk-Taking." Developmental Review : DR. U.S. National Library of Medicine, 28 Mar. 2008. Web. 07 Feb. 2016.


Freezing cells is difficult, almost an art form. It depends largely on the types of cells being frozen, the program to be used in freezing and the program used to thaw. You can end up with a massive loss in viability if a technician doesn't follow a freeze or thaw protocol to a tee, and there are release criteria where products of low viability cannot and should not be infused.

Being said, cryopreservation of blood for transfusion exists, and has since the Vietnam war. We're getting better at the process, but barriers such as cost and training probably still pose a hindrance.

Another barrier is maintenance of stocks, especially if you're considering monitoring your own blood supply. A cryogenic freezer would need to be maintained and monitored for constant -160-170°C. Cells do not undergo multiple freeze-thaws and thus once thawed you have a short shelf life.


How does the cell cycle affect stem cell fate?

If you are referring to cells that are differentiated in adults:
Some somatic cells in multi-cellular organisms are post-mitotic, that is, the cells cannot divide, or said in other words, they don't enter in S phase. This cells are said to be in G0 phase, because they keep synthesizing proteins but the won't replicate their DNA.
Another thing we could say about cell cycle having something to do with cell division, is that in G1 and G2 (and , of course in G0) different cell types, produce different proteins. ie: a skeletal muscle cell, produces lots of proteins associated with the contraction, but neurons not so much.

If you are referring to the first cell divisions in a multi-cellular organism's development, then:
in cleavage, the cells are dividing synchronously, and they avoid some cell cycle stages, like g1 or g2 (in cleavage, the cells are just dividing and replicating their DNA; the protein synthesis happens with mRNA inherited from the mother). In this stage, there is no cell growth at all. After some cell divisions, they have to start synthesize mRNA  and, because of that, they start to divide asynchronously. Eventually the cells (for this and also for many other reasons) get differentiated.

I hope this answer is useful :)


Are there any major noticeable limitations to genome sequence compression methods that use reference templates?

The most obvious drawback of the reference template method is that if you use it, you've already analysed data.

Usually, you get data from wet biologists. They sequence samples and upload sequences to a server. Often an uploading process is already automated. If you sequence in-house, the data is already on your server. If not - biologists do not want to do an extra job. Moreover, if it is not a big project you do not have that much data that transferring and storing it is the problem. So you'll get the data as *.fastq.gz files.

Then you make QC, align reads and make an SNV-calling or expression analysis or whatever you want. Aligning and SNV-calling could be painful, complicated (Copy Number Variation, heterozygosity etc) and time-consuming. It is the problem. Resulting data usually is stored as Variant Call Format (VCF). Under the influence of CRAM and 1K Genome Project which uses it, VCF has been developed.


Is Klebsiella pneumoniae found in the throat of healthy people?

Klebsiella species, including pneumoniae, are normal members of the healthy human oral microbiome.

Klebsiella and Providencia emerge as lone survivors following long-term starvation of oral microbiota

Saliva microbiomes from 6 healthy adults were analyzed by 16S sequencing over a starvation timecourse, where oral microbes were cultured in minimal medium (PBS or 1:1 PBS:cell-free saliva).  Figure 1 shows that the genus Klebsiella is initially low abundance in the healthy oral microbiome, but the proportion of Klebsiella increases over the starvation timecourse in the two media tested.  An excerpt from the results:

  At day 1, several species of Streptococcus were recovered, as were Gamella sanguinis, Klebsiella pneumoniae, and Klebsiella oxytoca. At day 20, K. pneumoniae, K. oxytoca, Enterobacter homaechei, and Providencia alcalifaciens were the only recoverable species. Finally, at day 84 and day 100, only K. pneumoniae and P. alcalifaciens were recoverable under the conditions tested

Given the proximity of the mouth to the throat, I think it's fair to say that K. pneumoniae is likely a member of the healthy human throat.

If that's not convincing, you can check the supplemental data from this paper, which looked at 16S data associated with throat tissue samples from 29 patients with laryngeal carcinoma and 31 control patients with vocal cord polyps.  Looking at the relative abundance of different phyla, they found that Proteobacteria (the phylum containing the genus Klebsiella) accounts for 11% of the recovered 16S reads on average for all patients (range 0–67.1%).  The authors claim to have recovered 218 genera and >3000 unique OTUs at 97% similarity, though they only report the ~30 most abundant genera in their differential abundance analyses, and it doesn't look like they included the full dataset in this publication.


How to generate protein graphics for illustrating articles?

All comments are great, there are numerous software programs that allow you to make such images.

Gathering information about the insulin structure

By simply clicking on the image in wikipedia it will provide you with  valuable information:

  Created by Isaac Yonemoto created with en:pymol, en:inkscape, and
  en:gimp from NMR structure 1ai0 in the en:pdb. Ref: Chang, X.,
  Jorgensen, A.M., Bardrum, P., Led, J.J.

So the creators used pymol, inkscape and gimp, but let's dig a bit deeper. Unfortunately Isaac Yonemoto, the editor of this wiki, did not provide a direct link to the original publication (see wiki file history). However by searching the author names in combination with insulin we quickly find the article: Solution structures of the R6 human insulin hexamer. In the first paragraph we see:

  The atomic coordinates of the 20 refined hexamer structures and the
  NMR-derived restraints have been deposited in the Brookhaven Data Bank
  (PDB ID codes 1AIY and 1AI0 for the symmetric and the nonsymmetric
  hexamer, respectively)

You can find the structure that was depicted in this wiki article by searching the PDB id.

Creation vs visualization
You can interpret 'create' in your question in two ways here:

Creating this whole structure from nothing
Visualizing a structure someone else determined

If you refer to the former you should look at the article corresponding to this structure. Note that this is quite detailed and requires  knowledge of several concepts, such as molecular dynamics and NMR spectroscopy. If you refer to the latter than you should take a look at the programs mentioned earlier such as pymol, inkscape and gimp

Not generalizable
This boils down to what @David already said in his comment:

  You are surely aware that Wikipedia's contributors (not users) are
  completely independent and thus use whatever software they choose to
  create molecular images.


1) Pain can aggravate hypotension, so painkillers may help to prevent shock.

A severely wounded person with significant blood loss can develop hemorrhagic shock due to drop in blood volume and consequently drop of blood pressure and insufficient perfusion of vital organs.

It is known that pain can trigger vasovagal syncope, also known as neurocardiogenic syncope in which a person faints due to sudden drop of heart rate and arterial vasodilation resulting in drop of blood pressure and reduced brain blood perfusion.

Here is an example how carbamazepine, which prevented pain, also prevented the episodes of neurocardiogenic syncope (The Korean Journal of Pain):

  A 65 year-old male patient diagnosed with glossopharyngeal neuralgia
  complained of severe paroxysmal pain in his right chin and ear
  followed by bradycardia, aystole and syncope. We report a case
  successfully treated with a permanent pacemaker and carbamazepine in a
  patient with GPN who had syncopal attacks preceded by paroxysms of
  pain.

In an injured person who is at risk to develop hemorrhagic shock, severe pain could cause neurocardiogenic syncope that could proceed into shock, so, it sounds logical that painkillers could help to prevent shock.

From the first quote in the question (the patient was convinced he was receiving a strong painkiller), we cannot conclude that the painkiller prevented shock, because this has not even started to develop.

2) Analgesics for a person in severe pain who has lost blood and is in danger of developing shock.

According to Pain Control in Trauma Patients (Trauma Reports, 2011, fentanyl can be appropriate painkiller in shock since it does not aggravate hypotension:

  Fentanyl is the best known synthetic agent and is widely used in pain
  control. It is 50 to 100 times more potent than morphine and has the
  added benefit of not causing histamine release and peripheral
  vasodilation, as found with morphine administration. Based on this
  physiology, fentanyl should not impact blood pressure as much as other
  narcotics and, therefore, is preferential in the critically ill trauma
  population who may have tenuous cardiovascular status from hypovolemic
  shock.

Morphine can cause hypotension, so it may aggravate shock. According to prescribing information for morphine sulfate oral solution by FDA.gov, 2018:

  In patients with circulatory shock, Morphine Sulfate Oral Solution may
  cause vasodilation that can further reduce cardiac output and blood
  pressure. Avoid the use of Morphine Sulfate Oral Solution in patients
  with circulatory shock.

In conclusion, painkillers may help to prevent shock by reducing pain.


What are the total number of action potentials in the human brain?

If firing rate is from 1 Hz to 200 Hz, 100 trillion to 20 quadrillion synaptic firings. Neuronal (say, measured from soma) firings  will add up to 86 billion to 17.2 trillion action potentials per second.

It important to remember, that synaptic firings "sum up" in soma or interfere between each other, so the are more of those.
Read more: http://neuroblog.stanford.edu/?p=4541


Birds are both flying dinosaurs and flying reptiles. Yes, that's potentially confusing.

To understand the apparent contradiction, you have to understand how modern classification of organisms works (phylogenetic systematics). Under the old (Linnean) classification system, Reptilia (reptiles) was an order and Aves (birds) was a separate order. Phylogenetic systematics, which has completely replaced the Linnean system, views all organisms as interrelated in a nested set of monophyletic groups (clades). It's like a set of venn diagrams, where all organisms fall into a giant circle and then successively smaller circles classify more and more specific groups.

The clade Reptilia includes snakes, lizards, crocodiles, and lots of extinct groups, including dinosaurs. So all dinosaurs are reptiles. The clade Dinosauria includes all the extinct dinosaurs (Stegosaurus, Triceratops, sauropods, etc.), including theropod dinosaurs, which include well known dinosaurs like Tyrannosaurus and Allosaurus. Based on a mountain on anatomical evidence, including lots of transitional fossils, living birds are a sub-group of theropod dinosaurs.

So all birds (Aves) are theropod dinosaurs (Dinosauria: Theropoda). All dinosaurs are reptiles. Therefore, birds are dinosaurs and reptiles. They are just more closely related to dinosaurs than to other reptiles.

The tricky part is that most people have an intuitive idea of what "reptiles" and "dinosaurs" are. To a systematist, whose job it is to classify organisms, these terms don't mean the same thing as they do to most people. Systematists think about groups like Reptilia and Dinosauria and how those groups are related to one another. So they have no problem saying that birds are dinosaurs and reptiles, because birds are nested within both of those groups.

A few words about pterosaurs

Along with birds and bats, pterosaurs are the other clade of vertebrates capable of powered, flapping flight. Pterosaurs fall within Reptilia (and Diapsida and Archosauria) along with Dinosauria, which includes birds. There are a lot of other extinct lineages in the tree that are not shown, e.g., ornithodirans that are not dinosaurs and not pterosaurs. Pterosaurs and birds share anatomical features that all reptiles, diapsids, archosaurs, and ornithodirans have, which is how we know that they are more closely related to each other than to other groups, like crocodiles. But their flight structures evolved independently and are anatomically distinct fro one another. So pterosaurs are flying reptiles but not flying dinosaurs.

These images might help you understand the above explanation.


What is the name of this flower? The photo was taken in the Okanagan Valley, British Columbia


blood clots inside the body have an unfortunate tendency to get into the bloodstream and cause blockages, leading to severe problems such as strokes or heart attacks

This statement is primarily true only for blood clots within blood vessels, especially in the veins. When you are talking about bruising, you are talking about clots outside of the vasculature.

When a blood clot occurs in an artery, it can block that artery or break off, flow downstream, and block some smaller distal vessel. These events are most severe when they affect crucial organs like the brain and heart ("stroke" or "heart attack"), though of course any organ can be damaged in this way. However, blood clots in arteries can't ever directly affect a tissue that is not distal from where the clot starts, because they can never pass through capillaries or travel backward.

When a blood clot occurs in a vein and is dislodged, it can follow the increasingly larger venous system back to the heart, where it can cause a pulmonary embolism (blockage in the lungs) or, via a patent foramen ovale, travel to the left-side circulation and end up anywhere, including the coronary arteries or blood vessels of the brain. Similarly, clots that form in the venous return from the lungs to the heart or in the left side of the heart itself can travel anywhere (except the lungs) and create a blockage.

For a clot outside the vasculature, for it to have an effect somewhere else systemically it must re-enter the vasculature. This is simply not possible in most situations, because the vessels involved are very small, and during bleeding the blood is flowing out of vessels: there is no pressure gradient to push the clot back into the vessels.

In more severe cases of injury where major vessels are involved, clotting in those major vessels can indeed be a problem, but not for common occurrences of bruising.

(see also @anongoodnurse's answer that contains a good clarification of what exactly a bruise is, as well as how there are risks from very serious bruises but not the same way the original question implied)


Why do we feel headache after ice cold drink?

The cold drink causes the blood in blood vessels of gums to freeze. This stimulates nerve endings and causes a sensation in brain.


Examining milk for presence of harmful bacteria

A simple way to know if milk contains any bacterial contaminations is to take ~5 ml of the milk and add a couple of drops of methylene blue to it. If the milk is sterile, it will stay blue. If any bacteria are present they tend to take up the dye, leaving the sample colourless after ~1 hour. A more extensive way would be to plate 3-5 dilutions of the milk sample on LB or nutrient agar.
You don't have to do much extensive sampling. Just make sure that you take a couple of well-stirred samples.


Could a virus produce prions, leading to prion disease?

Perhaps not prions themselves, but viruses may possibly contain "pieces" or domains of proteins with prion-like chemical activity, which can catalyse refolding of prions from normal to disease state.

Mutation rates put limits on the size of RNA viruses. There is a higher cost for the average RNA virus to allot precious genomic space on encoding a normal protein that would take decades to be pathogenic, and which does not seem to help make copies of the virus.

Because DNA is a more stable molecule, and DNA polymerase has a higher fidelity rate than RNA polymerase, DNA viruses can have a larger genome. They could more easily carry code for encoding prion-like domains inside proteins.

There's a recent paper from George and Victor Tetz that looks for these so-called "prionogenic domains" (regions which encode portions of another protein that could potentially have prion-like behavior) in a catalog of viral genomes, and they find approximately three times more such domains in DNA viruses than in RNA viruses:

  We determined that more PrDs can be found in the DNA-viruses compared with their numbers in the RNA-viruses, and in the enveloped viruses, compared with that in the non-enveloped ones. This may be partially explained by the larger genome size and protein numbers in DNA-viruses.

While the domains themselves are usually part of proteins that are not themselves prions, infection could lead to expression of those proteins, which in turn provides the domain templates that invoke misfolding in the host of normal prions into pathogenic (disease-causing) prions:

  Some viruses may be implicated in the prion misfolding in humans since it was observed that the de novo appearance of prions can be facilitated by another PrD-containing protein

Also! There are retroviruses that have integrated themselves in our genome over millions of years. These are called "endogenous retroviruses" or ERVs, and have been called "junk DNA" by some biologists. However, some get expressed along with our normal genes:

  Although a large percentage of ERVs are replication-defective or are suppressed by host defense mechanisms, some ERVs can be expressed and replicated. The activation of an ERV gene can bring positive co-opted functions to the host, which may be evolutionarily maintained [13,20]. For instance, some ERV proteins may provide important functions during normal development; for example, human protein syncytine-1, which is an ERV Env protein, is involved in the formation of the syncytial layer in the placenta [30,31]. Moreover, the expression of Env proteins encoded by ERVs has been suggested to mediate host resistance to exogenous pathogens [32,33]. However, because of their analogy to exogenous retroviruses, the activation of certain ERVs has been frequently implicated in disease.

The authors observed that some people who develop Creutzfeldt–Jakob disease (CJD) have ERVs that get overexpressed:

  To evaluate the possible relationship between HERVs and human prion disease, we examined the retroviral sequences in cerebrospinal fluid (CSF) obtained from individuals with sporadic CJD. The frequencies of several HERV families, including HERV-W, HERV-L, FRD and ERV-9, were significantly increased in the CSF of individuals with sporadic CJD compared to the frequencies observed in normal control CSF. In addition, when compared to individuals with other neurodegenerative diseases that exhibit similar symptoms to CJD, such as dementia, the incidence rate of HERV-W and HERV-L were significantly higher in the CSF of sporadic CJD patients. Moreover, the frequency of increased HERV-W and HERV-L in the same samples was much higher in sporadic CJD than in either normal or other neurodegenerative diseases CSF samples, and there was no correlation between individual parameters, such as sex and age [61].

The cause may not be expression of proteins with PrD, but with the triggering of signaling pathways that lead to inflammation of tissues, which sets up conditions for normal prions to malform into disease-causing prions:

  According to these studies, ERV proteins may be closely implicated in the pathogenesis of inflammatory diseases, such as multiple sclerosis and rheumatoid arthritis (RA) [51,54,68]. In prion diseases, a correlation between the inflammatory process and neurodegeneration has been suggested because of the activation of large numbers of glial cells and the up-regulated expression of proinflammatory cytokines, which are pathological features of prion diseases [69,70].

Life is complicated.


Do unique communities of bacteria form inside water storage in plants?

As stated in Plant Signal Behav. 2010 Dec; 5(12): 1568–1570:

  Phytopathogenic bacteria do not enter plant host cells, but proliferate in the intracellular space.

But as they can reach the apoplast, pathogenic bacteria can take advantage of environmental humidity levels and manipulate water content inside plant leaves to reproduce and spread infection as shown in
Nature volume539, pages524–529

So yes, bacteria can infect water inside plants but usually not inside the plant cells themselves. As they infect the intracellular space, they can spread in the water and infect the whole plant. It is also to mention that we are not speaking about the same bacteria as in standing water or something else. Viruses on the other hand can infect the plant cells themselves.


Could someone Identify this Insect Hive on my Balcony Grill

These are certainly paper wasps (Vespidae) building their paper nest. Looks like a species of Ropalidia, which are known from Singapore.

I know little about Ropalidia, it seems to be rather small and probably harmless, but our larger European wasps can sting and bite and are sometimes quite aggressive (this refers first of all to Vespula germanica).


Amino acid substitutions near the receptor binding site HA protein in type A H3N2 influenza strains?

Short answer: Yes, 156 is generally considered "near" the RBS, e.g. in this paper you can see it mapped onto the structure.

For a more general answer, you'll need to sit down and stare at 3D models of hemagglutinins (there are hundreds in the PDB), just like the rest of us. Antibody binding sites are not black and white, and interactions between influenza and antibodies are wildly complicated. What's "near" in some contexts might be "far" in others.

You might find the Influenza Research Database's Identify Sequence Features in Segments tool useful, particularly its annotation of hemagglutinin H3.

Be aware that numbering of amino acids can be confusing, since different groups may be using different starting points. There's a vague agreement on the "correct" numbering, but quite a few groups pay it lip service and then number their version however they like.


The whole point about using D' rather than D is because D' is bounded between -1 an 1 for any allele frequency, while the bounds for D depends upon the allele frequency of interest.

Recall the definition of D

$$D = p_{ab} - p_ap_b$$

Let, $D_{min}$ and $D_{max}$ be the minimal and maximal values of $D$ for a specific allele frequency.

For $p_a = p_b = 0.5$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.25$) and $D_{max}$ is when $p_{ab} = 1$ ($D_{max}=0.75$).

For $p_a = 0.8$ and  $p_b = 0.2$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.16$) and $D_{max}$ is when $p_{ab} = 0.2$ ($D_{max}=0.04$).


Because then it wouldn't be going anywhere, and the first part of the sentence is specifically about traveling.

Without more context that might make me wrong, I think the statement is intentionally tautological and is just meant to set up a problem to solve.

By "better or worse" I think the author means to generalize about conditions that an organism may prefer: nutrient concentrations, temperatures, etc.

Restated, I think the author is roughly saying "For cells to spend more time where conditions are best for them, they have to move on their own power."


Those Hardy-Weinberg equations are the general case, used for only two alleles.  This question is basically answered here, for three alleles; you've got a situation of four alleles.  That means you need to have:

$(p+q+r+s)^2=1$

Where $p$, $q$, $r$, and $s$ are the frequencies of your respective alleles.  This expands out to the rather unwieldy:

$p^2+2pq+2pr+2ps+q^2+2qr+2qs+r^2+2rs+s^2=1$

Now it becomes a plug 'n chug assignment; simply assign the frequencies and calculate.

   Assuming $p$ is Adh-1, $q$ is Adh-2, etc., $p^2=0.0121$, $2pq=0.1848$, and so on.


Math behind the Genetic Relationship Matrix

This expression is a mean
$$\frac{1}{m}\sum_{i=1}^m ...$$
($m$ is the number of SNPs) of the ratio
$$\frac{numerator}{denominator}$$
where the numerator is a covariance
$$(a_i-C)(b_i-C)$$
and the denominator is the expected heterozygosity (it is also the variance of binomial distribution with n=2)
$$2p_i(1-p_i)$$
Therefore, it represents how much do two individuals covary $(x_{ij})(x_{ik}-p_i)$ respectively to what is expected on average $2p_i(1-p_i)$ averaged over all SNPs $\frac{1}{m}\sum_{i=1}^m...$, where $m$ is the number of SNPs.
It is a relative measure (relative to the expected heterozygosity) of covariance between each individual (averaged over all SNPs).
Does it help?


Bacteria resistance to natural antibiotics?

For a natural immunity to evolve, two things have to happen:

The immunity has to actually occur. That means all the necessary mutations will need to be there to grant this bacterium resistance to penicillin. For penicillin, for example, bacteria that evolved such a resistance evolved to produce the enzyme beta-lactamase.
The immunity has to grant an advantage. Penicillin is produced by Penicillium, which is a mold found in environments with lots of oxygen. Lots of bacterial species have never encountered penicillin and the vast majority (for example anaerobic bacteria that don't infect humans) never will. In the absence of this pressure, a resistance to penicillin, even if it evolves, will likely deteriorate within a few generations because the individuals with the resistance do not have an advantage in survival. Producing an enzyme such as beta-lactamase is not without its costs (protein synthesis).

While bacteria van exchange genetic material in the form of plasmids between different species, so not all species would need to evolve beta-lactamase de novo, this is also only "helpful" if the bacteria a) come in contact with resistant bacteria species, and b) if this resistance confers an advantage for the receiving species.

Origins and Evolution of Antibiotic Resistance

Mechanisms of Bacterial Resistance to Antibiotics


What are these strings used to describe animals?

Those describe the genotype of an animal (or plant, virus etc.).

The nomenclature can be very varied and domain-specific, but for those two examples:

$dt^{sz}$ is a Syrian golden hamster model with a spontaneous mutation (i.e. occurred during breeding, without specific human intervention) which gives predisposition to seizures.
They are described in this paper:

Spontaneous seizures: a new mutation in Syrian golden hamsters. - Yoon et al. - J Hered 1976

  SPONTANEOUS motor seizures with tonic muscle spasms and severe paralytic states have been observed in inbred line BIO® 86.93 of Syrian hamsters
  (Mesocricetus auratus auratus). These animals had been inbred for 23 generations and maintained by Bio-Research Consultants. The seizures, which last from 2 to 5 hours, can be precipitated by mild stress, and occur in
  animals between the ages of 30 days and 60 days. Breeding tests have shown that the condition is transmitted as a simple recessive; accordingly, the gene symbol
  sz is proposed for this condition.

The lowercase indicates that the mutation is recessive that is, you need to have two copies of the mutation to see its effect (its phenotype).

dt comes from dystopia, another symptom of the mutation.

As for Rgs9-Cre/+;gtROSA/+ mouse, the genotype is a bit more complex.

Whenever you see /+ it means that the animal is heterozygous, that is, it only carries one copy of that specific gene.

For instance these are transgenic animals producing the bacterial protein Cre under the Rgs9 promoter. A promoter is a sequence of DNA that controls the expression of a certain gene. In this case the DNA sequence for the promoter of the gene Rgs9 was attached to the DNA sequence for Cre. This new construct was then inserted into the genome of the mouse.
The result is a mouse in which the cells that normally transcribe the Rgs9 gene also produce Cre.

This mouse line was then crossed with a reporter mouse line called gtROSA26, which expresses a certain protein called $\beta$-galactosidase in a Cre-dependent manner.

The gene for the galactosidase is present in all the cells, but only where Cre is present (in our case the Rgs9 positive cells) it will be transcribed.
Eventually the crossing leads to the expression of $\beta$-galactosidase in Rgs9 positive cells.
$\beta$-galactosidase has the nice property that it can change the colour of certain chemicals to blue, which allows to easily visualize the cells that produce it. This can help you answer questions like: "where is the Rgs9 gene transcribed?".

Wikipedia has a neat page on Gene nomenclature with lots of links to nomenclature guidelines.


The person cannot survive for long, in spite of the infinite supply of blood.

In real life

There is no blood delivery system that can add blood to the vascular system as fast as it would be lost by two bullet holes in the heart. But I guess that's covered by your conditions.

As mentioned in comments, where would the blood go? Despite a thoracic entry and exit wound, blood volume inside the thorax would not squirt out of those holes fast enough to prevent a life-threatening accumulation of blood which would interfere with expansion of the lungs, so unoxygenated blood = death.

Theoretical

I suspect this is what your teacher was hoping would be the answer. Blood - like most things - will follow the path of least resistance. Which has a higher resistance, the aorta and arteries  (if it hit both the right and left ventricles, the pulmonary vasculature as well) supplying life-sustaining blood to vital organs, or two holes? Theoretically, there would be little resistance against blood flow through the holes, so no flow into vasculature means death.

Regarding clotting, nope. Rate of blood flow would preclude a functional clot.

In real life, even with surgeons at the ready, this is a deadly scenario. One hole: doable (depending on the caliber of the bullet); plenty of people have survived this event. Two holes, it would take particular circumstances and would basically be a miracle.


In Darwinian evolutionary theory, does the environment has any role?

"According to Darwin, eventually, the fittest will survive"

Darwin never said this. Fitness and survival are two separate concepts.

In a simplistic version, fitness is measured by reproductive output. Survival is, well, survival. You can have higher output than your brother, but have a lower chance survival. In fact, the very act of producing offspring can negatively affect your ability to survive.

No, the environment is not an other organism, in any context. It is the place (stage, arena, etc) in which the measure of fitness (reproductive output) can be measured. The environment can directly influence and affect fitness, and other organisms (inter and intraspecific) ARE part of that environment.

A single isolated organism does not evolve, but can have offspring. However, you need a more than one organism for fitness to have any meaning in a Darwinian model.


How do plants take in only carbon dioxide?

Plants don't take in only CO2, they take in whatever the atmospheric concentration of gases is: gases travel freely across membranes, so it is difficult to select for certain gases.

What your teacher is explaining is based simply on the laws of diffusion in that diffusion results in a net flow from areas of high concentration to areas of low concentration. If CO2 is being used up in chemical reactions in the leaves of a plant through photosynthesis, that means that concentration of CO2 is low there, so the net diffusion of CO2 will be from outside the plant to inside.

Calling it a rush might be a bit misleading, but in general gases mix fairly rapidly (compared to, say, liquids). The plant doesn't really have to do anything to facilitate this except to have surface area available for gas exchange.


What kind of larvae are these. Lots of them in the basement in the summer, crawling around on the floor and the walls

Those are not larvae, but adult millipedes. Myriopoda, Diplopoda. https://en.wikipedia.org/wiki/Millipede
Here is a good link from the U of Minnesota on common arthropods in the basement.
https://extension.umn.edu/insect-relatives/sowbugs-millipedes-and-centipedes


What makes DNA sequences most different/recognizable from a biological perspective?

This isn't a question with a really well accepted answer yet, and comes up quite a lot in e.g. studies of population variation in transcription factor motifs.

Usually, we approximate the sequence preferences of a DNA-binding protein with a position weight matrix. A weight matrix will given you a score for two sequences,  so the simplest means of quantifying the relative binding strengths for two sequences is compare these scores. You could also, say, compare the relative chances of getting the scores under some background distribution of scores, which would arguably be more comparable between different factors.

The PWM score (and other means of describing sequence specificity) are only an approximation to what you're really interested though, which is the binding energy associated with the interaction. If you have detailed experimental evidence about how the protein binds, you might use that, and there are some papers that build models for approximating it from PWM scores as well. However the reality is that you can only ever roughly approximate what's happening in the cell, because of molecular crowding, and the many other factors that will be present on the chromatin fibre, so the difference in PWM scores is often what gets used.

Predicting the impact of a given change to a non coding DNA sequence is a hard problem. Sometimes you'll get a decent approximation, but in the end you're trying to do biochemistry from first principles, and we aren't there yet.


Regulation of the TCA cycle and glycolysis by adenine nucleotides

Summary

Glycolysis and the tricarboxylic acid cycle (TCA cycle) are distinct processes which are not necessarily linked sequentially. It is therefore not surprising that their modes of regulation are not identical and, in fact, involve far more complex regulation than mentioned in the question. The use of AMP rather than ADP as sensor of energy deficit depends on the action of adenylate kinase, which may differ between cytoplasm and mitochondria.

Relationship Between glycolysis and the TCA cycle

The expectation evident in the question that glycolysis and the TCA cycle should be controlled in exactly the same way assumes that either the two processes are inextricably linked or at least that the functioning of the TCA cycle is dependent on that of glycolysis. This is not the case, although the student can be excused this misimpression from the (perhaps unavoidable) way the topics are generally treated sequentially in text books of biochemistry.

The primary function of glycolysis is to produce ATP directly from ADP. The end-product of the pathway, pyruvate, is in some circumstances converted to acetyl CoA for the TCA cycle, and the NADH generated used for production of ATP generation via the electron transport chain (etc) and oxidative phosphorylation. However pyruvate has a variety of other possible fates depending on the type of organism or — in higher organisms — the tissue, and their overall metabolic requirements. For example in anaerobic metabolism — including exercising muscle tissue mentioned by the poster — the pyruvate may be reduced by reactions that regenerate NAD+ from NADH, e.g. conversion to lactate. It can serve as a precursor of the amino acids, alanine, valine and leucine. It can also be converted in the reaction catalysed by pyruvic carboxylase to oxaloacetate, the key intermediate that allows acetyl CoA to enter the TCA cycle. The importance of direct synthesis of oxaloacetate in this way is that it allows continuation of the cycle when intermediates are used for synthetic purposes (discussed below), in which circumstances oxaloacetate becomes depleted.

As regards the TCA cycle, there are sources of acetyl CoA other than pyruvate produced by glycolysis, and it has functions other than energy generation. Acetyl CoA can arise from the breakdown of fatty acids and of certain amino acids. In multicellular organisms, pyruvate can also be produced from lactate taken up from the blood, although in liver cells it is likely to be used for gluconeogenesis. And certain bacteria — acetic acid bacteria such as Acetobacter — can utilize the ethanol produced by fermentation in the TCA cycle. In addition to its function in energy generation some of its intermediates (α-ketoglutarate, succinyl CoA and oxaloacetate) are precursors of biosynthetic pathways, and the production of citrate from acetyl CoA is a means of transferring the latter out of the mitochondrion, where it is reconverted to acetyl CoA by the citrate cleavage enzyme (ATP citrate lyase).

It is therefore not surprising that there will be differences in the regulation of glycolysis and the TCA cycle, and, indeed, that there will be differences between different organisms — something generally not mentioned in elementary texts.

Regulation of Glycolysis

The prime function of glycolysis is the direct generation of ATP (“at the substrate level”), and flux of glucose through it is controlled by the regulatory effects of both ATP (–ve) and AMP (+ve) on phosphofructokinase, which was established and rationalized by D. E. Atkinson (Biochemistry 1968, 7, 11, 4030-4034) in terms of a response to the overall energy charge of the system.

This arises from the ability of adenylate kinase to reconvert ADP to ATP:

               2ADP → ATP + AMP

[from Atkinson and Walton (1967) J. Biol. Chem. 242 3239–3241]

It can be seen that AMP is a much better indicator of low energy charge than ADP in the circumstances represented by the graph above.

Citrate is also a negative effector of the enzyme, providing co-ordination between glycolysis and the TCA cycle. (Hormonal regulation via protein phosphorylation occurs in the tissues of higher eukaryotes.)

Regulation of the conversion of pyruvate to acetyl CoA

In order to enter the TCA cycle, pyruvate needs to be converted to acetyl CoA by the pyruvate dehydrogenase complex. The regulation of this enzyme determines the extent to which this occurs, and, hence, the extent to which pyruvate is metabolized by other processes. Negative regulators here are high concentrations of the reaction products, acetyl CoA and NADH, although in higher eukaryotes hormonally induced protein phosphorylation is important.

Regulation of the TCA cycle

Then first regulatory enzyme of the TCA cycle, isocitrate dehydrogenase, responds to the concentration of the key molecules involved oxidative phosphorylation: it is stimulated by ADP and +, and inhibited by ATP and NADH. It is worth reflecting on the consequences of inhibition. If a build-up of citrate occurs, this can feed back and inhibit phosphofructokinase in glycolysis. However the citrate can move to the cytoplasm of eukaryotes and be converted to acetyl CoA (for fatty acid synthesis) by the citrate cleavage enzyme, which is stimulated by ATP and inhibited by ADP.

A later regulatory stage is α-ketoglutarate dehydrogenase, which is inhibited by ATP, NADH and its product, succinyl CoA. Inhibition of this enzyme would allow a build-up of α-ketoglutarate, which is a precursor of several amino acids.

This the existence of several regulatory steps in pyruvate oxidation and the TCA cycle allows the use of the cycle for both energy generation and as a source of synthetic precursors. Hence it should be evident why its control is similar to that of glycolysis in some respects, but exhibits key differences.

[Berg et al. Biochemistry 5th ed, Figure 17.18]

But why isn’t AMP a regulatory molecule in the TCA cycle?

Glycolysis and the TCA cycle do not need to march in step, although when they are both responding to the need for ATP their key enzymes are regulated by adenine nucleotides, among other molecules. The original question (or a modification of it) remains as to why is AMP a positive effector of phosphofructokinase, but not of isocitrate dehydrogenase, which responds to ADP. It is interesting that in the section of Berg et al. discussing the concept of energy charge, a rather lame rider is added without further explanation to the effect that the ATP/ADP ratio can also act as an index of energy status.

I don’t know for certain, but suspect that the conditions under which Atkinson’s equation for energy charge is valid do not hold in the mitochondrion. This is supported by Sobol et al. (1978) Eur J. Biochem. 87 377–390 who found concentrations of AMP in rat liver mitochondria to be much lower than would be expected from equilibration with ATP and ADP through the adenylate kinase reaction. They suggested additional reaction of AMP with GTP in the mitochondrion might be responsible and also cited reports that adenylate kinase was absent from the matrix of rat liver mitochondria.
At least in rat liver, this would explain AMP would not be a useful regulatory molecule, whereas the ATP/ADP ratio would be indicative of the requirement for oxidative phosphorylation.


I don't believe you can produce a general function for this. It will depend on the exact gene and organism you are considering.

From a molecular point of view, the vast majority of recessive mutations result from a change producing either a non-functional protein product or a truncated product that is cleaned up by the cell. We can reasonably assume that most modifications significant enough to produce a phenotype will be of this class since there are more mutational sites which can produce a non-functioning product than can produce a product of changed function but the exact ratio of one to the other is not going to be equal across different genes and organisms.

Note as well that the whole notion of recessive and dominant traits is probably an over-simplification and, in fact, there are subtle differences between homozygotes and heterozygotes in many, perhaps most, cases so I'm not sure how useful an estimate would be even if you had one.


ATP Binding dwell time

Here is a very dodgy derivation of the binding dwell time (note I am the OP). For this we have $$E+S\rightarrow ES$$
Where $E$ is the enzyme and $S$ is the substrate (keeping this general). We can write our rate equation as:
$$rate=k[E][S]$$
But we can also write the rate as:
$$rate=-\frac{d[E]}{dt}$$
so that:
$$\frac{d[E]}{dt}=-k[E][S]$$
Now here is the bit that I think is a bit dodgy, we are going to assume that $[S]$ is approximately constant. So that:
$$[E]=Ae^{-k[S]t}$$
We can take $n=[E]V$ to represent the number of enzymes left, where $V$ is the volume, then letting $n_0=VA=constant$:
$$n=n_0e^{-k[S]t}$$
The probability of been within the time $t$ is then given by:
$$F(t)=1-e^{-k[S]t}$$
Which is our commutative distribution function. Differentiating this gives our probability density function:
$$f(t)=k[S]e^{-k[s]t}$$

Interim dwell time

The interim dwell time (also called the catalytic dwell time) involves two steps[7]:
1. The cleavage of the enzyme bound ATP.
2. The release of the hydrolysed products.

Each of which is going to follow the distribution (analogous to the above) of:

$$p_i(t)=k_i e^{-k_i t_i}$$
For $i=1,2$ respectively. The joint probability distribution is found by the convolution of these two [8]:
$$p_T(t)=\int^{\tau}_0 p_1(t) p_2(\tau-t)dt$$
Which gives:
$$p_T(t)=\frac{k_1 k_2}{k_1-k_2} (e^{-k_2 \tau}-e^{-k_1\tau})$$

Edit

Although starting from deterministic equations (which actually doesn't really matter), this method does hold and is simple. The type of reaction is called a pseudo-1st-order reaction (or 2nd order class 2) which explains my approximation for $[S]$ been constant. See [9] and [10]

Sources for additional info

https://youtu.be/X_YXTWU2maY?list=PLbKSbFnKYVY3j6ubaW1zgTXj5C4443v8s
http://www.nature.com/articles/srep08773
http://www.ks.uiuc.edu/Research/atp_hydrolysis/
http://www.pnas.org/content/85/17/6314.full.pdf
https://books.google.co.uk/books?id=uIxwICNmLKEC&pg=PA199&lpg=PA199&dq=catalytic+dwell+time+distribution+%5Batp%5D&source=bl&ots=u8oBcVNCDc&sig=PKvdVAwT0WxdqTuVwMxhU3RfSwM&hl=en&sa=X&ved=0CCAQ6AEwADgKahUKEwiGhKDalufHAhXkadsKHc54ADs#v=onepage&q=catalytic%20dwell%20time%20distribution%20%5Batp%5D&f=false
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://www.ncbi.nlm.nih.gov/pubmed/16258036
http://crystal.harvard.edu/PDFs/floyd_biophysj.2010.pdf
http://glutxi.umassmed.edu/grad/GradKinetics.pdf
http://chemwiki.ucdavis.edu/Physical_Chemistry/Kinetics/Reaction_Rates/Second-Order_Reactions/Pseudo-1st-order_reactions


Terminology of the sequences of promoters in relation to DNA strands

It appears that this question is one of terminology, so I am answering it as such.

Convention for representing features in DNA sequences

The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U). Like any other nucleic acid sequence§, it is always written in the 5ʹ to 3ʹ direction in the same manner as the mRNA transcribed from it, without this being explicitly stated.

† An exception might be hemi-methylation, in which case both strands would be shown.

‡ I call this the sense strand. I discuss the nomenclature further below.

§ An exception is that tRNA anticodons are sometimes written in the 3ʹ to 5ʹ direction for ease of comparison with the codon, but in this case the directionality is indicated.

Origin and justification for this convention

Historical. The amino acid sequence of the protein (the product of the gene) is central to this convention because knowledge of the genetic code, and hence representation of the region of the mRNA that encodes protein — and by extension the DNA — was the first sequence information to be known.
Logical consistency.  Later other sequences features were identified (some of which initially may have just been genetic features), e.g. ribosome binding sites, polyadenylation addition signals, transcription start sites, promoters, transcription factor recognition sites. It was logically consistent to represent them on the same strand as the coding sequence.
Functional agnosticism. In many cases the function of a sequence followed its description, so there was no reason initially to place it on any particular strand. However, even if it were thought that the function of some sequence were to be recognized on the opposite strand (what I would call the anti-sense strand), it would be unwise scientifically to  change the representation to indicate this. Science progresses and interpretation changes. Better to separate concrete descriptive features from conclusions about their function.

It couldn’t ever be an ATAT box

Even if you represented the TATA box on the anti-sense strand, it could never be called an ‘ATAT box’ (as suggested by the poster) because, according to the basic convention, ATAT is 5ʹ-ATAT-3ʹ, and on the antisense strand the sequence is 3ʹ-ATAT-5ʹ, i.e. TATA!

Terminology for referring to the two strands of dsDNA

Whereas the above is the convention followed universally, the following is just my opinion. In science terminology is important to communicates ideas unambiguously, so I think it worthwhile explaining the ambiguity in some of the terms, the use of which I discourage.

Sense and anti-sense
This is my preferred term because, although not perfect, it avoids the pitfalls of the others. The idea seems to me clear that when you read the string of codons that encode the amino acid sequence from this strand they ‘make sense’. (Anti-sense is used in preference to non-sense, as ‘nonsense’ was the term used historically for mutations that converted amino acid codons into stop codons.) It can also be extended to non-protein coding genes (e.g. for tRNA), where ‘sense’ correlates with the sequence of the gene product.

I shall use ‘sense’ and ‘anti-sense’ as reference terminology in discussing other terms.

Coding and non-coding
This has the disadvantage that it cannot be extended to non-protein coding genes. However my primary objection is that it can cause confusion, as coding only unambiguously refers to mRNA. As the anti-sense strand is the template for RNA polymerase, one might make the mental association between this and ‘coding’, whereas it is the sense strand that is meant in this (admittedly common) usage.

Template and non-template
Template might be a more logical term for the anti-sense strand as this is the template for transcription by the RNA polymerase (although mRNA is also a template — for translation). However it is used only infrequently.

Plus and minus
This terminology is used for single-stranded (especially RNA) viruses to represent the whole genome, where in plus-strand viruses the genome is also the mRNA, i.e. the sense strand. One problem here is that it can be confusing for the beginner, who by extrapolation may assume that in double-stranded DNA genomes one strand is the sense strand for all genes. It is not.  Which brings me to my final point…

…whatever terminology you use, it is better to make sure it is clear that you are referring to the sense or anti-sense strand of a gene, not of the whole genome. You need to employ some other terminology to distinguish between the two strands of e.g. bacterial or plasmid DNA if it is necessary to distinguish them.


Do non-enzyme catalysed reaction pathways exist?

If by enzyme you mean "protein" aka polypeptide, than there are such things as catalitic RNAs. Those are molecules of RNA that facilitate chemical reactions but don't change themselves (definition of catalyst). I think that, based on the discovery of such RNAs, it is now believed that life might have started from or with the help of catalytic RNAs (please forgive the speculative tone, see self-replicating RNAs).

You might find this article interesting: The Road to Non-Enzymatic Molecular Networks, which describes non-enzymatic networks. The problem with searching this topic is that most current publications, seem to me, to concentrate on way to transfer enzymatic reactions into inorganic catalysis systems--because those systems can be more clean and easy to expand--than purifying enzymes for biotech.


Evolution of the haplo-diplontic life cycle

I just want to report the finding of one paper here. I don't know much about the rest of the literature and can't comment on it.

Otto et al. (2015) investigate this question in sexually reproducing organisms. As I understand it, they assume that the amount of time spent in on phase of the life cycle is proportional to the amount of selection happening in this phase. With a theoretical model Otto et al. (2015) showed that there is a sexual conflict over the length of the haploid phase. Mothers favour a longer haploid phase while fathers favour a shorter haploid phase. The outcome of the model depends upon who is in control of the length of this phase.

For mothers, producing a baby is often costly (see Bateman's principle). As such, the mother might want to ensure that its baby has high fitness. In the haploid phase, deleterious recessive alleles are no masked by their dominant counterpart and hence can be purged out of the population. A long haploid phase, therefore allows purging of deleterious alleles and make the diploid phase more resistant which is in the mothers interest.

Among fathers, the evolutionary pressures are different. Fathers evolve to mask mutations carried by their haploid gametes (e.g., by provisioning with diploid gene products), causing their sperm to be more competitive. As such, a father has interest that the haploid phase is short.


Could be a blue rutila fly (Family Tachinidae) http://www.brisbaneinsects.com/brisbane_tachinids/BlueRutiliaFly.html. Or the green rutila fly, which is similar.

Or the golden head rutila:


It's caused by a sudden shift in the pressure needed to circulate blood to your brain which your body fails to respond to sufficiently quickly. This results in a sudden loss of blood pressure termed Orthostatic Hypotension which, in term, results in a transitory reduction in the blood supply necessary for brain function. You experience a momentary loss of vision for the same reason that you would if someone strangles you.


Function of testosterone in women and estrogen in men

As you know by now, both males and females have testosterone and estradiol. Of course, their levels are different in each sex, but both hormones are important to males and females. A human male with zero blood concentration of estradiol or a human female with zero blood concentration of testosterone wouldn't be possible.

Here are some famous examples:

Role of testosterone in human females:

Increase libido1,2
Modulate physiology of vaginal tissue3

Role of estradiol in human males:

Help to regulate spermatogenesis4
Reduce bone loss5


It might be helpful if you showed us what sort of data you are looking at since copy number variations and gene expression can each be detected in similar but distinct ways.

Generally speaking, both gene expression and CNVs are detected by counting the number of reads that map to a given genomic region. The difference is that CNVs are detected using DNA sequencing while gene expression is detected using RNA sequencing. This is an important distinction because CNVs are a more stable genomic feature than gene expression. Reviewing the Central Dogma might help if this is confusing.

In the context of your problem, the main thing to understand is that CNVs can exert an influence on gene expression but gene expression cannot exert an influence on CNVs. Having fewer copies of a gene means that the process of transcribing RNA to express it cannot proceed as quickly as normal. So in an organism with gene X showing copy number loss, it makes sense to expect diminished expression of gene X than in organisms whose genome includes more copies of that gene X. If you're asking for an undergraduate class, chances are this is all you're expected to understand about "copy number regulation": the maximum transcription rate of a gene is dependent on how many copies of that gene are available for transcription.

Gene regulation becomes important for understanding how an organism with fewer than normal copies of gene X in its DNA might have the same amount of gene X RNA expressed as an organism with a normal number of copies of gene X. Suppose that some molecule, M, is necessary for expression of X but degrades after a short time. The cell will send M to the nucleus whenever it needs X to be expressed and the number of X transcripts produced per molecule of M will be dependent on the number of X copies available for transcription. If M is abundant and can be continually sent to the nucleus, then the cell with fewer copies of X can theoretically produce as much X as the cell with a normal number of X copies although it'll take a bit longer. If instead M is a finite resource within the cell, then the amount of X expressed in cells with fewer copies of the gene should be consistently lower than cells with more copies.

Of course if M happens to be produced by a gene exhibiting copy number gain/loss then that could also play an important role in how much X RNA transcripts you ultimately detect (even in the event that X actually has a neutral copy number). Hope this helps.


If I workout, will this inherited trait (of being stronger) not be passed down to my offspring (Lamarck's theory on evolution)?

Indeed, whether you work out or not will not change how strong your offspring will be. This is exactly why Lamarck's was wrong.

I would note however that Behaviour can be heritable and Your behaviour can affect your kids environment

Behaviour can be heritable

The probability of you working out is affected by your genes and so if you have a genetic predisposition for willing to work out, this will be passed on.

Assuming there are genetic predisposition for liking to work out, the fact that you worked out would not increase the probability of your kid to work out via genetic inheritance but the fact that you have a genetic predisposition for liking to work out will increase the probability that your kid will have the same preference and will work out

By the way, if you want to learn more about the concept f heritability you should have a look at Why is a heritability coefficient not an index of how “genetic” something is?

Your behaviour can affect your kids environment

Working out won't affect your genes but it will likely affect the environment in which the kid will grow. Here are three examples

Teaching

If you eat healthy, you will probably teach your kids to eat healthy too.

Womb environment

Also, if you eat healthy and are a woman, you will likely give the right nutrients to your offspring while still in the womb (assuming you are a lady).

Epigenetics

Your environment will cause epigenetic changes (changes not in DNA but in the very close environment of the DNA such as typically histone tail methylation). These epigenetics modifications will be directly passed to the foetus.

More information

A post your question is almost a duplicate of...

Is it the case that all changes in phenotype during life are not inheritable?

A post on heritability

Why is a heritability coefficient not an index of how “genetic” something is?

And finally an answer that talks about non-genetic inheritance

Why does evolution only involve heritable traits?


is ventricular depolarisation same as depolarisation during nerve impulse conduction?

Depolarisation of nerve (here Purkinje fibres) causes Action Potential (bcoz of opening of voltage gated Na channels) which causes opening of Ca++ channels in membrane of heart muscle- results in ventricular contraction
So ventricular depolarisation is actually action potential in heart muscle of ventricles
So both terms are related
Ventricular depolarisation is a consequence of nerve impulse(depolarisation of nerve here Purkinje fibres )
Thnks
Ps: read bracket portion separately


What biotechnology can be used to treat lazy eye, and possibly cure lazy eye?

In order to treat amblyopia you first have to treat the initial problem with the eyes that caused it, which is a medical issue and probably not what you are asking anyway. However, as wikipedia states, "after the underlying cause is fixed, vision is not restored right away, as the mechanism also involves the brain."

As a rule of thumb anything related to brain functions (in humans) is so complex that we don't really have the (bio)technology to just cure it. Sure, their are some advancements in a few areas, but especially if you want biotechnology to do this, you'll probably have to wait at least 10+ years for a medically save and readily usable method.


What is the creature with the lowest neuron count that demonstrates cognition beyond reflexes?

Indeed, C. elegans nematodes (which are the ones you are talking about) do not show cognitive responses. AFAIK, Drosophila melanogaster is also able to learn and display some quite complex behaviors, but no cognitive functions. I believe the "simplest" organism known to display what could be called "cognitive" functions is the honeybee (see for example this article).

But as to your question:

  to demonstrate something more than mere scripted actions

I would also ask "what is a scripted action?" and to what extend a complex, cognitive response from a monkey or a human isn't also scripted (though through many different interacting pathways)?


What would happen if a person had the right side of their body totally removed (including the brain)?

They would die.

Let's imagine that we perfectly cut a person down the middle. That would mean cutting the spinal cord in half, probably damaging the tissue so much that the remaining half wouldn't work well. The liver would be gone. The intestines and bladder would just be open. The heart would have to be adjusted to the left. The surgery would probably cause so much blood loss that they wouldn't even survive to die of other organ failure.

And you already alluded to the mismatch between what side of the brain controls what side of the body, so if you kept the pseudocorpse "alive" on an IV, heart lung machine, and hemodialysis, they'd probably still be paralyzed.


Giving a simple answer is difficult as the field of humoral immunology is quite extensive. Here is an abbreviated overview.
Our body produces myriads of different antibodies during an immune response, not just one. It is impractical to isolate and sequence one antibody protein as their sequence differs in very subtle ways. N-terminal sequencing like Edman degradation is not practical as it covers only a few dozen residues at most. Perhaps proteolytic digest of an antibody and peptide sequencing is possible, but again this requires a large amount of a pure antibody. Protein sequencing is not practical.
Instead, people sequence the DNA corresponding to a given antibody instead of sequencing the antibody protein itself. As a given B cell expresses one antibody in large amounts, Milstein and Kohler (Nobel laureates) devised a technique to fuse B cells with tumor cells, creating hybridomas. Each hybridoma thus produces a single antibody. Such hybridomas may be cultured – monocultured in fact - in the lab to large amounts, leading to the production of a uniform, single antibody, termed monoclonal antibody. The corresponding DNA sequence of such monoclonal antibody may be readily sequenced.
I would think it feasible to create a library of individual hybridoma monocultures using a patient’s B cells, and then select the hybridoma producing the best monoclonal antibody from the library, and sequence that DNA. Epitope binning [https://en.wikipedia.org/wiki/Epitope_binning] is one example of a technique to identify the best antibody. The successful hybridoma may then be culture to large scale to produce lots of that exact antibody.
Administering such purified antibodies to a patient is not straightforward as this foreign protein will be itself recognized by the patient's immune system and cleared. There are techniques to reduce the immunogenicity of a given antibody, but that will be a lengthy discussion in itself.


“Gene expression level” is an imprecise and partially ambiguous term
  that should be avoided.

Many (but not all) genes have the information to produce proteins†, but there is no need for this information to be used at any given time — it depends on the requirements of the organism or cell. For example the DNA of lung cells contains the information to produce the protein chains of haemoglobin, but it is never used in those cells. We can say that “the gene is not expressed”.

So the absence of expression is fairly easy. However, for a protein-coding gene the meaning and quantitation of expression is more difficult. That is because in expressing the information in the gene the DNA is first transcribed into mRNA by RNA polymerase, and then that information that encodes a protein can be translated into protein on the ribosome.

The word level refers to quantification, and is a sloppy substitute for quantity or perhaps rate (quantity produced in unit time) or perhaps relative quantity.

But the main difficulty is whether in quantifying gene expression you measure the quantity of mRNA synthesised under standard conditions or the quantity of protein produced.

If you are a bioinformatician encountering this term, my bet is that it is in relation to the currently (2018) popular RNA-Seq technique, which in fact provides relative measurements of the quantity of RNAs of different types produced under standard conditions. This is generally expressed in units called FPKM — Fragments Per Kilobase of transcript per Million mapped reads. The difference between this technique and the northern blotting mentioned by @Hawkeye, is that the latter is used to detect a single mRNA, whereas RNA-Seq applies to all the mRNAs that are present in a sample.

In the field of proteomics, it is possible that the term is being used in relation to the amount of protein produced, which may be roughly quantified by two-dimensional gel electrophoresis.

†Some genes encode RNAs that do not encode proteins (ribosomal RNAs, transfer RNAs, RNAs involved in splicing and in modification of rRNA, microRNAs etc.). The expression of the genes for these will end with the synthesis of the RNA.


Do lobsters possess a nervous system to feel pain?

Yes they feel pain, at least in certain areas of their body without a doubt. Research has been done to test whether they feel pain consciously (a signal to the brain that is perceived allows for learned response) or if it is just a reflex response (Nociception), and there is good evidence they actually perceive it especially in the antenna.

source

Source 2


Can anyone help me identify what type of horns these are?

Those look very much like "Catalina" goat horns. They're a popular trophy game to hunt, specifically for these sorts of displays. The goats themselves originate in Spain but are commonly found in the United States, now.


Are there special constants in biology that define organism's morphology?

I don't know if this is what you mean, but take a look at BioNumbers.

Also, mathematical constants like pi are different from physical constants. Mathematical constants are true in a mathematical (logic) sense, and do not need to be related to any physical quantity. They are derived by logic. Physical constants, on the other hand, typically describe an observed relation between two types of quantities. They are derived by measurement.


Has evolution made a mistake with prehistoric animals?

There are two questions here.

Dinosaurs were larger because their basic anatomy is better at being large than mammals. Their spine is better braced (no lumbar region), their breathing mechanism scales better, and their hip structure is stronger. This is called a preadaptation, or when an organism or group of organisms just starts with a head start on a particular adaptation due to unrelated reasons. It is the same reason mammals are the only terrestrial vertebrates to have echolocation: they are the only group with advanced amplification equipment in the ear to give it a head start.
Any era has its giants. Today is the time of the largest whales, largest trees, largest frogs, and largest horse to ever exist. Size is often a decent advantage: it makes you more resistant to resource fluctuation, it's just not a good for surviving global mass extinction inducing bolide impacts.

Evolution has no foresight. Evolution often produces and locks in counterproductive adaptations in the long run; while an adaptation may be an advantage in the short term, it may lock the organism into a disadvantaged position in the long run.
Sexual displays are a classic example: some quirk in peacock brains meant early female peacocks really liked more flamboyant males, that drove peacocks to the point modern males are incredibly vulnerable to predators and can barely fly due to carrying around huge superfluous tails. Both males and females would be better off preferring/having something less detrimental, but a feedback loop has locked in that detrimental feature. Males without it can't find mates, and females who do not prefer large tails male offspring also can't find mates. The term for this is fisherian or runaway selection. As an another example of counterproductive selection, many organisms when no longer controlled by predators or other factors will expand their numbers and consume resources to the point their populations collapse because there are too few resources to sustain them. Parasites often face this: a host with too many parasites dies, which is bad for the parasites but if the host can't fight off the parasites many are perfectly happy to kill their host and then starve.

Another aspect of evolution not having foresight is it cannot prepare you for extremely rare events, like mountains falling from the sky.


It depends on the kind of organism.

When the cell with two nuclei will try to go through mitosis, the nuclear membranes will fragment, releasing all genetic material to the cytoplasm, where it will behave normally, as if it came from only one nucleus. The DNA will divide and move into two daughter cells, each of which will assemble its one nucleus from the membrane fragmnets. However, each daughter nucleus will have double the normal number of chromosomes - one whole set from each of the old nuclei.

(In fact, this is what happens in humans after fertilization - the male and female pronuclei never merge, they just copy their DNA and divide it simultaneously into two daughter cells. The pronuclei are haploid, so the resulting daughter cells are diploid.)

What happens later, to the tetraploidic cells from your question, when they try to develop into a full organism, may end better or worse.

For exapmple many plants will just grow normally, only form bigger plants (modern wheat is such an example - it may be tetra- or even hexaploidic, meaning it has up to 6 sets of chromosomes).

For animals this is usually fatal, but some, like the xenopus, seem to be unaffected.


Bug identification - Beetle, grasshopper, moth-like and it also flies

That is a mole cricket, Order Orthoptera, family Gryllotalpidae
https://en.wikipedia.org/wiki/Mole_cricket


Difference between Fulminant and Acute Meningococcemias

When we say "Fulminant meningococcemia" we mean failure of adrenal glands due to haemorrhage of infectious origin, or Waterhouse–Friderichsen syndrome

and acute is related to time of signs appearance, opposed to chronic disease.


What nutrients do I lose in the water when I boil vegetables?

Vitamin C and the B complex vitamins are water soluble.   Thiamine and folate are also heat labile.

Overall there are hundreds or often thousands of kinds of small molecules (not protein or DNA) in the cell and many of them are water soluble or heat labile.  Plants especially have many unusual small molecules.  Its not known how many of them affect human health, but may affect factors like the gut microbiome quite a bit and have an effect on well being if not mortality.

Some people think that live uncooked vegetables have enzymes and other proteins which are good for you since cooked proteins are denatured and may be taken in differently.  At the very least they are probably easier to digest when they are not heat denatured.


Did researchers evolve multicellular yeast or did they just turn on multicellularity?

You're right:

  Within the Fungi, simple linear multicellularity of hyphae occurs in all major clades (see below), but only Ascomycota and Basidomycota display more complex two- and three- dimensional multicellularity in the form of sexual spore- producing fruiting bodies. In both of these groups, reversals to unicellular lifeforms have occurred, for example, Saccharomyces and many other related yeasts in the Saccharomycotina (Ascomycota) or Cryptococcus albidus and related species in the hymenomycete clade of Basidiomycota (de Hoog et al. 2000, p. 130).

Medina, M., A. G. Collins, J. W. Taylor, J. W. Valentine, J. H. Lipps, L. A. Amaral Zettler and M. L. Sogin (2003). "Phylogeny of Opisthokonta and the evolution of multicellularity and complexity in Fungi and Metazoa." International Journal of Astrobiology 2(3): 203-211. doi:10.1017/S1473550403001551
(PDF)

Update: The authors responded to criticism like this on The Loom, here's an excerpt:

  Our yeast are not utilizing ‘latent’ multicellular genes and reverting back to their wild state. The initial evolution of snowflake yeast is the result of mutations that break the normal mitotic reproductive process, preventing daughter cells from being released as they normally would when division is complete. Again, we know from knockout libraries that this phenotype can be a consequence of many different mutations. This is a loss of function, not a gain of function. You could probably evolve a similar phenotype in nearly any microbe (other than bacteria, binary fission is a fundamentally different process). We find that it is actually much harder to go back to unicellularity once snowflake yeast have evolved, because there are many more ways to break something via mutation than fix it.


Standing genetic variation is when there is more than one allele at locus in the population at the time-point in question. When an allele goes to fixation there is no standing genetic variation at the locus until new mutations occur. Loci where alleles are not fixed are described as having standing genetic variation.

  "Standing genetic variation: the presence of more than one allele at a locus in a
  population."

from Barrett and Schluter 2007


Will salting the ground kill insects and spiders?

Dusting the area with a diatomaceous earth based insecticide ought to do the trick, while being essentially non-toxic. If you want to prevent plant growth there too then of course salt the earth.

See Efficacy of modified diatomaceous earth on different cockroach species (Orthoptera, Blattellidae) and silverfish (Thysanura, Lepismatidae)


Can sexual reproduction create new genetic information?

Homologous Recombination not only shuffles different mutations together, but similar sequences near each other from gene duplication events and from regions with highly repetitive sequences can recombine and cause gross changes in the sequence of the genome in hot spots.


shRNA knockdown not showing with Western

I assume that you transfected the plasmid directly not producing viruses. If you want stable transformants, you might want to subculture them and maintain a bit longer. It is because efficiency of integration of plasmids into genome could not be that high--less than 0.1% of population obtain stable resistance by integration into genome. After 6 days, cells were still healthy in your case. This means you might get good transfection efficiency and after several times of cell division, your plasmids were diluted and the effects might be low even if cells maintain resistance against puromycin.

If transient expression (KD) works in your experiment, you might want to check expression level of your target at day 2 or 3. If you prefer stable cell lines, you can increase puromycin concentration, and if you agree, you pick up single colonies after cells not having plasmids in genome are dead. Among these colonies, some have more plasmid copies other have less. You can choose cells least expressing your targets as well as moderately expressing cells if you want. Because you might want to see expression level dependency.

For some cells, 5ug/ml puromycine is used according to this link.


What are gram negative and positive bacteria?

The Gram stain is one of a large number of techniques used to characterize bacteria. In particular, a bacterial species is usually either Gram-positive (purple when stained) or Gram-negative (pink when stained). In Gram-postive bacteria, the cell wall is thicker and has much more peptidoglycan compared to Gram-negative bacteria. The chemicals in the stain react with these molecules in the cell wall and result in the purple color. All of this information is well covered in the Wikipedia article on the subject.


Does the sun light have to have *direct access* to fruits to make them sweet?

It would depend if the fruit has the ability to sense or capture light. This depends on chlorophyll mostly, found in cellular organelles called chloroplasts. If the fruit is incapable of capturing light, the light can still have an indirect impact by being captures on leaves, since plants circulate nutrients - this is why roots can grow without having access to sunlight.

Here's a few excerpts from the following paper (https://www.ncbi.nlm.nih.gov/pubmed/11337414):

"To date, molecular regulation of the role of light in fruit ripening has been studied most thoroughly in tomato, and available evidence suggests that light has its greatest impact on pigmentation, with apparently little effect on additional ripening phenomena."

"The green to red color transition typical of ripening tomato fruit is largely due to the developmental transition of chloroplasts to chromoplasts; as photosynthetic membranes are degraded, chlorophyll is metabolized, and carotenoids, including β-carotene and lycopene, accumulate."

In plain English, the pigment that captures and absorbs sunlight for metabolic reasons (photosynthesis) gets transformed into a pigment which absorbs sunlight for other reasons, such as 'looking tasty' or protection from ionizing radiation. Essentially the same thing happens to leaves in autumn - the green chlorophyll pigment, which absorbs the energy of the sun for the plant to grow, becomes the orange carotene, and the leaf slowly dies off.

Interesting sidenote: biological pigments are very important molecules in ecology and in cell biology. Take a closer look: https://en.wikipedia.org/wiki/Biological_pigment

As for your question about how ripening occurs... Google would do a better job than most.


HeLa cells themselves are not pigmented, and usually appear translucent/gray under light microscopy. The growth medium may however be colored, and a common color is magenta.

The tumors themselves will appear purple, as most tumors do, due to the broken vascularization. Tumors commonly secrete growth factors leading to angiogenesis, but the resulting vessel networks are convoluted and not well organized, commonly full of anastomoses. The resulting poor vascularization leads to significant hypoxia, which results in a bluish coloring of the blood.


What happens between two nodes in an evolutionary tree?

Your answer is A. for one simple reason, two different nodes represent at least one notable/measurable difference between groups, so between any two nodes there must be at least one difference.

Look at this example, whether A and B represents Mammals and Birds or two subspecies of chimp, or two strains of virus the fact they are two separate nodes means there is some difference between them. When constructing a tree there has to be at least one character difference to have more than one node. A tree with no differences is just a dot by itself.

Also an organisms does not stay the same between a node an the tip (the tip is a node) to use the below example the starred node between A and B is the most recent common ancestor of A and B which is not the same thing as A or B.


Is there any stem cell or biogel method that exist for muscle and tendon lengthening?

Limb lengthening surgery is usually used to treat sequelae caused by bone disease, trauma, pygmyism or inflammation. I personally do not recommend to use surgical methods to increase height. Typically Limb Lengthening requires Achilles pre-lengthening surgery and a lot of postoperative rehabilitation. Moreover, Limb lengthening surgery may cause pain, infection, muscle atrophy, joint stiffness and delayed bone healing. There's a lot of related research cause this study is timely for some patients.

ALDEGHERI, R., RENZI-BRIVIO, L., & AGOSTINI, S. (1989). The callotasis method of limb lengthening. Clinical Orthopaedics and Related Research, 241, 137-145.

De Bastiani, G., Aldegheri, R., Renzi-Brivio, L., & Trivella, G. (1987). Limb lengthening by callus distraction (callotasis). Journal of Pediatric Orthopaedics, 7(2), 129-134.

Paley, D. (1988). Current techniques of limb lengthening. Journal of Pediatric Orthopaedics, 8(1), 73-92.

Paley, D. (1990). Problems, obstacles, and complications of limb lengthening by the ilizarov technique. Clinical Orthopaedics and Related Research, 250, 81-104.

Szoke, G., Lee, S. H., Simpson, A. H., & Prescott, J. (2005). Response of the tendon during limb lengthening. The Journal of Bone and Joint Surgery.British Volume, 87(4), 583-587.


Why do tears fall from our eyes when we ride a bike too fast?

Our eyes need to be covered with a thin film of liquid all the time. When riding fast, the wind flow pushes the liquid away from your cornea. Your eye compensates for that by producing more tear.