Is the increased/decreased enzyme activity (tyrosinase) caused by an environmental factor (UV radiation) considered to be gene expression?

Unless there's a feedback mechanism shutting off gene expression (which controls the proteins made by a cell), activation or deactivation of an enzyme is not in itself a matter of gene expression, it's a matter of external factors controlling the enzyme's activity. You need to decide on what exactly causes skin pigmentation: the enzyme or cell proliferation, and what is under the control of gene expression and what isn't.

Most of what you find on ultraviolet light and melanin will be somehow related to melanomas, the formation of which does involve gene expression, so it's important to keep the two separated.

Ultraviolet light does cause proliferation of melanocytes, which cause the skin to darken. Melanocytes impart melanin to keratinocytes; these cells then are what give you a tan. The keratinocytes undergo constant turnover, so are eventually shed, and in the absence of continued exposure to UV radiation, there is no need to keep producing melanin-heavy keratinocytes.

  The keratins and proteins within the stratum corneum act mainly by scattering and absorbing the UV. UV-R sets in action an integrated mechanism for the formation and delivery of melanin within melanosomes from melanocytes to keratinocytes. This mechanism is probably triggered by keratinocytes, which respond to UV-R with bursts of mitoses and with increased production of ET-1 and POMC, thus creating a new demand for melanosomes. The mitotic rate of basal keratinocytes increases a day after UV exposure, reaches a maximum 2 days later, and maintains this level for ∼1 wk. It then declines, and the skin regains its original thickness after 1–2 months if there has been no subsequent exposure.

Continued exposure to UV light stimulates the melanocytes to grow. This increases the chance of the development of melanomas. Since skin cells containing melanin are shed (there's no getting around that), in light-skinned individuals, keeping a tan is to keep injuring the skin and risking carcinogenesis.

Melanin Pigmentation in Mammalian Skin and Its Hormonal Regulation
Human skin pigmentation: melanocytes modulate skin color in response to stress
Mechanism of UV-related carcinogenesis and its contribution to nevi/melanoma


Does the given pedigree show a Y-linked dominant trait?

You're right that this could just as well be Y-linked dominant (althought that is pretty rare due to the small size of the chromosome).

The only reason pointing more towards autosomal dominant is the mention of "extra fingers and toes". Most cases of polydactyly are inherited in an autosomal dominant way.

Does seem like an unfair question, though, since (at least in theory) there's more than one possible answer.


Which magnoliophyta groups are NOT pollinated by bees and why?

Flowering plants evolved before bees, so clearly in the ~100 million years, they must have been pollinated by other methods. Some plants still retain this ancestral characteristic.

This paper shows a species Magnolia tamaulipana (Magnoliaceae) which is pollinated by beetles.


Did cyanobacteria commit evolutionary suicide by producing oxygen?

Oxygen is, indeed, highly toxic to cells, due to its oxidizing power, i.e., the ability to remove electrons from another substances. Since the first carbon-reducing organisms started to increase the amount of molecular oxygen in the atmosphere, more than 2 billion years ago, life on earth has been dramatically changed by this compound: you can even consider that aerobic respiration appeared originally as a mechanism of reducing the toxic molecular oxygen to the innocuous water.

Today, organisms that use water to reduce carbon dioxide, releasing oxygen as a by-product, have molecular mechanisms (as aerobic respiration, for instance) to protect them from the very oxygen they produce.

But your question is quite interesting: how did the first photosynthetic organisms protected themselves against the oxygen they started producing?

This is a catch 22. An interesting solution was proposed by a team of geobiologists from Caltech: There was a little amount of molecular oxygen in the ocean's water before the appearance of photosynthesis. This small amount of oxygen was able to promote the evolution of biochemical mechanisms protecting organisms from its toxicity. Some of those organisms, then, were capable to develop photosynthesis and protect themselves against the huge amount of oxygen that they started releasing. According to the team:

  Low levels of peroxides and molecular oxygen generated during Archean and earliest Proterozoic non-Snowball glacial intervals could have driven the evolution of oxygen-mediating and -using enzymes and thereby paved the way for the eventual appearance of oxygenic photosynthesis.

Source: Liang, M., Hartman, H., Kopp, R.E., Kirschvink, J.L. and Yung, Y.L. (2006) "Production of hydrogen peroxide in the atmosphere of a snowball earth and the origin of oxygenic photosynthesis", Proceedings of the National Academy of Sciences, 103(50), pp. 18896–18899. doi: 10.1073/pnas.0608839103.

EDIT: according to your comment, all you want to know is "whether cyanobacteria is able to survive oxygen". Well, that's even easier to answer:

Cyanobacteria can perform aerobic respiration. That means that they can easily use protons and electrons obtained from organic matter to reduce molecular oxygen to H2O:

  Cyanobacteria... are among the very few groups that can perform oxygenic photosynthesis and respiration simultaneously in the same compartment,and many cyanobacterial species are able to fix nitrogen. Therefore, they can survive and prosper under a wide range of environmental conditions.

Source: Photosynthesis and Respiration in Cyanobacteria


Are thunder and lightning necessary for any organisms?

Lightning results in nitrogen fixation (Draphco et al., 1967; Hill et al., 1980). It is one of the main abiotic nitrogen fixation mechanisms. As you would know very well, nitrogen fixation is important for all organisms.


In what situations, when reacting to impressions, are the signals sent directly from the thalamus to the hypothalamus?

As @Pyssling states, it has to do with fear, and how we process situations that are potentially dangerous. There is a distinction between the two concurrent processes that you describe, that go under the title "short route vs long route" or "low road vs high road" (possibly more titles).

The short route (or low road) is the immediate process/reaction/response, which would enable os to avoid death in certain situations - This works on an instinctive level. The long route (or high road) is the process/reaction/response that could be defined as a thorough evaluation of the input/signal that we receive.

This site has descriptions and images that can be read on three "levels of explanation", and I find them highly informative.
http://thebrain.mcgill.ca/flash/a/a_04/a_04_cr/a_04_cr_peu/a_04_cr_peu.html

Here is a youtube video on the subject "How fear is wired in the brain" that deals with the same topic. https://www.youtube.com/watch?v=vl_B6nz3UOQ

I am in no way an expert and have stumbled upon these sites based on personal interests, so I do not know if someone may be able to criticize their validity / quality, but I found them excellent.


Is there any biological basis for the emphasis on the value of the firstborn son?

There are lots of cases reported now that suggest that overall the firstborn child is usually more intelligent. The articles supporting this are based on behavioural and economic study though, so the biological basis is a little lacking.
It's also not clear if this is nature or nurture. The firstborn may benefit from their parents undivided attention disproportionately.
Here's the press release for it. And the coverage from the Independent
and Forbes
I read somewhere that the firstborn is more likely to be overweight too, but I can't find the article now. Other people may know other traits that are supposed to differ between children.


One way to identify mechanisms by which the body tames the microbes in the mouth is to observe what happens when those mechanisms are impaired:

  Deviation from symbiosis among the bacterial community
  leads to “dysbiosis”, a state of community disturbance. Dysbiosis
  occurs due to many confounding factors that predispose a shift in the
  composition and relative abundance of microbial communities.
  (Dentistry Journal)

1) Immunity

Normal innate, cellular and humoral immunity helps to prevent oral flora from causing infections.

a) When the immunity is impaired due to a disease (HIV/AIDS, cancer...) or long-term treatment with antibiotics, steroids, immunosuppressants or chemotherapeutics, a part of normal flora, such as the yeast Candida, can overgrow and cause oral thrush.

  Host defense against infections with Candida spp. depends on rapid
  activation of an acute inflammatory response by innate immunity,
  followed by an incremental stimulation of specific immune responses
  mediated by T-cells (cellular immunity) or B-cells (humoral immunity). (Immunology of oral candidiasis, J Pharm Bioallied Sci.)

Picture 1: Oral candidiasis (source: Wikipedia, creative commons license)

b) Impaired immunity can result in osteomyelitis of the mandible, caused, for example, by the Actinomyces bacteria:

  Systemic factors such as diabetes mellitus, agranulocytosis, leukemia,
  severe anemia, malnutrition, or alcohol abuse affect immune
  surveillance and lead to impairing the osteomyelitis

  Actinomycotic druses and filaments were detected from the sequestrum
  of the fracture site (Rapidly Progressing Osteomyelitis of the
  Mandible, Case Reports in Dentistry)

2) Saliva

Saliva helps to prevent mouth infections by flushing microbes into the gut and by the antimicrobial substances.

  Among such protective factors, the flushing effect of saliva flow is
  the most important one...(Antimicrobial function of human
  saliva--how important is it for oral health?, Acta Odontol
  Scand.)

  Importantly, saliva is crucial for defense against microbial species,
  as it is rich in antimicrobial compounds such as hydrogen peroxide,
  lactoferrin, and lysozymes...disruptions in saliva secretion increase the frequency of oral
  conditions such as oral candidiasis, gum disease, and tooth decay
  (caries), as well as respiratory tract infections (The power of
  saliva: Antimicrobial and beyond, PLoS)

Impaired saliva excretion due to a disease (salivary stones, Sjögren's syndrome, untreated diabetes, radiation injury) or drugs (antihypertensives, antidepressants, tranquilizers, diuretics, antihistamines...) can result in dry mouth (xerostomia), which increases the risk of oral thrush and other mouth infections.

3) Lack of substrate for microbial overgrowth

Clean healthy mouth does not contain enough food for microbial overgrowth.

On the other hand, in untreated diabetes mellitus, the abundance of glucose in the saliva promotes the overgrowth of the yeast Candida (oral thrush):

  A dry mouth coupled with a higher amount of glucose in the saliva can
  also make for favourable conditions for thrush.
  (Diabetes.co.uk)

Mouth full of food debris due to poor hygiene can promote bacterial overgrowth:

  Periodontitis is caused by certain bacteria (known as periodontal
  bacteria) and by the local inflammation triggered by those bacteria.
  Although these periodontal bacteria are naturally present in the
  mouth, they are only harmful when the conditions are right for them to
  increase dramatically in numbers. This happens when a layer of
  bacteria and food debris, known as plaque, builds up and is left
  undisturbed on the teeth...(What is periodontitis, European
  Federation of Periodontology)

The bacteria from normal oral flora often involved in periodontitis: Porphyromonas and Streptococcus (Lumenlearning.com).

4) pH

The normal pH in the mouth is 6.2-7.6 (Journal of Indian Society of Periodontology). When it falls under certain value known as critical pH (~5.5), acids derived from bacterial fermentation of dietary sugars start to dissolve tooth enamel and cause caries. The bacterium Streptococcus mutans is a part of normal oral flora, but is commonly involved in caries (Lumenlearning.com).

5) Low susceptibility of mouth mucosa for certain microbial toxins

Certain microbes, such as Staphyloccocus aureus, which are a part of normal mouth flora do not likely cause infections in the mouth, even when they appear in the mouth in much greater amounts, for example, in food poisoning and even if these microbes can cause severe diarrhea (Centers of Disease Control and Prevention). This is because the mouth mucosa is not susceptible for the toxins secreted by these bacteria, while the stomach or intestinal mucosa is.


I don't think it is an adaption, but the that diet plays a dominant role. The feces of cows in intensively fertilized agricultural fields, with grasses rich in protein, has no shape at all. See picture below.

The feces of cows in natural areas has much more structure. (image has copyright, so can only link)


Do axonal conduction delays have a function?

Your point #1 is correct, signal propagation is not instantaneous in real physical world. But for some models it is "good enough" to approximate action potential to go through axon in an instance.

There is also biological role of signal propagation timing. One example, is classic Hebbian learning model. Based on "fire together - wire together" idea, connected neurons that become active relatively close in time, will increase synaptic connectivity, illustrated here:


Is it a limitation of the eyes, or the brain, that we can't see a moving bullet?

It's less a problem of speed and more of raw photon count. Assuming a brightly lit day, the bullet will move so fast that it doesn't reflect enough photons to register against the background. High speed images of bullets usually involve a very bright flash (and other controlled settings) for the camera to pick it up. (Also, a very short flash helps the bullet to appear stationary in the image.

On the other hand, seeing where your bullets are going is pretty useful. Therefore tracer bullets were created, which are essentially a pyrotechnic flare that you substitute in every 5th bullet, typically in machine gun ammunition. Proof that if you make a bullet bright enough, you can register it just fine.

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


explanation of conjugation experiment in bacteria

There are three variables being shown here:

The amount of time samples were stored in the freezer to allow $^{32}$P decay (x-axis),
The length of time samples were allowed to grow in a nonradioactive environment before being frozen (points with different symbols), and
The rate of $\beta$-galactosidase production when cells were thawed and grown in the presence of the transcriptional inducer IPTG (y-axis).

Let's break those down a bit more:

The x-axis measures "fraction of $^{32}$P decay." In terms of the experimental protocol, this translates to "length of time left in the freezer." For the $^{32}$P-decay experiments, samples are stored in the freezer for various lengths of time, where metabolic processes, like DNA replication or enzyme production, are shut down or drastically slowed. Although metabolism has been shut down, $^{32}$P can still beta-decay into $^{31}$S (according to Wikipedia), which promotes the breakdown of any DNA containing (formerly) radioactive isotopes. The implication is that the longer you leave samples in the freezer, the more $^{32}$P will decay and the more formerly radioactive DNA will be degraded. So you can read the trend in the x-axis either as "increasing fraction of $^{32}$P decay", "increasing amount of time left in freezer," or "decreasing fraction of intact $z^+$ DNA." The different points corresponding to, say, "48 minutes past mating" correspond to samples that were frozen down 48 minutes past mating but kept in the freezer for different lengths of time.

The y-axis measures "percent survival of enzyme-forming capacity." I think that it's safe to interpret this as the rate of $\beta$-galactosidase production relative to the rate with no $^{32}$P-decay. In other words, if you plot $\beta$-galactosidase production over time (as in Figure 5) for different conditions, you'll measure a slope, the rate of enzyme production. If you normalize all these rates from different conditions by the rate when there was no radioactivity (and thus no degradation of $z^+$ DNA in the freezer), you'll get the values plotted on the y-axis.

The final interpretation of this plot is that the $\beta$-galactosidase production rate is sensitive to the loss of the introduced $z^+$ DNA when the loss occurs soon after mating, but if cells are allowed to grow enough to divide once or twice before DNA degradation, then the loss of the original conjugated $z^+$ DNA does not affect the $\beta$-galactosidase production rate. This data is consistent with the idea that the DNA form of a gene is constantly required for sustained $\beta$-galactosidase production, and after several rounds of division the $z^+$ DNA has been replicated and is no longer radioactive and prone to degradation.

There's a lot of data in this plot (ah, the elegance of 1960s molecular biology!) so it can take a while to digest. Hope this helps!


Why are vaccines containing attenuated microorganisms preferable to those containing dead microorganisms instead?

It's not necessarily true that attenuated vaccines are "preferable" to killed vaccines. It's a case by case basis. In some cases one or the other simply isn't possible or practical. It may not be possible to make a vaccine that's attenuated enough, for example. Or a killed vaccine may not be effective.

Here are some pros and cons of attenuated vaccines:

more likely to follow the natural path of infection, so there might be more immunity at the specific site of infection. For example, attenuated vaccines against gut pathogens might drive gut-specific immunity.
Might replicate in the host so that the actual amount of antigen seen by the host is greater than the amount delivered -- so you can deliver a much smaller dose to get similar immunity
Might cause more inflammation. Inflammation can drive a much stronger immune response because the body "thinks" it's being attacked by a dangerous pathogen

Cons:

Might cause more inflammation. Inflammation can cause tissue damage or local pain
May be less safe. Replicating in the host may give the opportunity to mutate and become more dangerous
May be more fragile. A killed vaccine could be relatively temperature stable, while an attenuated vaccine might need to be kept in a very narrow temperature range so it doesn't die and become ineffective. That might make it difficult to use in, say, developing countries

There are many more points that could be made but the overall picture is that attenuated vaccines might be more effective but more dangerous. Attenuated vaccines that are used today have been shown to be safe as well as effective, and killed vaccines that are in use have been shown to be effective as well as safe, so these are concerns during development of new vaccines, not in use of present ones.


The one on the left is a Lunate Zale Moth (Zale lunata).
See Western Washington University's PNW moths page for more detailed info.

The one on the right is a Forage Looper Moth (Caenurgina erechtea).
See here for an image similar to the one in the question.
And again take a look at Western Washington University's PNW moths page for more detailed info.


What is the minimum air pressure the human body can tolerate if oxygen supply is not an issue?

Disregarding hypoxia, the lowest atmospheric pressure the human body can withstand is around 6 percent sea level pressure, or 61.8 millibars, below that pressure the water and blood in your body starts to boil. Harry George Armstrong, a physician, and an airman, was the first to recognise this limit, which on Earth occurs at an altitude of roughly 63,000 feet, beyond which humans absolutely cannot survive in an unpressurised environment. The limit was named in his honour and so is called the Armstrong Limit. The lowest atmospheric pressure humans can breathe in, with a pure oxygen supply on hand, is roughly around 12.2 percent sea level air pressure or 121.7 millibars, the pressure found at 49,000 feet. Or, as a slightly madder alternative example, in a terraforming Mars situation, which might arise one day; a fit person could in theory walk around outside without a spacesuit on, but breathing from an oxygen tank, only when the atmospheric pressure got above about 120 millibars, and hope to survive for long.


Why do many fruit trees have five-petaled flowers?

Peach, apricot, plum, pear, apple, cherry trees are plants of the same family, Rosaceae, so they are closely related. They share many more aspects than the five petals. In fact, other plants in this family, and even many other dicots have five petal, simply because their share a common ancestry.


What are the (evolutionary) advantages of secondary transport?

I think an easy analogy for why this approach evolves is to think of how humans use electricity (or energy more broadly).

Although it is feasible to have localized electricity generators (for example, a solar panel on a simple calculator), it's typically more efficient to have centralized electricity production. With that organization, changes to the electricity generating machinery can proceed without any changes needed at the end user. If the power plant improves efficiency by 10%, that improves the efficiency of the entire system without a change needed in every lightbulb, refrigerator, and phone charger.

Once an ion gradient is established, different independent systems can use it to perform otherwise energetically unfavorable tasks. Of course this is not the only way evolution could proceed: as linked in a comment there are several general explanations for why evolution doesn't produce every possible combination. There are in fact a lot of proteins that use ATP directly.

The sodium-potassium ATPase that powers one of the major secondary transport systems is particularly interesting because it moves 5 ions at a time, making it very efficient. It would waste ATP if it only exchanged 2 ions at a time. By producing that gradient, other proteins can then evolve to use this gradient at an appropriate energy level rather than needing to work on a "1 ATP = 1 cycle" basis.


What is this? Found crawling across ground under oak tree. Six arms waving, I broke off 1 trying to pick it up. Less than 1 inch long

That is a Hag moth caterpillar

Don't touch.


What exactly is extreme heterozygosity and how does it work?

Without reading the article, given the context that you have mentioned, I think extreme heterozygousity means that most of the individuals in the population are heterozygous (much higher than 50%). So there might be some kind of selection pressure that gives heterozygous individuals a reproductive benefit.


Do we instinctially interpret birdsongs as a sign that there are no predators present?

Crows and gulls would probably also flee predators but their songs are definitely not really pleasant to listen to! I know it, they woke me up last week-end $\ddot \smile$. The canadian goose or the common starling (see here) are other examples of not really pleasant songs.

Too a selectionist view of evolutionary processes

It is important not to make the mistake to see anything as an adaptation (a result of natural selection only). Evolution is way more than natural selection and it encompasses tons of stochastic processes. This answer has a paragraph on the subject of not thinking of anything as a result of natural selection. This kind of over-consideration of adaptive processes in evolution is a common mistake especially when thinking about how human behaviour evolved.

Evolutionary psychology and evolution of appreciation of bird songs

The field of evolutionary psychology may interest you but note that it is a field that is sometimes still at the limit between psychology, philosophy and biology.

Appreciation of art as a by-product

Appreciation of art (like birds songs) and beauty is a pretty poorly understood subject yet. The first hypotheses came from Darwin and Gould. They pretty much argued that we enjoy sex, grasp facial expressions (kin recognition), have to like logical proof to appreciate learning and acquire language, efficient communication (cooperative hunting), appreciate put oneself into others thoughts (Machiavellian intelligence),  etc... As a result of those selection pressure, we may have evolved, so-called by-products. A by-product is a phenotypic trait that hasn't been directly selected for but that has been  selected via its correlation to some other phenotypic trait that is under positive selection and that is correlated. If this is true, then there would have a correlation between cognitive abilities and art appreciation and therefore a correlation between art appreciation and fitness.

Appreciation of art due to sexual selection

Some have argued that looking at the importance of art appreciation and intelligence in today's mate choice, it is likely that art appreciation may have been reinforced by sexual selection.

Either sexual selection may have reinforced a trait that was correlated to fitness ("evolution of appreciation of art as a by-product" hypothesis).

It is also possible that sexual selection may have selected for art appreciation without art appreciation being correlated with fitness but just because it asks for a big brain and lots of energy (brains consumes lots of energy) and being able to appreciate arts means that the individual has extra-energy to spare and is therefore very fit (handicap principle).


Do plant cells recycle carbon dioxide from their respiration during photosynthesis?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884119/
This paper found mitochondria move to be next to chloroplasts when exposed to light. So carbon dioxide is  more likely to be recycled in lighted conditions.


Terminology is what is holding you back.
What chromosome implies depends on context, i.e. is it replicated or not.

In Meiosis. Gametes arise from Germline cells that have 23 PAIRS of chromosomes. That means, that while there are 23 different chromosomes they come in doubles/pairs. This is the typical X like shape we think about when we hear chromosomes.
Another way, chromosome can means either 1X or 2 single chromatid

MEIOSIS I -- 23X chromosome pairs are duplicate and end up as 46X chromosome pairs (46 pairs of X OR, 92 separate chromatid)

These 46X are divided equally among two daughter cells just like in mitosis. Where now each daughter cell receives 23X = 23 pairs.

MEIOSIS II. The daughter cells in end of Meiosis I divide without DNA replication and the 23 pairs are split among 2 new cells. So now each new daughter cell (in total 4) has 23 individual chromatid (individual chromosomes)
and these are the gametes.

When the gametes fertilize to form a zygote, the zugote product ends up 24X each.

Each X contains, 1 chromatid (|) from the father and 1 chromatid {|} from the mother.

Haploid means once copy of each chromosome.
23
Diploid means two copies chromosomes or 23X

Ref
- Allison Q.N,.(2015), Freeman Biological Science.


Is there a good site or software to see if a primer pair spans an exon junction?

If there is a such a site, I have never encountered it. Since you say you have the genomic coordinates for each primer it seems to me like all you need is a list of the genomic coordinates of every transcribed exon in the human genome. Assuming that is correct then you are in luck because such lists do exist in the form of a GFF3 file. You should be able to obtain a comprehensive annotated GFF3 file of the human genome from the EnsEMBL website. It is possible that the UCSC browser has a similar file (except in their '.bed' format) but I  am less familiar with the contents of that site.


Can cell division be stopped during prophase?

I'm unaware of such stop occurring at a mitotic prophase, but if your definition of "cell division" includes meiosis, the answer is yes: in several species, the oocyte stops at the first prophase (prophase I), in a resting phase called "dictyotene": https://en.m.wikipedia.org/wiki/Dictyate


How is the appropriately-stratified gut microbiome acquired in organisms performing horizontal transmission?

tl;dr it really might be due mostly to random chance, in terms of intentional mechanisms at least.

One thing that is important to remember about the gut tube is that conditions of life for microflora vary dramatically from one end to the other. This is true of nutrient availability, pH, and antimicrobial load. For example, the bacterial load of the lower intestinal tract is approximately seven orders of magnitude higher than the upper GI tract (stomach). They're just completely different places.

In some cases you can try to impute the bacterial assemblage in some part of the gut to a specific biological cause furnished by the host, for example the role of bile salts in controlling which organisms are able to colonize certain locations.

But a more parsimonious explanation is that the bacteria are growing in the places where they are good at growing. This brings up the old ecological saying: "Everything is everywhere, but the environment selects." We aren't necessarily trying explicitly to reinforce a certain assemblage, that's just the assemblage that works in niches with very low pH, very high nutrient load, bile salts, etc. And most of those features are unavoidable consequences of the gut's main function, digestion/excretion.

It certainly doesn't seem that e.g. behavioral strategies for exposing yourself to the "right" microbes gets you the right microbes in the right places. Recall that fecal microbiome transplant is one of the most successful strategies- just take some healthy poop and put it into a sick person's GI tract, they get better! That's not a very controlled horizontal transmission strategy.

You could propose that there is some second-order selection going on in which we have constructed GI niches in such a way that they encourage certain assemblages. Certainly, dysbiosis occurs and is bad in such cases as e.g. C. difficile infection, we would like to avoid those. Probably some coevolution has occurred between host and microbe, for example immune responses and butyrate production. That Foster paper has some more examples of possible mechanisms for a couple of specific cases, for example mucus. But they are probably not sufficient to explain the full compartmentalization of the microbiome in the way that you seem to be asking.


What experiment for first time showed DNA is anti-parallel?

The definitive proof came with the crystal structure of B-DNA (see Watson & Crick, 1953). Anti-parallel strands is the configuration that best explained the diffraction data while not violating chemistry (bond lengths and angles, no steric clashes, etc.).

The relevant sentence from the article is:

  the sequences of the atoms in the two chains run in opposite directions

I underlined this sentence in the following screenshot of the article:


It appears to be a Boxelder bug, which are common in areas of North America with maples, ash, or other host trees:

 (photo by Katja Schulz via Wikimedia Commons)


Is there a realistic "family tree" model for the human population?

Well, there are some questions regarding what population. I don't have 50 rep, so I can't really ask for clarifications; populations range a lot, from your typical avoidance of inbreeding (laws against cousin marriage) to Tamils with their high rates of first cousin marriage (so high that they don't have any pedigree inbreeding depression due to selection, so it's not unhealthy).

Mating in humans is often assortative for many traits including education, vocation, etc. When the Americas were settled (after aboriginal Americans were devastated by disease), skin color was a source of assortative mating. Arguably it still is. On the other hand, people tend to mate disassortatively for traits such as Major Histocompatibility Complex.
Furthermore, isolation in human populations tends to be by distance (though this is of course changing, leading to a lot of admixture in recent population history).

As a result, what your population is will have a huge impact on your results; you'll need to calculate f for any particular locus, and take a look at admixture. If f is 0, then you have a random mating scenario (neither preference nor avoidance of inbreeding, and neither assortative nor disassortative mating).

TL;DR if you're doing a very simple analysis on dummy data, you can probably get away with assuming that mating is totally random. But if we're talking about actual populations, you'll need to run the models/calculations of f and other population measures.


Does the Abbott ID NOW coronavirus test return a positive result if you take it while you're still in the incubation period?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

  It seems like Abbott's ID Now test works by detecting the virus directly as opposed to checking for antibodies?

Yes, the ID NOW test performs a quantitative real-time RT-PCR assay to amplify reverse-transcribed viral RNA, specifically targeting the SARS-CoV-2 RdRp gene.

The product insert for the COVID-19 test for the Abbott ID NOW product describes the "analytical sensitivity" or "limit of detection" (LOD), which describes the true positive rate.

The LOD described in the product insert is the lowest amount of viral genome in the collected sample that you need to get a true positive in 95% or more of administered tests, in units of "genome equivalents per mL".

This is effectively the minimum number of copies of viral genome per mL of assayed sample needed to give a true positive in 95% or more tests. Its LOD (125 copies/mL) is comparable with other tests (example).

A false negative can result if there is insufficient virus copies in the sample, or if there is test material contamination or the test is not performed correctly.

This assay includes positive and negative controls, which help to identify potential problems with how the assay was performed. Controls are important, given the many millions of tests that will be done to identify infected carriers of SARS-CoV-2 — the assay must be done correctly and without contaminants, in order to give the best statistical odds for the correct diagnosis of those who will be tested.


Why do some moles grow longer and darker hair than the rest of the skin?

Before answering the question (about the hairs) I will first go in some detail about what moles actually are:

  Moles are growths on the skin that are usually brown or black.  They
  are formed by clusters of melanocytes, the pigmented cells responsible
  for your skin color.  Moles typically appear during the first 30 years
  of life, can be flat or raised, and can darken with sun exposure,
  puberty, or pregnancy.

There are no articles covering this topic in detail (most of them are about the skin cancer, if you are interested in this topic check out this article). However there are some medicial experts talking about the hair growth.

  Joshua Zeichner, M.D., Director of Cosmetic & Clinical Research at the
  Mount Sinai Hospital in New York City. "If the mole also contains a
  hair follicle, the hyper-pigmentation can cause the hair that comes
  out of it to be coarser and darker."

Junji Takano, a Japanese health researcher said the following about this topic:

  This is due to the fact that capillaries of a mole are growing rapidly
  and excessively, and this includes the hair follicles

Actually moles are benign tumors(wiki), the cells in the body in charge of normal skin color, are being produced at an extremely fast rate. Thus causing the melanocytes to form in clusters instead of spread out, causing abnormal skin pigmentation in some areas of the body(wiki). So based on the above quotes this "fast production" also affects the hairs which are present in this piece of skin. More interesting is that people hate these hairs (which make sense offcourse) but in most of the cases this is a sign that this mole isn't cancerous:

  A mole that has a hair growing out of it usually means that is was
  present since birth or at a young age and is typically normal.

references: first quote, second quote, third quote, last quote


Identification - What kind of animal leaves these tracks?

The only candidate I could imagine is hare.
Sometimes it leaves a single track from its fore-limbs (from a theoretical point of view, I'd say it happens when the snow is relatively deep.)


Why do living fossils like crocodiles remain so constant and not evolve?

Evolution is a process of change by four mechanisms; mutation, migration, drift, and selection.

You are correct in thinking that, because crocodiles have been around for a long time, they could have accumulated many new mutations in that time, relative to other more recent species. However, mutation is only one of the important mechanisms underlying evolution.

How different are ancestral and modern crocodiles?

It seems the appearance of crocodiles has been fairly unchanged since their occurrence ~85 million years ago (mya).

How can they remain so unchanged?

Genetic variation may have been low in the ancestral population, this would reduce the potential for evolutionary change, as most change would have to occur through new mutations. It seems the populations of ancestral crocodiles were quite small, such that a genetic bottleneck may have occurred (which would reduce genetic variation). Mutation rates seem to be relatively low in crocodiles (also see here) which would reduce the rate at which novel mutation occurs, reducing the potential for evolution.

Note that many mutations will be neutral in their effect (or "synonymous") so won't have an obvious phenotypic effect, so there may be substantial evolution at the genetic level despite the phenotypic similarity.

Low rates of evolutionary change could suggests some other things may have also played a factor. Given that the populations have been through multiple genetic bottlenecks, genetic drift could have slowed down rates of evolution eroding genetic variance, removing rare mutations from the population.

If selection has been fairly constant over time then there is less chance that changes will occur. If selection were to change and favour new adaptations then these are likely to spread, but if selection remains fairly constant over time then it will continue to favour the same mutations. After a long time of consistent selection it is likely that most mutations will be deleterious (have a negative effect) and be removed from the population by selection. Darwin suggested that living fossils could occur because the environment they are in has remained fairly constant (from this link).


It would be incorrect to assume that

  every change has a significance

from an evolutionary point of view. In many cases, the changes could be happening at an age where it does not affect it's selection, since it's past the reproductive age. This could certainly be true for greying of hair.

If you want to understand from the point of view of an evolutionary theory, there are at least two possible explanations. One is the Mutation Accumulation (MA) theory. It says that mutations causing late life deleterious effects can build up in the genome more than diseases that cause early life deleterious effects. This is for the simple reason that cases of the latter would be eliminated as they will usually affect in the reproductive period, but chances of a 60 year old grey-haired man to have offsprings is low. In essence, if a trait reduces survival in the post-reproduction period (which is the case here), then the effect of selection is weak for it. So, since grey hair arrive so late, they might not really be selected out.

Another is the Antagonistic Pleiotropy theory. Pleiotropy means a single gene having more than effect. So it says that if a gene improves fitness early on, but causes an undesired effect later in life, it will be selected for in the population. This is simply because the later deleterious effect does not affect the advantage the gene provides at the stage were reproduction happens. So, it is possible that the gene responsible for grey hair may also be making you more fit.

So, in summary, there seems to be no direct advantage of having grey hair. It could be the result of Mutation Accumulation, or the antagonistic pleitropy effects of the responsible gene.

You can read more about it in this and this answer.


Books about famous experiments in biology - 'methods of investigation'

Although it's not stricly about biology, A short history of nearly everything by Bill Bryson, especially chapter 5, is a good start to look for historical experiments.


Do nematodes have organ-level organisation?

In Fig.1 is shown the body plan of a round worm:

Fig. 1. Nematode. source: University of Illinois

You ask whether there is an organization in terms of organs; an organ is:

  A group of tissues that perform a specific function or group of functions;

A tissue is:

  An aggregate of cells in an organism that have similar structure and function;

As you can see in Fig. 1, there are clearly organs present, including a mouth, pharynx, reproductive organs, among others. They fulfill different tasks and contain various tissues, each dedicated to specific functions. Hence, they fulfill the definitional requirement of being organs.


In my opinion they should mean the template strand, and they probably do. Perhaps if we had a link to the paper we could have examined the language more closely.

Here is a paper which uses the term in that sense:

  Mugal, CF et al. (2008) Transcription-Induced Mutational Strand Bias and Its Effect on Substitution Rates in Human Genes. Molecular Biology and Evolution 26,131-142

In the abstract (which I have linked to) the authors make a clear reference to the transcribed strand in contrast to the coding strand (i.e. the strand of DNA with the same sequence as the RNA transcript):

  All three [mutational rates] considered are found to be on average higher on the coding strand and lower on the transcribed strand...

There are also definitions confirming this at this Wikipedia page.


The meaning of the "Score" in ScanProsite

The score provides an indication of well a specific profile (which is a weight matrix) matches the profile for the domain. Section II.B. Profiles development explains this in further detail.

A paper that outlines the development of PROSITE notes that they primarily use a cut-off of 8.5 and explains the score thus;

  the raw scores in PROSITE profiles are converted into so-called ‘log10
  per residue E-values’, allowing the computation of the number of
  expected matches with equal or higher score in a database of a given
  size. For instance a match with a normalised score of 9.0 or higher is
  expected to occur about once in a database of one billion residues.


Is there a molecular basis to intelligence?

As a Drosophila biologist, I will attempt to address the above question by giving an examples from the Drosophila field. When this paper (http://www.ncbi.nlm.nih.gov/pubmed/7720066) in Cell came out, it sent shockwaves around the world since it showed a molecular mechanism by which production of cAMP and activation PKA, effects CREB transcriptional activation and in turn formation of the long-term memory (LTM) in flies. Some of these CREB over expressing flies could learn a task after simply one try whereas wild-types had to do it several times! This work was later followed by mouse studies (http://www.pnas.org/content/100/18/10518.full.pdf) and comparisons to RTS patients were made. At that time there were discussions of CREB being responsible for intelligence however now there is nice nature review/meta-analysis paper (http://www.nature.com/srep/2014/140225/srep04176/pdf/srep04176.pdf), which says there are no evidence connecting CREB and IQ. This paper performs a literature based investigation and identifies several candidates that are testable and can act as biomarkers for intelligence related therapeutic approach to mental retardation. According to their screen dopamine and norepinephrine pathways seems to be important in IQ-related biological processes.

Hope this helps!


What attracts cells to: pathogens, professional antigen-presenting cells, and cells with an antigen on its MHC-1 protein?

What attracts leukocytes and antibodies to pathogens in the first
  place?

They just bump into them. If secreted antibody is already present in the blood then complement system can be activated.

  What attracts CD4+ cells to professional antigen-presenting cells
  (APC)?

APC release chemokines. All that is known is that this is a CC-type chemokine and signals via CCR4/CCR8 receptors. See this list of articles (from Google Scholar). This study reports a peptide called Chemrin that promotes chemotaxis via ChemR23 receptor.

  What attracts CD8+ cells to cells with an antigen on a MHC-1 protein?

CD8+/NK cells are activated by CD4+ cells before they kill their target. The MHC-1+antigenic peptide is just a mark for the cells that are to be attacked, as far as I understand.

  What attracts macrophages to pathogens that have been tagged with
  antibodies?

Complement factors.

NOTE: Many of these concepts are old but still relevant. You should check out recent articles in this area for novel/atypical mechanisms.


Growing Mouth Bacteria in a bowl of sugar water

I like the concept of this demonstration for teaching science!
As rotaredom's comment pointed out, bacteria does not grow in plain water with sugar. Bacteria require a nitrogen source, trace minerals and vitamins to grow in significant numbers.
I have a few recommendations that you can try, but I attached an extensive guide to kitchen microbiology below.

Growing the microbes in diluted milk (~ 1:10 dilution) + salt (a pinch for half glass) with and without added sugar (1 teaspoon for half a glass) might be a good starting point. Add yeast extract if you have some (not bakers yeast, but this is the killed version of that).

Make sure to boil and cool the milk, the container and other ingredients to keep conditions sterile.

Avoid a cotton swab if you can (as the cotton might not be sterile), I would take some milk solution, swirl it in my mouth and spit it back into the same container.

Also have a sterile culture in the experiment, without the oral microbes for comparison and a great teaching point.

Grow the microbes for 2-4 days with an air permeable cap (the air allows faster growing aerobic organisms, the cap ensures dust does not fall in)
Extensive source: Microbiology at Home: A short non-laboratory manual for enthusiasts and bioartists
PS: I'm studying PhD to be a microbiologist


Why do I see so many handicapped dorbeetles?

I do not know for certain but one possibility is an internal parasite.

A number of parasites have been documented to alter the behavior of the hosts to suit the life cycle needs of the parasite.  For example, Toxoplasma is a parasite use rats and cats as hosts. Toxoplasma alters the behavior of the rats so that they no longer respond to the smell of a cat. That makes the rats much more likely to be captured by the cats, which transfers the parasite to the cat from the rat (Berdoy et al. 2000).

This YouTube video shows how a fungal parasite of ants alters the ant behavior to help the fungus reproduce.

My favorite example, which I use in my introductory biology course, is Euhaplorchis californiensis, a parasitic fluke. The parasite lives in marshy habitats, such as Carpinteria Marsh in California, USA. This parasite uses wading birds (herons and egrets), a snail and a fish as it's host.  The adult lives in the gut of the wading birds. Eggs from the adults pass out with the bird feces. Horn snails consume the fecal material and the eggs.  The eggs hatch inside the snail. The larvae actually castrate the snails so that the snails cannot reproduce. Instead, the snails only feed, which provides nutrients for the parasite larvae. The larvae then leave the snail and swim into the marsh, where they are consumed by the California killifish (Fundulus parvipinnis). The parasite works its way from the gut of the fish to the brain, where it releases chemicals that alter the behavior of the killifish. Normally, if a killifish sees a wading bird, it would dive deep. Instead, the parasitized fishes no longer dive. They remain near the surface and swim eratically. This behavior makes it much easier for the wading bird to see and catch the killifish. The parasite is transfered back to the wading bird, and its life cycle begins again. Details of this fascinating life cycle can be found in (Shaw et al. 2010).

Therefore, it is possible that the behavior of the dorbeetles is being influenced by an internal parasite. These dung beetles may consume a parasite when they ingest dung from a certain species. The parasite could alter the behavior of the beetle making them more vulnerable to a particular predator, thereby continuing the next step of the parasite's life cycle.

Your description of the beetle behavior would fit this hypothesis but I stress that I do not know this. I raise the idea as one possibility among many.

A good not technical book on parasites is Parasite Rex by Carl Zimmer. It covers the biology of parasites, the many ways that parasites can affect their hosts, and the creative scientific minds that uncover the complex life histories of many parasites. (I have no connection to the author or the book.)  The book covers the above examples and more in some detail.


Who created the codon wheel chart (not as a table)

It is very difficult to answer this one for certain but I think the codon wheel representation is sometimes attributed to Rosemarie Swanson who represented the amino acid code using Gray code (or reflected binary code).

Swanson's work actually went quite a bit deeper than the simplified codon wheels you find in ordinary textbooks (ordering by size of the amino acid and position within the chain as well). You can have a look for yourself here in her 1984 article A unifying concept for the amino acid code in Bulletin of Mathematical Biology.

DISCLAIMER: I do not claim that I know the answer to this question for certain nor can I. However, I cannot find official publications earlier than Swanson's 1984 paper showing a circular representation of the amino acid code.


What type of flask should I use to culture NTERA2 embryonic cancer stem cells?

I found a protocol by ATCC for NTERM2 cells, and it didn't mention any specific flask, so any cell culture flask would do. Since ATCC is basically a cell culture bank I trust that their protocol is valid.


Check for:

https://www.youtube.com/watch?v=6uKDpHM-OsI
https://www.youtube.com/watch?v=3jPtZByr740
https://www.youtube.com/watch?v=Kh1HnMFolgw
https://www.youtube.com/watch?v=M5dduAX8iuI

The third one was filmed by BBC. The fourth one is a closer look of the nest complemented with a fairly good analysis.
The first two are reasonably good, but the third one is just awesome for your purpose!


What is this? In Florida. Found in plant bed under rosemary tree that gecko' enjoy hiding aloe plants also growing.

I only know this because I have seen them before in the tropics, but this is probably Clathrus ruber (Wikipedia).  So interesting!

EDIT: Also mentioned in these questions 1 and 2 so perhaps this will get marked as a duplicate.


Why does human facial and head hair continue to grow?

How humans evolved to have head / beard hair that continues to grow longer than other animals is a topic that many anthropologists & biologists are still not sure about & there is no general consensus as to "why" yet.

The three main views that I am aware of however are :

1) Evolution of the "Aquatic Ape." (Ingram, 2000: Morgan 1997; 1982)

Infants, in order to hold onto their mothers in the water, would latch onto her hair. Limiting separation from the mother & increasing chances of survivability
Longer hair meant that infants / small children would need to swim less in order to get to their mother
Believed to be supported even further when you consider that aquatic mammals are almost always hairless, indicating that at one point, humans were highly "aquatic" mammals.

2) No real benefit, but used as a tool for "mate selection." (Darwin, 1871; Cooper 1971)

The view held by many of the Darwin school of thought (I do not mean that as a derogatory), is that at first, "hairiness" was sexually attractive, but eventually "hairlessness" became more sexually attractive in most places (i.e. the face to see facial expressions & socialize better; Wong & Simmons 2001)
A sign of "virility" & "health" as can be seen in the mate-selection behavior of lions. Which is true even today as human diagnostic material for health (Klevay, 1972).

3) Practical evolutionary benefits for the human species specifically

A lot of body heat escapes from the head, probably the most important part of your body. Hair is a good insulator that can keep in heat. This increases survivability in colder climates. (Wong & Simmons 2001; Bubenick 2003). (A disputed but considered credible reason, especially when you compare hair length and types across different regions throughout history)
Protection against damaging UV rays (while still permitting adequate Vit.D3 to come through) & some protection from free-radicals or other harmful particles. Because we became bi-pedal, the head was the main area exposed to the sun (as well as some of our back). Extending hair's usefulness to even hot environments, while other body hair became less important with the development of sweat glands (Wheeler 1985).
Heightened "Situational Awareness" through "Touch sense." A concept that may seem silly at first but has some evidence to support the theory. Though the hair is not "alive," it is connected to the follicles & your nerves. In a nutshell, it may help to increase "sensory awareness" & "data gathering" of your environment, which would favor longer hair. This would be an asset in survivability (Kardong 2002; keratin.com 2010; Sabah 1974; washington.edu)
Though not a collegiate Journal article, if reasonably credible, this small article is an interesting case for supporting hair & "Touch sense" in "recent history" & in combat-survival : http://www.sott.net/article/234783-The-Truth-About-Hair-and-Why-Indians-Would-Keep-Their-Hair-Long.

I personally lean 90% "Evolutionary benefits" & 10% "Mate selection" as to reasons why humans' hair continues to grow longer than other animals. Beard & head.

Hope this info was a little helpful.
There are copious amounts of other respectable articles on each point, but I only referenced a few.


How non-invasive blood glucose concentration measurement work?

This is not a new thing, by checking the articles about non-invasive glucose level measurement, it started in the early 90's.

  Near-infrared (NIR) spectra of the human inner lip were obtained by
  using a special optimized accessory for diffuse reflectance
  measurements. The partial-least squares (PLS) multivariate calibration
  algorithm was applied for linear regression of the spectral data
  between 9000 and 5500 cm−1 (λ = 1.1-1.8 μm) against blood glucose
  concentrations determined by a standard clinical enzymatic method.
  Calibration experiments with a single person were carried out under
  varying conditions, as well as with a population of 133 different
  patients, with capillary and venous blood glucose concentration values
  provided. A genuine correlation between the blood glucose
  concentrations and the NIR-spectra can be proven. A time lag of about
  10 min for the glucose concentration in the spectroscopically probed
  tissue volume vs. the capillary concentration can be estimated.
  Mean-square prediction errors obtained by cross-validation were in the
  range of 45 to 55 mg/dL. An analysis of different variance factors
  showed that the major contribution to the average prediction
  uncertainty was due to the reduced measurement reproducibility, i.e.,
  variations in lip position and contact pressure. The results
  demonstrate the feasibility of using diffuse reflectance
  NIR-spectroscopy for the noninvasive measurement of blood glucose.

1993 - Noninvasive Blood Glucose Assay by Near-Infrared Diffuse Reflectance Spectroscopy of the Human Inner Lip

There are multiple approaches, mostly spectroscopy, but dielectric properties (e.g. conductivity) can depend on glucose levels too. Saliva can be used to measure glucose levels as well.

2014 - Non-invasive glucose monitoring using impedance spectroscopy
2014 - Broadband Tissue Mimicking Phantoms and a Patch Resonator for Evaluating Noninvasive Monitoring of Blood Glucose Levels
2014 - A paper strip based non-invasive glucose biosensor for salivary analysis

The details of each technology you can find of wikipedia.


Why does a high osmotic pressure pull water in, yet a high hydrostatic pressure pushes water out?

Great question, the answer has to do with the definition of osmotic pressure and the difference between this pressure and "hydrostatic pressure" which is the water pressure you are thinking of.

Here is the definition of "osmotic pressure" given by Google:

  the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis, often used to express the concentration of the solution.

Osmotic pressure in this definition is best illustrated by the commonly used tool to show osmotic pressure, often seen in a textbook as something like this:

In this picture, osmotic pressure is roughly how hard do you have to push down on the water on the right to make the levels the same on the left and right, despite the difference in concentrations. Osmotic pressure is not a pressure of water, as your question seems to imply, it is a pressure of the solutes in the water.

If it helps, I think it would be appropriate to think of this as sort of a "suction" on the water. Net flow of water stops when:

osmotic pressure - hydrostatic pressure = 0

...on the right side of the diagram.


Are there any DNA viruses with junk DNA in them?

Viruses typically don't have junk DNA-so to speak because of their tiny size. When the particles (of virus) are so small, there really isn't any space for "junk" or extra DNA.
That being said, while viral DNA replication, there may be some errors that may make the virus DNA unable to code for proteins or "junk". While this is an interesting proposition, the mutations that occur in almost cases do not make non functional proteins but mutated proteins which make the viruses more virulent (more true in case of RNA viruses...which mutate a lot faster).
Regarding virus infecting virus, putting its own code it "kind of happens" but not as you would expect. I am listing 2 such examples here-

There are some viruses called satellite viruses and viroids which depend on "donor" larger viruses for some of the proteins they need for replication. This means a satellite virus can survive in a host only if the donor virus is present.

In animals like pigs, when different strains of Influenza virus infect together, while virus assembly genetic material (RNA) of one strain can enter into the other....creating completely novel strain.

Hope that answers your question. Please feel free to ask for clarification. Thank you and have a nice day.


Understanding Membrane / Resting Potential from the perspective of ions?

Ah, what a classic biophysics problem.

One first needs to understand how a membrane gets a potential. The lipid bilayer is a large sea of hydrophobic interactions that essentially prevents any ion from crossing. As a result, Na+ and K+ concentrations remain constant and different on the cytoplasmic side and the extracellular side. However, ions can pass through ion channels like the K+ channel. It is important to understand that in K+ channels, only K+ can pass and these channels are actually selective against Na+ (answer to question 1).

There are two potentials at work here. First is a chemical potential created by the flux of K+ from high K+ to low K+. The second is a counteracting membrane potential created by a charge imbalance. Note, that the swapping of a few ions will a) result in a negligible change in the concentration ie. the chemical potential, b) result in a large change in the membrane potential. At some point, the flux out due to the chemical potential and the flux in due to the membrane potential will be equilvant and the cell will reach a resting potential otherwise known at the Nernst potential or equilibrium potential (technically a steady state).

When a cell depolarizes by closing these channels, the local charge will quickly go back to an equilibrium or a non-charged state.

So why K+ rather than Na+? For typical cells, the extracellular concentration of Na+ is 145 mM and cytoplasmic is 12 mM. For K+, it is 4 mM and 155 mM respectively. Doing the appropriate calculations of the Nerst potential, for Na+ it is +67 mV and for K+ it is -98 mV. Qualitatively we can see that this would result in vastly different things.

Most of this information can be found from Pollard and Earnshaw's Cell Biology


Differentiating Taenia solium and Taenia saginata Infections

Taenia solium is more dangerous:

  T. saginata is relatively innocuous, since only the intestinal tapeworm phase occurs in man, whereas infection with T. solium has major health effects due to extraintestinal infection by the larval or cyst phase in the CNS [1].

The most feared complication of Taenia solium is cysticercosis. Taenia saginata can lead in extreme cases to intestinal obstruction.

Preventive measures:

improved hygiene
adequate thermal processing of meat [2]
preventing contamination of animals (pigs and cattle) [3]

Differential diagnosis:

PCR [1, 4]
Hematoxylin-Eosin Staining [1]

References:

Mayta H, Talley A, Gilman RH, Jimenez J, Verastegui M, Ruiz M, Garcia HH, Gonzalez AE. Differentiating Taenia solium and Taenia saginata infections by simple hematoxylin-eosin staining and PCR-restriction enzyme analysis. J. Clin. Microbiol. 2000 Jan;38(1):133-7. PubMed PMID: 10618076. Cited text is from full text article available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC86038/
Wikipedia contributors, "Taenia saginata," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_saginata&oldid=618599196 (accessed July 28, 2014).
Wikipedia contributors, "Taenia solium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Taenia_solium&oldid=618599210 (accessed July 28, 2014).
Luis Miguel González, Estrella Montero, Leslie J. S. Harrison, R. Michael E. Parkhouse, and Teresa Garate. Differential Diagnosis of Taenia saginata and Taenia solium Infection by PCR. J. Clin. Microbiol. February 2000 vol. 38 no. 2 737-744


If mantis shrimp have 16 photoreceptors then how many other colors on the spectrum are there?

The first source you posted pretty much answers your question. Here are some others, probably referring to the same study but talking about it differently:
The Mantis Shrimp Sees Like A Satellite (National Geographic; this article is referred to in your first source)
Study Offers Insights into Unique Color Vision of Mantis Shrimp
Mantis shrimp's super colour vision debunked (Nature)
Here is the paper that those three articles are based on:
A Different Form of Color Vision in Mantis Shrimp
And what seems to be the author's (slightly more recent) thesis on the subject:
Colour vision in mantis shrimps: understanding one of the most complex visual systems in the world
The big thing to understand is that there is no such thing as "the color spectrum". There is the electromagnetic spectrum, which is one-dimensional: you can describe an electromagnetic wave's position on the spectrum with one number, its wavelength. But if you look at a picture of the electromagnetic spectrum with the colors associated you can notice something immediately:

You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other.
That's because the point of color vision isn't to detect variations along the electromagnetic spectrum per se; the aim is to allow our brains to get more information about the world around, based on the fact that light comes in many different wavelengths. Different objects will reflect different combinations of those wavelengths, meaning being able to tell some of those wavelengths apart improves our ability to tell objects apart based on those differences.
The key here is that there isn't a perfect way of doing this; nobody has a system where you detect the exact wavelength of each photon and tell exactly how many of each wavelength you receive. What human eyes do is have some specific receptors be more receptive to some wavelengths than others, and then the brain compares how excited each receptor is and puts all that information together to generate a sense of "color", which is basically a way of telling some things apart when they reflect certain different wavelengths. It's related to wavelength, but isn't the same thing; for example our brains recognize wavelengths that excite the red and green receptors equally as "yellow". This includes wavelengths that fall between the red and green wavelengths, but also combinations of red and green wavelengths. That's how you get the color wheel, the ability to make some colors out of others, and the fact you can generate all colors that we see from three primary colors. An organism with an extra receptor between the red and green would be able to tell those different combinations of wavelengths apart so that "yellow" to us would look like several different possible colors to them. Conversely, trichromatic humans are able to tell colors apart, like red and green, that are one single color to dichromatic mammals.
So the answer to "how many colors on the spectrum are there" is "there is no universal color spectrum". Every organism with its own system of light receptors can theoretically have its own color spectrum; how many colors they see is a question of how many different combinations of wavelengths they can tell apart, and that's a function of how many receptors they have but there can also be other factors (like the sensitivity of given receptors, how much processing power they're dedicating to color vision, exploiting different aspects of physics that affect wavelength... In humans even language and culture can influence color discrimination to some extent).
And where does the mantis shrimp come in? Well this is interesting, because it's been generally thought as you put it that the mantis shrimp would be able to see many more colors than we do, due to its much more numerous receptors, but the recent studies mentioned in the first source you linked to suggest that the mantis shrimp is worse at discriminating colors than we are, i.e. it sees fewer colors. However it appears its color vision functions very differently, and that's where the 16 different receptors come in. It's possible that the different receptors allow the mantis shrimp not to detect more colors, but to process the colors it does detect much faster. To quote the Nature article:

If the shrimp eye compared adjacent spectra, like the human eye does, it would have allowed the animals to discriminate between wavelengths as close as 1–5 nanometres, the authors say. Instead, each type of photoreceptor seems to pick up a specific colour, identifying it in a way that is less sensitive than the human eye but does not require brain-power-heavy comparisons. That probably gives the predatory shrimp a speed advantage in distinguishing between different-coloured prey, says Roy Caldwell, a behavioural ecologist at the University of California, Berkeley.

And the National Geographic one:

Their working hypothesis is that the mantis shrimps analyse the outputs from all of their 12 receptors at once. Rather than making comparisons between those receptors, they pass the entire pattern of outputs onto the brain, without any processing. “One could imagine that they have a look-up table in their brain,” says Marshall. So rather than discriminating between colours like we do, their eyes are adapted for recognising colours.
“Oddly enough, the closest device to stomatopods would be a satellite,” says Marshall. “Remote sensing algorithms have look-up tables of colour to fill in the image that the satellite forms.”

For your other questions:

How many photoreceptors is possible?

Theoretically the limit would only be how many you can pack in an eye and how many chemical pigments exist, but in practice there is a trade-off between color and spatial discrimination (after all any color receptor is a light receptor that's limiting itself to certain wavelengths only, so you lose in overall light perception). Another article in the Science journal the article on Mantis shrimp color vision appeared in suggests the optimal number is isn't over 4 (in organisms that use our system of color vision of course, not the mantis shrimp's):

In fact, theory predicts that two to four receptor types are optimal for discriminating the spectra of natural materials and maximizing the number of objects that could be distinguished by color.

And:

How much of the spectrum is not ever going to be seen by any creature ever?

Again, considering every set of photoreceptors leads to its own color spectrum (and every brain probably cooks it to its own sauce beyond that), that question applied to the set of all colors isn't really meaningful. The answer would probably be along the lines of "almost all of it" because the set of actual color vision systems in the natural world is an infinitesimal percentage of the set of theoretically possible color vision systems... but it's not like those colors are "out there to be seen" in anything but the most abstract sense; they exist in the same sense that a child that's the combination of a sperm and egg that haven't met exists.
If by "spectrum" we mean "electromagnetic spectrum", then there is likely an upper and lower bound to the wavelengths that can be detected, where wavelengths on the upper bound are too deadly for a cell to survive let alone detect (though bodies can and do sacrifice cells to exploit inhospitable environments, see the cells lining our stomachs, so even that might not be an absolute obstacle), and on the lower bound aren't energetic enough to cause pigment molecules to react to them. I don't know what those bounds are though; it's likely that more important constraints are how useful it is to detect those higher and lower wavelengths, that any organism would bother evolving the ability. (also, for the lower wavelengths, whether their detection is associated with forming an image. For example we can detect infrared radiation as heat but we don't think of that as "seeing". On the other hand "eyespots" that detect visible light without forming an image are often thought of as a primitive form of sight; there is a level of arbitrariness there but it's also true that lower wavelengths have different optical properties).


Transfer of antibodies from mother to fetus

Both are technically correct.  Here's a review that goes into some detail about the process: IgG Placental Transfer in Healthy and Pathological Pregnancies.  It's worth a read if you're interested in the subject.  In particular, it cites a study of immunoglobulin transport which:

  demonstrated a continuous rise in IgG levels in the fetal circulation between 17 and 41 weeks of gestation. Fetal IgG concentrations were only 5%–10% of the maternal levels at weeks 17–22 but reached 50% of the maternal concentrations at weeks 28–32. The majority of IgG is acquired by the fetus during the last 4 weeks of pregnancy, and fetal IgG concentrations usually exceed maternal ones by 20%–30% at full term.

So it begins a wee bit before week 17, so definitely within the second trimester, but it is only by the third that concentrations begin to be truly meaningful.  However, most of the antibody acquired, going above the maternal level, is done in the last month.


What could an increase in systolic blood pressure and decrease in diastolic mean?

First, a couple of considerations

Heart rate (HR) is lower when seating, and even lower when lying. I assume that participants were seated when the first measure was taken.
Cardiac output is not constant during the day. Depending on the moment, some factors such as digestion have an impact in Cardiac output, so take that into account when carrying out the experiments.

Normal walking may cause that blood pressure pattern. I think that you should not consider the increase in systolic pressure if it is not significant, as something as simple as crossing your legs when seated can increase your systolic pressure and normally diastolic pressure provides more information for physicians. Relaxation techniques usually decrease heart rate, which can affect the blood pressure. However, the point in this case seems to be that HR remains constant. I suppose that Mean Arterial Pressure $(MAP)$ has decreased.

If we part from:

$\textit{MAP} = (CO \cdot SVR) + CVP$
where $CO$ is cardiac output, $SVR$  is systemic vascular resistance and $CVP$ central venous pressure.

$CVP$ is usually depreciable. $CO$ is defined by $SV \cdot HR$, where $SV$ is the stroke volume. Then, if the HR is constant, only $SV$ or $SVR$ could have changed. Maybe the heart is pulsating more vigorously, or a vasodilation is decreasing $SVR$. I find the latter more likely. However, I don´t know why the smooth muscle could be relaxing. Make sure that heart rate is not changing and consider your sample size.
I hope it helps, at least to focus you search on cardiac regulation. It is difficult to conclude anything without seeing the data but I tried to answer from my limited knowledge since I am not specialized in cardiac physiology.


How to determine if a plant is autotrophic or heterotrophic?

This in part depends on how you define heterotrophic. The most common definition is the inability to synthesise energy-containing molecules, most commonly by fixing carbon through photosynthesis (but dont forget chemotrophs). However, I've sometimes seen definitions that also include dependency on external sources for nutrition (e.g. nitrogen) but also to supplement carbon sources.

Using the first, main definition a lack of chlorophyll is a sufficient trait to define heterotrophic plants, which clearly places Orobanche (lacks chlorophyll) in the heterotroph category. If you use the second definition you will include more species, but it also becomes much more tricky to draw the line between autotrophs and heterotrophs. I know that Melampyrum pratense is a hemiparasite, but don't know exactly to what extent, and therefore cannot say if it is accurate to label it as heterotrophic (using the second looser definition - it has fully functional photosynthesis). Checking whether a hemiparasitic plant can establish, survive and reproduce without its host should be a useful way to establish if it is a obligate or facultative hemiparasite (I suspect that Melampyrum pratense will be found in the latter category). Myco-heterotrophy can also be obligate and facultative, and can involve transfer of both carbon sources and nutrients, see Merckx et al (2009) for a review. Insect-eating plants such as the Venus flytrap are however sometimes called partial heterotrophs, based on the fact that they get part/most of their nitrogen from insect trapping, while still obtaining their energy from photosynthesis.


Short answer
Noise-induced hearing loss affects primarily the mid-frequencies, because the inner ear is most sensitive to these frequencies.
Background
Noise-induced hearing loss occurs typically in the mid-frequencies (Rabinowitz, 2000), typically around 4 kHz (3 - 6 kHz), see Fig. 1. This can be explained by the fact that the human ear is most sensitive in this frequency range (Fig. 2). In turn this relates with the frequency range where speech understanding is most important, namely between roughly 2 and 6 kHz (Killion & Mueller, 2000). Hence, noise exposure neither targets the base, nor the apical parts of the cochlea, as claimed by asker and answerer, respectively. High-frequency hair cells in the rat cochlea have been shown to be very susceptible to damaging noise, but the low-frequency hair cells may go unscathed (source: eMedicine).
The other answerer claims that

parts of our hearing apparatus responsible for perceiving these
[low-frequency] sounds are more fragile...

Hence, the claim that low-frequency regions in the cochlea are more sensitive than the more basal parts is not a claim supported by the bulk of the literature. In fact, as a rule of thumb, cochlear damage (inner ear damage) occurs most frequently first in the base, where the high frequencies are resolved. This holds for age-induced HL where high frequencies are lost first (Ciorba et al., 2011), as well as chemically-induced HL (Campo et al, 2013, barred some specific organic solvents that apparently do not follow this rule (Cappaert et al., 2002.

Fig. 1. Typical audiogram of noise-induced hearing loss showing loss of functional hearing at the mid-frequencies (Rabinowitz, 2000)

Fig. 2. Relation between perceived loudness and intensity (equal-loudness curves) for a normal-hearing person. source: Lumen Phsyics
References
- Campo et al., Dis Mon (2013); 59(4): 119–38
- Cappaert et al., Neurotoxicol Teratol (2002); 24: 503–10
- Ciorba et al., J Laryngol Otol (2011); 125(8):776-80
- Killion & Mueller, The Hearing Journal (2010); 63(1): 10-7
- Rabinowitz, Am Fam Physician (2000); 61*(9):2749-56


What is the location of the Hypoglossal nerve?

The following image of a cadaver shows the hypoglossal highlighted:

 Source: StudyBlue

You can see the flap of skin/muscle that has been removed to get an understanding of the thickness of tissues separating the nerve from outside the body.

Additionally, here is an image showing a person receiving an operation. You can see the relative depth of the nerve fairly well:

 Source: Cambridge University Press


Does anyone know what kind of caterpillar this is?

Looks similar to a Rusty Tussock Moth (Orgyia antiqua) caterpillar, but you might want to check the bugguide page for the species, or submit your photo there for a second opinion.


What are some potential consequences for attempting to cure Type one Diabetes?

High school biology apparently failed to teach you that many conditions, like type I diabetes are not classically Mendelian. The term "carrier" does not apply to you...you are just someone with a predilection who hasn't developed the condition (but who might...I have heard of someone developing type I diabetes in college)

  Scientists develop a modified virus that contains a normal person's
  beta cell genetic makeup,

How much DNA do you think you can cram into a virus?  Not having the right beta cell DNA is almost certainly not the cause of type I diabetes, anyway.

  The virus and beta cells reproduce, and the body detects the virus,
  but not the beta cells.

How do you think the immune system responds when it detects a virus?  Hint, it kills the hosting cell.

A virus that induced a small percentage of pancreatic alpha cells to undifferentiate and redifferentiate beta cells might work...but you would still have the same immune system that went agro on your beta cells the first time.  They might do the same when exposed to new beta cells.  And there is a fine line between undiffernetiated cells and cancerous cells.


A good question (if a little mixed up on transcription vs. translation!)

AUG is not always the start codon, but whatever the codon is it will always code for Methionine (or fMet, but still a variation on Met), even if the codon codes for a different amino acid otherwise. A  separate transfer RNA (tRNAi, the initiator tRNA) is used for the arrangement of this first step, guided by eIF2 [in eukarya].

In this respect it's less a question of "why AUG" than "why this specific initiator tRNA", the answer being that it's got certain sequence elements and modifications that distinguish it from the elongating tRNAs which bind elongation factors and hence are targeted to the ribosomal A and B sites instead of the ribosomal P site (with function being dependent on form, basically it's shaped to set up transcription rather than to elongate an existing nascent chain polypeptide).

  "Identity elements appear to finely tune the structure of the initiator tRNA, and growing evidence suggests that the body of the tRNA is involved in transmitting the signal that the start codon has been found to the rest of the pre-initiation complex." — Kolitz and Lorsch, 2010

The other start codons are just from natural chemical variation (or evolution, whichever way you want to look at it) giving rise to different codon-recognising protein shapes.

The machinery for starting translation works, and as such is "conserved" - evolution has kept it, and that's why it is always the same codon (more or less). Archaea have a very similar shaped tRNAi acceptor stem, and is an equally good ligand, which shows how ancient the system is and gives an idea of how fundamentally difficult it must be for an organism to change a system like this through mutation (3.5 billion years of evolution can't be wrong! etc. haha).

Not to just gloss over the part where I said that non-AUG codons get used too (in yeast and mammalian cells), the following is from a study in which it was found changing 1 (and only 1) of the AUG bases still permitted translation initiation:

  "Naturally occurring misrecognition indicates that discriminating two base-paired near-cognate codons from the perfect three-base-paired AUG
  codon is subject to mistakes. Mutations in translation
  initiation factors, such as eIF1 and eIF2b, further increase the levels of these mistakes.

  Two base-pairing interactions between non-AUG codons and the anticodon of
  the Met-tRNAi are sufﬁcient to trigger translation initiation, suggesting that wild-type eIF1 plays a role in
  monitoring proper base-pairing interactions when scanning for the AUG start site. It would be predicted that
  the Met-tRNAi, not a cognate tRNA matching an individual non-AUG codon, is used in translation initiation at these non-AUG start codons.

  The translation initiation complex will bind only the Met-tRNAi as
  opposed to other tRNAs because Met-tRNAi has unique
  sequence and structural features that allow it to be
  loaded onto eIF2 of the ternary complex and enable it
  to ﬁt into the P site of the ribosome" — Maduzia et al, 2010

Basically the consensus is that it's not really possible to say why the methionine codon, "it's just a structural thing", which is a bit of a circular argument really.


Polyploidy, or why plants of different species can produce fertile offspring hybrids more frequently than animals?

While I do not know if there is a definitive answer to this question, I suspect that at least part of the answer can be found in the fact that animals typically have much more complex and delicate mechanical interactions in their bodies than plants.

From a mechanical perspective, plants are pretty simple. They move, but generally quite slowly and via very simple mechanical principles, and the interconnection between different tissues and organs is mostly via chemical and fluid flow.  Many plants are also highly flexible in their size and also change their size by orders of magnitude even after sexually mature.

Animals, by contrast, are often ferociously complex and intricate systems of joints and complex and highly differentiated organs. They also tend to have a well-defined typical size of mature individuals, which doesn't vary all that much compared to plants.

When you have a change in ploidy, a major effect is to multiply or divid the levels of gene expression, based on the change in number of copies.  Where that interacts with the processes of morphogenesis, it will thus often have radical effects on the size or growth patterns of the effected tissues or organs.

With a more intricately connected and scale-sensitive system like an animal, it seems then unsurprising that such changes might be much more difficult to survive.


Key points of Wagner's theory of innovation

Wagner does not propose any new theory. He uses the word innovation to mean evolutionary adaptations that manifest qualitatively different traits. In fact, he has himself not defined it properly in the mentioned book. This is what he has written about the term innovation:

  It may be difficult to define rigorously what an evolutionary
  innovation is [538,616]. However, these and countless other examples
  show that it is usually easy to recognize: a new feature that endows
  its bearer with qualitatively new, often game changing abilities.
  These may not only mean the difference between life and death in a
  given environment (just think of biosynthetic abilities), they may
  also create broad platforms for future innovations, as did innovations
  of photosynthesis and of complex nervous systems.

However the examples he cites in the introduction are not as obvious as he says. Lets say the evolution of nervous system. The innovation that would have led to evolution of nervous system could have been the evolution of electrically excitable cells.

Actually, throughout the introduction he does not actually clarify the meaning of innovation. In page-3 he does list some features of innovation but it is all still vague. Without a rigorous definition nothing is easy to recognize and classify (especially in theoretical terms).

I do not have the book and cannot look through the entirety of it. However, based on what I have read in some of his papers I can comment something about what he possibly means by innovation.

In certain dynamical systems, some parameter changes can lead to qualitative differences in the output (bifurcations). Steven Strogatz's book on Non-linear Dynamics and Chaos is a nice and easy read on this topic.

If you look at some of Wagner's research papers, you would understand this idea better. Some of these papers are about how some parameter changes can affect the overall outcome (which may be drastic). For example, in this paper the authors talk about how differences in cell division rates can affect the outcome of a cell differentiation event.

He also talks about metabolic innovations which refer to changes in metabolic reactions and network leading to new products/optimized growth etc. Details of this can be found in his lab's papers on Metabolic Flux Balance Analysis.

There is nothing new or drastically different about all of this. This is just an addition that was unknown during Darwin's time. All that he says is still quite in agreement with the current evolutionary theory. (But personally, I find the opening of the book too vague).

As far as empirical corroboration is concerned, you may have a look at his lab's research papers.


If one endures the same form pain over a long period of time, would the pain begin to lose intensity?

Under the assumption that the temperature experienced is not high enough to simply burn the nerves responsible for the pain (which would lead to insensible regions), yes and it would due to what is called receptor desensitization. In the case of burning pain the receptor involved is called the transient-receptor potential channel V1 (TRPV1). It is the same receptor involve in the oral burning sensation of spiciness.

Now two scenarios are possible given your question, namely a constant stimulus over a long period and "oscillating" stimuli (i.e. a repetition of stimuli followed by non-stimulated periods).

Constant stimulus

I provided a similar answer to this question: What features cause mechano sensory adaptation?. This is the scenario where you keep the painful stimulus constant over a period of time. Here desensitization, i.e. reduction in pain feeling, is due to a direct receptor desensitization. This happens because the receptor is internalized (also called receptor-mediated endocytosis) into the cell after being activated and it takes some times for the receptor to reach the cell membrane again meaning if the stimulus remains constant, pretty much no receptors will be left on the cell membrane.  After decades long term desensitization will occur and is slightly different in it's mechanism compared to standard desensitization as described hereafter.

"Oscillating" stimuli

In the case you are talking about a chronic pain interrupted by periods of non stimulation then long term desensitization will occur. In this scenario, the concentration of receptors will be reduced semi-permanently (i.e. reduced expression of the receptor) in the receptor cells reducing the pain signal. This is what happens with spiciness sensation. People eating regularly very spicy will physiologically be less sensitive to spices as they have less receptors sensing the spices provoking a reduced burning sensation.

Just as a footnote, very long chronic pain will also change the brain wiring of the pain signal but as I don't know enough about neurobiology I will leave that appart.


Why did whales end up larger than most sauropods and what is a whale's limits?

As best we can tell food availability is the relevant limits in whales.  its true that the bigger an animal gets the more energy efficient it is, it needs less food proportionally but still needs more total amounts of food. There is a limit to how much food you can find and eat, especially in the lean parts of the year. This is actually why we see dwarfism on islands lower food availability favors smaller size (less overall food needs). Finding food and even feeding itself takes energy and it reaches a point where the energy you expend is equal to or less than the energy you can extract from your food.
There are other limits like blood pressure, internal surface area, digestion time, heat buildup, but whales have not reached any of these.
https://science.sciencemag.org/content/366/6471/1367


nontechnical understanding of a mammalian expression system

The general principle of the expression system is simple: it is a biological machine that uses cell media as its input (i.e. a broth of simple nutrients, including the protein building blocks) to generate its output, a specific protein of interest, according to its "settings", if you will, which is the DNA plasmid that describe which protein will be made. The cogs of the machine are carefully engineered mammalian cells that both create protein from nutrient, and multiply themselves to increase production capacity.
In a perfect expression system, there would be no need to know the underlying biology of the system: just provide the specified broth with a correctly formatted DNA plasmid, let it simmer for a specified duration at a given temperature, and voila!
The value proposition of a commercial system for its users is being as close as possible to this perfect system, i.e. not having to "roll your own" from first principle (after all, the general processes underlying protein expression are covered in an undergrad biology education) which would entail a great deal of effort and expenses. In some way, this is similar to the business model of cloud providers like AWS: abstract the low-level sysadmin-type stuff to provide a reliable platform for applications.
This is useful in both an R&D context (you can iterate on the protein and specific process steps for your product, not on the expression system) and a production context (you have a reliable expression system, that conform to regulatory requirements, with vendor technical support).
However, even the vendors have not entirely abstracted the biology of protein expression, and the specific working of the system is part of the differentiating features of a specific commercial product versus other products in the same line, and competing solutions from other vendors. You have asked clarification on a few technical terms:

host cell lines: The carefully engineered mammalian cells, which have been tuned to product protein in great quantity, while maintaining quality (e.g. avoiding aggregates) and, typically, specific requirement on post-translational modifications necessary for the application the protein was designed for. It must be easily to culture in large batch. There cells are a blank slate in which the DNA plasmid will be inserted to start useful production. A vendor's expression system will feature a cell line that tries to fulfil these something conflicting requirements.
vectors: How to format the DNA plasmid (= protein recipe) and get it into the host cell line. For mamalian system this will typically be viruses that can infect the host cell line to deliver the plasmid. The reliability and ease of use of the vector system, as well as compliance with regulatory standards in a pharmaceutical environment is also a differencing feature of an expression system.
cell culture media: Specific cell line will have different "nutritional requirement", as such vendors will have specific "recipes" for the nutrient broth in which to grow the cells of the system. This is more or less directly dependant on cell line, so less of a differentiating factor per se.
know-how: Biological processes tend to be messy, so some troubleshooting is expected even in commercial systems. Documentation as well as expert technical support can be an important selling point.

Ultimately you will need to understand to some degree the biology underlying the particular
expression system to be able to compare it horizontally to competing solutions from other vendors,
and vertically to other methods of producing proteins (e.g. prokaryotic expression system, cell-free systems), and, if you are in a customer-facing position, to be able to answer some domain-specific question on the spot. Here is an overview, here is another from a different vendor. I would suggest asking more specific question after perusing these.


Is it mostly true that predators or parasites traverse wider spatial areas than their prey or hosts?

The ability of prey to find refuge in predator-free habitats is a fundamental hypothesis for predator-prey stability. The availablility of predator-free patches allows the prey metapopulation to maintain positive population growth in some patches, despite being decimated by predators in other patches. If the predators are far superior dispersers, they would eat all the prey, possibly driving the prey—and themselves—extinct.

That being said, it's difficult to make generalizations about spatial food webs. In nature, prey, predator, and parasite populations persist due to a multitude of factors, including the spatial configuration of suitable habitats, their dispersal rates, interactions with competitors and mutualists, etc. For example, in a system where carnivores hunt herbivores, sure, the predator may disperse across the landscape, hunting across more than one herbivore metapopulation; in other systems, such as those that may be more spatiotemporally variable (e.g., prone to disturbance and local extinctions), the ability of the prey to disperse faster than the predator could be a crucial aspect of predator-prey stability.

Some theoretical resources include: Comins et al. 1992, Holt 2002,
Amarasekare 2008.

A foundational experiment is that of Huffaker, who dispersed mites on oranges: Huffaker 1958. Also, take a look at work on host-phage interactions: Schrag and Mittler 1996.

For Google Scholar searches, try various combinations of the following words: spatial, host, parasite, predator, prey, stability, coexistence, food web.


Are PVC&PET bacteria found inside homes?

If you read the Wikipedia article carefully, and the recent article in PNAS on improving the enzymes responsible for TET degradation, it is evident that Ideonella sakaiensis is the only example so far known of a bacterium that can use PET as an energy source. As it is a Japanese marine bacterium it will not be found in “domestic spaces”.

The requirement for an aqueous environment is presumably related to the need for the enzymes the bacterium secretes to gain access to the plastic and the products of the digestion to be reabsorbed, and perhaps also for access to essential nitrogen, not present in the plastics. The rarity of bacteria that have evolved this facility presumably relates to the ‘difficulty’ of the chemistry — or its difference from that involved in degrading other carbon sources — although there is some similarity to cutinase, the enzyme in certain fungi that can digest the cuticle of plants.


Does Sympaticus and lymphatic circulation cause feeling of thirsty after short shower?

I think the mechanism is the stimulation of the skin systemically i.e. the most important endocrine organ which we have.
The irritation of skin in the shower is

mechanical turbulent stream of water in acceleration

1) hitting (start) your skin from different directions (many flows) in many different flows
it's you who causes the systemic stimulation effect!
water steam in acceleration all the time; moving its direction; in ellipsoidal tracts
water stream flowing slowly on your skin towards periphery mostly
causing smooth but continuos irritation of your skin

activation of smooth muscles in synchronous order which boost lymphatic circulation

mechanical turbulent stream of air (temperature change of skin)

this one is not in accelerative move, since there is no forces which keep the subsequent air and skin together
very little impact, unless extreme situation (etc in Alaska)

I would think that the increased lymphatic circulation irritates the walls of lymphatic circulation which causes an increase in the need of water there.
So water would diffuse from vascular space inside blood vessels (extravascular space) into the lymphatic system.
The decrease in blood pressure through baroreflexive arch and hypothalamus (some nuclei too) would then be sensed as the feeling of thirsty.

Water in shower on the skin accelerates, since it changes its direction all the time from the beginning of the stream until the end.
I think it is the steady change of irritation's location in ellipsoidal tracts that stimulates hypothalamus.
I think it is not the strength of the stream but the changing direction that is cause of the irritation.
Of course, there is little changes in the strength of the total stream.
I think this is not so significant than the change of the direction of the water flow causing the irritation.

In short, I say that accelerative water streams massage lymphatic system in ellipsoidal tracts.