Your classmate is forgetting that the child will have to inherit one allele (A or a) from each parent. Suppose the dad is affected---so his genotype is Aa. He has a 50% chance of passing the A on to his kid. That means the kid has a 50% chance of being affected.

If your classmate was right, then it would be possible for both the kid's alleles to come from just one parent. You have to pick one allele from each parent.


Dragonish caterpillar from North Vietnam

My comment above is actually likely wrong.

Instead, I think this is possibly the larva of the rose-myrtle lappet moth (Trabala vishnou) in the Lasiocampidae. (It may also be the larva of the closely-related roseapple caterpillar, Trabala pallida -- see here and here).

I don't know this group of moths at all, but a series of failed "Lymantriinae" searches and otherwise successful image searches led me to this genus and these species. Lack of reputable resources available in English online make differentiation between species in this genus very difficult for me. Below are some images of Trabala caterpillars:

 Images Source: Koh Chang Nature

You can see a very smilar image to the ones above on flickr.


You're right that if there was really a complete lack of Trp, then the cell wouldn't be able to make the enzymes. But the cell doesn't have to wait until [Trp] drops all the way to zero -- it can induce expression of the operon when the concentration gets sufficiently low (in practice there's some continous relationship between [Trp] and expression). Note that there's always going to be a little bit of Trp around as there are constantly proteins being degraded (and resynthesized).

But you're on to something -- in fact there is some bias towards lower usage of a particular amino acid in enzymes that are responsible for synthesizing that amino acid. Here's the paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1839009/ although the effect isn't that high for Tryptophan.


Enzyme kinetics: recommended literature to grasp the concepts better

I always used the book "Enzyme Structure and Mechanism" by Alan Fersht. (Structure and Mechanism in Protein Science: A Guide to Enzyme Catalysis and Protein Folding is the latest version, published in 1998.) Both in some courses I did and when working on (complex) enzymatic mechanisms. It's a classic (so a bit old maybe), but it covers all the basics and includes most of the common complex mechanisms like ping-pong. I don't know if it will teach you how to analyze multivariate data, so maybe you need something else for that.


I don't know if lambda for estimating divergence times works in the same way as it does for scaling internal tree nodes, but I'm going to assume it does given the context of your question.

My gut reaction was: of course it must because K is the ratio of observed to expected variance and tip variance is moderated in part by branch lengths. So if you change the node positions, the expected tip variance should also change.

A quick simulation shows that this appears to be true.

library("ape")
library("picante")
library("geiger")

set.seed(5)

tree <- rtree(30)
y <- rTraitCont(tree)

lambdas <- seq(1.0, 0.05, by = -0.05)
M <- data.frame(lambda = lambdas, k = numeric(length(lambdas)))

for (lambda in lambdas){
  tree_trans <- rescale(x = tree,
                        model = "lambda", lambda = lambda)
  M$k[M$lambda == lambda] <- phylosignal(y, tree_trans)$K
}

plot(k ~ lambda, data = M)

Generate a tree with 30 tips and generate random data along the branches. Then rescale the tree for a series of lambda values and calculate k for each lambda scaling.


Hypersensitivity Simultaneously in Ear canals

This answer is based on embryological studies and is limited.
I will extend it later when understand better.

Sensory areas

maculae acusticae - walls of utricle and saccule (this most probable area)
cristae acusticae - change in body position

Nerve

vestibular fibers of cranial nerve VIII (TODO each branchial arch has a nerve - how these differentiate between different arches?)

Embryonal Ganglion

statoacoustic (spinal) ganglion (19.5 C Fig)

Embryonal ganglion splits into two

cochlear portion
vestibular portion

which supply sensory cells of organ of Corti, and those of the saccule, utricle and semicircular canals, respectively

Branchial Arches

Each arch has a vessel, cartilage and nerve.
The task is to understand which part of embryonal ear is able to start hypersensitivity reaction.

Middle ear

Tympanic Cavity and Auditory Tube

origin endoderm (1st pharyngeal pouch) - malleus and incus
malleus - 2nd a.a.a.

Eardrum or Tympanic Membrane

ectodermal epithelial lining at bottom of auditory meatus
endodermal epithelial lining of the tympanic cavity
intermediate layer of connective tissue (See Langmans' Fig 19.9B). TODO this part is superficially covered in Langmans.

Auricle

6 mesenchymal proliferations at dorsal ends of 1-2 a.a.a.

TODO I must look again embryonal slides of ear to see where the nerves occur first and how they develop.

Sources

Langmans Medical Embryology, 12th ed, 2011
My notes of Embryology classes, Spring 2014 (I did not have all my notes now so must study these things again after holiday)


How do trees use Adhesion and Cohesion to move water against gravity?

The mechanism is called "capillary action". It requires a tube of a small diameter and happens because of the adhesion of water to the walls and the cohesion within the water (=surface tension).


Are there any pairs of animal species that regularly prey on other?

Caiman and Anacondas - though each hunts the other at a stage of development when the hunter is larger.1 2
Occasionally this occurs with Orcas and Sharks.3
Some species of shark3
Spiders and mantids4
Alligators and catfish (catfish prey on infant alligators)
Many species of predatory fish
Some species of constrictor and venomous snake.
Some frogs and Epomis circumscriptus / Epomis dejeani5
Some amphipods6
In Antiquity, hominids and lions7 8
Big cats preying on eachother, among other large predators:

Carnivores eat a variety of vertebrates: e.g. desert coyotes eat … carnivores (roadrunners, reptiles, and mammals)… Carnivorous mammals often overlap substantially in diet (30). Many “readily prey on other carnivores” (125), e.g. tigers prey on bears (black, brown, and sloth bears), dogs, wolves, lynx, and badgers (125): leopards prey on lions, cheetahs, wild dogs, and spotted hyenas (also raptors, crocodiles, and pythons; …
Leopards are mutual predators with lions, spotted hyenas, tigers, large raptorial birds, crocodiles, and pythons…

The Ecology and Evolution of Intraguild Predation: Potential Competitors That Eat Each Other


How do both autotrophic and heterotrophic successions end up having Gross Production = Respiration?

The author is saying that 1) Mature ecosystems tend to have a balance between production (=P) and use (=R, respiration) of biomass. This is actually tautological because the author would probably define a mature ecosystem as one where this is true (P=R).

If it starts out P > R, the autotrophs are dominant: more biomass is being produced than used up. It is possible, for a time, that P will increase as, for example, plants grow more leaves, but R is growing too, and there is an eventual limit on P, which at maximum depends on the light available to the ecosystem. As biomass grows, so does the amount of biomass to potentially decay, so eventually R will always catch up to P, until there is balance.

If it starts out P < R, that means you are using up biomass faster than you are creating it. This case is even simpler: you will gradually run out of biomass, and R will decrease.

In either case, when the author is talking about P = R, this is going to be in relative terms; there might still be variations between them, for example seasonal variation, but on average over years or decades you would expect P = R in a mature, stable ecosystem.


Can we digest food as well as herbivores

Humans do not have microflora that can hydrolyze cellulose, but plant-eating herbivores do. One advantage of that though is that the cellulose helps move food through your gut and aids digestion. Herbivores have fermentation chambers in their alimentary canals that contain mutualistic bacteria and protists that can break down the cellulose for them; some of the microorganisms also use some of the sugars from the digested cellulose to produce nutrients vital to the animal, such as vitamins and amino acids. Also, herbivores have longer alimentary canals relative to their body size, due to the fact that plant matter is harder to digest because of the cell walls.

Here is an excerpt on herbivore teeth structure, taken from Campbell Biology, 10th Edition.

  "Herbivores, such as horse and deer, usually have premolars and molars with broad ridged surfaces that grind through tough plant material. The incisors and canines are generally modified for biting off pieces of vegetation. In some herbivores, canines are absent" (Reece et al. 906).

References:

  Reece, Urry, Cain, Wasserman, Minorsky, and Jackson. Campbell Biology. 10th ed. N.p.: Pearson, 2014. Print.


Formal definition of a 'genetic trait reservoir'?

In this context, "trait reservoir" refers to the set of all possible alleles for all the different genes in the organism. The more different alleles the organism has, the more possible genotypes it might have. The Nature paper might have referred specifically to the set of known allelic variants.


Why are there more stomatal openings on the lower surface of a dicot leaf?

Firstly, it is not necessary that all dicots have stomata on their lower surface of their leaves. The lotus Nelumbo nucifera has its stomata on its upper surface, due to the lower surface of its leaves being in contact with water, and therefore unable to transpire effectively.

The reason that stomata are usually on the lower surface has been analysed in this paper, which rejects the commonly held hypothesis that stomata appear on the lower surface of leaves (hypostomatous) as a response to dryness, by citing that hypostomatous leaves are relatively less common in dry environments.

The paper then analyses the correlation observed between parameters of leaves and their stomatal locations.

By using a number of computational models (which conclude that given the set of assumptions in the paper, leaves should not generally be hypostomatous), the paper addresses the faults of the model and concludes that there is no one single reason why leaves are usually hypostomatous, and then brings up a couple other possibilities that may help in explaining the majority of plants being hypostomatous.


Why do some people become more aggressive when tired?

From Poor sleep as a potential causal factor in aggression and violence

  In most people poor sleep will not evoke actual physical aggression, but certain individuals, such as forensic psychiatric
  patients, may be particularly vulnerable to the emotional
  dysregulating effects of sleep disturbances

  The relation between sleep problems and aggression may be mediated by the negative effect of sleep loss on prefrontal cortical functioning. This most likely contributes to loss of control over emotions, including loss of the regulation of aggressive impulses to context-appropriate behavior.

  Other potential contributing mechanisms connecting sleep problems to aggression and violence are most likely found within the central serotonergic and the hypothalamic-pituitary-adrenal-axis. Individual variation within these neurobiological systems may be responsible for amplified aggressive responses induced by sleep loss in certain individuals.


From which end of mRNA does transcription start?

They're both correct. The confusion stems from the book talking about the anticoding strand as well as the newly-formed coding RNA strand, whereas Khan Academy talks only about the coding strand.

From the book:

  The anticoding strand is transcribed from 3' to 5'.
  Therefore the coding strand is produced from 5' to 3', meaning the very first nucleotide added by the RNA polymerase is the 5' end, and you add to it in the 3' direction.

From Khan Academy:

  The RNA polymerase produces a strand of RNA from 5' to 3'.


Normal pressure in the eye1,2 is between 10 and 21 mmHg (somewhere around 1.3-2.8 kPa or 0.01-0.03 atm) with pathology occurring at around 30 mmHg.3  Clearly the cornea can handle that, but how much more?  There's a lot more evidence as far as I could see for how well surgeries hold up, with 150-300+ mmHg (20-40 kPa, 0.2-0.4 atm).4  One source5 from 1998 cites work supposedly showing that the stroma:

  gives the cornea 100 times more strength than is necessary to withstand the maximum intraocular pressure under physiological conditions.

So maybe around 200 kPa, for just the stroma?  Interestingly, a new eye layer was discovered earlier this year; this Dua's Layer is incredibly thin - 15 microns - but can withstand pressures of around 100-200 kPa (750-1500 mmHg, 1-2 atm).6,7  The large range there is due to some conflicting numbers in those links; the 200 kPa is the more widely reported one, but again, that's just for one layer.

Then, of course, there is this: a beautiful 2009 thesis by Jill Aliza Bisplinghoff from Virginia Tech which thoroughly examines the issue.  As an answer to your question, it includes the following such gems:

  The high rate pressurization of 20 human eyes resulted in a mean rupture pressure of 0.97 ± 0.29 MPa (7275.60 ± 2175.18 mm Hg)... A student T-test revealed that the difference in the rupture pressure between the equatorial mean of 0.93 ± 0.30 MPa (6975.57 ± 2250.19 mm Hg) and the meridional mean of 1.13 ± 0.21 MPa (8475.70 ± 1575.13 mm Hg) was not significant (p=0.16)

and

  A pneumatic cannon was used to impact eyes with a variety of projectiles at multiple velocities... The projectiles selected for the test series included a 6.35 mm diameter metal ball, a 9.25 mm diameter aluminum rod, and an 11.16 mm diameter aluminum rod... A range of internal eye pressures were produced that varied from 1256 mmHg (24.3 psi) to 22843 mmHg (442 psi)... [and] resulted in zero globe rupture.


We do, all the time. Here's a nice graphic from Dr. Douglas Theobald. (Images copyright 2000 Smithsonian Institution.):

That's 14 Hominid species, ranging from about 4 M.Y. ago to a modern human skull ("N").

Here's a nice genealogy as well (although these change frequently as more evidence is gathered):


Does consuming sodium benzoate (preservative E211) cause problems during pregnancy?

There is some evidence to support the idea that sodium benzoate may be detrimental to the development of the foetus:

TERATOGENIC EFFECTS: Classified POSSIBLE for human.
DEVELOPMENTAL TOXICITY: Classified Reproductive system/toxin/female, Reproductive system/ toxin/male [SUSPECTED].

MSDS for Sodium Benzoate
This has been shown experimentally in rats by Minor & Becker in 1971.  They introduced high doses of up to 1000 mgkg-1 intraperitoneally and recorded reduction in foetal weight and "gross anomalies".  Whilst I struggled to find a copy of their original paper, it is referenced in the Catalog of Teratogenic Agents1 (Thomas H. Shepard).
There is some evidence to refute this, however.  The Acceptable Daily Intake limits on sodium benzoate is a maximum of 5mgkg-1, at this dose there is no noticeable effect of exposure. (2,3)  The latter paper by EC food safety standards goes further:

There appear to be sufficient studies to conclude absence of teratogenic potential, with an overall NOAEL* for developmental toxicity of 500 mg/kg bw/day, based on effects on fetal weight.

*(No observed adverse effect level)
So the consensus from the food safety bodies suggests that E211 should not pose harm to an unborn child in the quantities allowed to be present as an additive.

1 Emire, Ronald J. "306: Benzoate, Sodium." Catalog of Teratogenic Agents. By Thomas H. Shepherd. JHU, 2004. 44-45. Google Books. Google. Web. 10 Feb. 2012.
2 Nair, B. "Final Report on the Safety Assessment of Benzyl Alcohol, Benzoic Acid, and Sodium Benzoate." International Journal of Toxicology 20.3 (2001). International Journal of Toxicology. Web. 10 Feb. 2012.
3 Scientific Committee on Food. Opinion of the Scientific Committee on Food on Benzoic acid and its salts. Rep. 24 Sept. 2002. EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL. 10 Feb. 2012


Homeopathic magnesium lotions don't* contain magnesium, so it seems a little irrelevant whether or not magnesium can be absorbed through the skin. However, magnesium ions can definitely be absorbed through the skin. There's no reason why that should reduce muscle pain(especially because ions would disperse throughout the bloodstream etc etc), but magnesium can be absorbed through the skin fairly efficiently.

*Footnote: they do, but not on purpose. If correctly prepared they would contain zero atoms of magnesium(depending on what 'strength' they are), but that kind of purity is impossible.


Does anyone know what this purple plant is? (picture taken in Turkey)

This shrub is called Tradescantia pallida. You can read more about this shrub on this website https://florafaunaweb.nparks.gov.sg/Special-Pages/plant-detail.aspx?id=2521

I hope this helps you


What is the difficulty with cloning and genetic engineering in humans?

The question you are asking is an ethical problem rather than a biological one. This particular nature article highlights the problem I am speaking about.
In brief, children afflicted with SCID were subjected to what at the time was termed as a pioneering retroviral treatment. The idea being you replace the defective gene with the real one, in case of the quoted study, of 11 patients, 9 were cured and one of these babies developed leukemia due to the treatment. This was one of the first trials and it showed how these treatments can go awry.

Fast forward to today, last year you may have heard, something called the three parent babies garnered a lot of attention. This is basically mitochondrial donation, where a third-party provides mitochondria for IVFs for reasons where parents opting for IVFs may not be able to undergo successful IVFs due to mitochondrial mutations. This posed and still poses a serious ethical question, because what you are doing is mixing heritable DNA between lineages, please note that most geneticists will never cross this line, i.e. editing the genome such that the offspring carries the edited genome. Almost always the modified individuals are sterile (I know of no GMO crop which is not sterile)

But not to say, we have done nothing in terms of genetic engineering.

Scientists for the same reason (A human life is more important than any animal's) are wary of editing the human genome directly, so we now we also have something called siRNA treatment is just one example. And this is a list of siRNA based drugs which were in various stages of clinical trials in 2013. I know of a few which entered trial since then.

Lastly, this is just the tip of the iceberg, there's a whole lot which could be said on this topic, but it boils down to the same ethical problems.

Just so you know, since 2001, we have a lot of newer genome editing tools, such as TALENs and CRISPR-Cas. But remember, they still have the same problem as retroviruses from 2001, the issue about off-targets.

What if your tool targets a region which it isn't supposed to target?

Will another child develop a condition due to the treatment?

To avoid such an issue, we need to understand much better how the genome works, and sadly still we don't know enough. I cannot quote the study here because I have no idea where it is published, but at a recent conference I heard a talk from a lady about how retroviral integration works. The idea being, if retroviruses don't need specific integration sites, they should integrate at the first genomic region they encounter, that is not the case. I will not go into more detail. But I hope you have some food for thought.

UPDATE ON Genetic Engineering at a preconception stage

This is a link to the Nature article on Venter's minimal cell. There also exists an artificial Yeast genome page. The point I am trying to make is, we are really at the basic stages even now.

I will outline to you the behemoth scale problem we are facing.

2002: The first human genome draft is published. All the media is rife with stories about how we are going to unlock the secret to life.

Since then, DNA methylation and histone modifications have come to the foray as regulators of genome functionality.

We knew that DNA was transcribed into RNA and translated into protein. Noncoding RNAs came to the foray and messed up everything.

We thought that DNA functionality was governed by DNA methylation and Histone modifications, come 2009, we saw the first major article on Chromatin architecture. We understood that the genome has switches called Enhancers and promoters which regulated when and for how long RNA is transcribed. But sometimes these switches were so far away, we did not know how they switched on their target genes.

The problem can be summarized as this, making an artificial bacteria is easier than a human. In humans you have multiple layers of regulation, there's the DNA, where one part is silent (heterochromatin) and one part is active (Euchromatin), DNA methylation and histone modifications affect how genes are expressed, these modifications allow opening of the DNA so that genes can be expressed, The DNA is further compartmentalised (architecture) so that switches only affect nearby genes in 3D space. Non-coding RNAs act as messenger in such areas relaying proteins to their target DNA regions. So the cell is a mess!

Not to say that goat biology is simpler, just that a goat's life is cheaper than a human's. So we wouldn't feel a thing while "euthanising" goats for the advancement of mankind.


What is the difference between taxonomical aids Flora, Manual and Catalogue?

A Flora describes plants and where they live. Floras typically include a dichotomous key for identification purposes and often times will include range maps as well. Floras are almost always designed to be simultaneously regionally constrained and regionally exhaustive/complete (i.e., includes all plants that grow in that region or at least all taxonomic divisions of specified taxa). See Example.

A manual applies much more broadly to plants, and typically instructs you on a subject (e.g., identification/differentiation of species).  A manual does not need to be exhaustive and its scope is typically user defined (though often based on the scale/range of it's underlying subject). However, some have used the term manual to be more or less synonymous with Flora or otherwise similar document (e.g., see here).

A catalog is simply a listing of all species organized in some way. These are usually alphabetical (vs. taxonomically organized like a typical Flora). You will also never find a key in a catalog and will often find less phytographic detail.

See Chapter 6 in Describing Species: Practical Taxonomic Procedure for Biologists by Judith Winston for further assistance.


5,6-dihydrouracil and 5,6-dihydroxyuracil - how they arise in DNA?

Dihydrouracil oxidase can catalyse the reduction of uracil to dihydrouracil in the presence of hydrogen peroxide. The reduction of uracil to dihydrouracil can also be catalysed by dihydrouracil dehydrogenase using NADH.

According to this paper, 5,6-dihydroxycytosine can be formed by treating cytosine or DNA with osmium tetroxide, an extremely strong oxidising agent. Since they are both pyrimidines (and in fact cytosine often spontaneously hydrolyses to uracil), uracil will also be affected by the same oxidation. 5,6-dihydroxyuracil was also detected within the oxidised DNA sample as a result of oxidation and demethylation of thymine.

  The presence of 5,6-dihydroxyuracil (peak 11 in
  Fig. 1) can be explained analogously to the formation
  of 5-hydroxy-5-methylbarbituric acid from thymine on
  permanganate oxidation (lida & Hayatsu, 1970, 1971)
  (Scheme 2). The actual oxidation products ofcytosine, i.e.
  structures (I) and (II), were not observed in DNA. As the
  calf thymus DNA used in this work did not contain uracil,
  the uracil derivatives discussed above could not have been
  formed from uracil in DNA.


What type of photosynthesis is performed by phytoplankton?

I'm not sure that all phytoplankton perform the same type of photosynthesis.

Originally, people thought that they all performed C4, on the basis of genome sequencing, which revealed the presence of genes important for C4 photosynthesis.  However, experiments on individual species seemed to indicate that the phytoplankton were performing multiple types of photosynthesis (source).

EDIT: CAM is unlikely, as that is an adaptation for dry environments.

EDIT 2: and of course, some phytoplankton appear to have both C3 and C4 pathways. In short, you can't generalize.


Has the human 7-day week had any impact on the evolution of species?

I have no clear evidence of a specific species, but two pieces of the puzzle:

species can adapt to living in cities: birds living in cities are bolder (i.e. allow humans to come closer before flying away), and apparently even some genetic changes can be detected.
it may be possible for species to evolve a circaseptan rhythm: beach beetles may have a seven-day rhythm to accommodate for different heights of the tides (spring/neap tide). (PubMed / PDF)


What exactly is the neural receptive field?

I think is closer to 2. It is the subset of sensory space that elicits a reaction in a given neural population.

So you should:

Pick your neural population. Usually it is a single neuron (but can be easily extrapolated to bigger populations). It may be a sensory neuron, or a neuron in a higher processing region.
Determine your sensory space. That is, you should decide the kind of stimuli you'll be dealing with. For example, not only "visual stimuli", but you should identify the parameters, or independent variables, you will vary in your experiment.
Define a criterion to discriminate between reaction and non-reaction. This implies to choose what is the dependent variable in your study (for example neuron firing rate). Then you could define what features in the relation $\frac{dependent\:variables}{independent\:variables}$ you will search for. That is the tuning curve (which well may be a high dimensional curve).
Perform your experiment and analyze your curve. The region of parameters (independent variables) whose reaction goes above threshold according to your criterion is the receptive field. Sometimes is not trivial to define such a criterion (see: http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0040092)

A good general reference is the article in Scholarpedia: http://www.scholarpedia.org/article/Receptive_field

This type of analysis is very useful for position coding, that is, when you expect that the activation of a specific region in the brain correlates to stimuli in a region of sensory space. But sometimes things are more complicated (e.g Olfactory coding http://www.jneurosci.org/content/30/27/9017.full).


What is a lip? (upper lip and lower lip)

Source

  The upper lip extends from the base of the nose superiorly to the nasolabial folds laterally and to the free edge of the vermilion border inferiorly. The lower lip extends from the superior free vermilion edge superiorly, to the commissures laterally, and to the mandible inferiorly. Around the circumferential vermilion-skin border, a fine line of pale skin accentuates the color difference between the vermilion and normal skin. Along the upper vermilion-skin border, 2 paramedian elevations of the vermilion form the Cupid bow. Two raised vertical columns of tissue form a midline depression called the philtrum. The philtrum is located between the paramedian elevations of the vermilion and the columella above. The labiomental crease passes horizontally in an inverted U-shape across the lower lip, which intraorally corresponds to the depth of the gingivolabial sulcus.

This includes vermilion as well. Dont forget the mucous part inside mouth.

This whole is lip.

As for upper cutaneous lip or cutaneous upper lip, it wont matter, both are same and are used interchangeably. And quite frequently
used is upper cutaneous lip.
As for latinisation, you can use labium for lip, no such specific word for upper or lower lip, is know to me. But, you can try superior cutaneous labium and inferior cutaneous labium, if you want.


When was the purpose of bone marrow discovered?

Answer: In the late 1800s, by a few different guys building on each other.
I personally had no idea, but a little searching around found this little gem, which seems up our alley: The origins of bone marrow as the seedbed of our blood: from antiquity to the time of Osler.  It's only ten pages so definitely worth a read, but a few passages of note:

Neumann and Bizzozero... are credited with making the initial observations leading to the recognition of the marrow as the seat of blood formation... In his report published in October 1868, Neumann described the presence of nucleated red blood cells in the bone marrow sap of humans and rabbits by squeezing bone. He was the first to conclude that during postembryonic life, erythropoiesis was taking place in the marrow.

However, Neumann concluded erroneously that the proliferation of marrow cells occurred inside the blood vessels of the marrow; the concept of marrow sinusoids was not coined until Minot's description in 1901.

It later says that, in the mid-1880s Osler stated

that there can be no doubt that nucleated red cells originate in the bone marrow...

It's actually a pretty interesting read, all in all, and like all of the best discoveries in science, it seems like a few people built on each others' work over the years, with a bunch sort of figuring it out around the same time.


What is the scientific name of this plant that is possibly called ogre ears?

This (lovely) succulent is Crassula ovata variety "Gollum", known also as "gollum jade" or "finger jade".  Search for the name and you'll find lots of commercial sources.  One informative source is here.


What makes a DNA sequence motif a DNA sequence motif?

Motif means a pattern. For any array of objects to be called a pattern, it has to have at least more than one instance.
To define more precisely, a motif should have significantly (statistical) higher occurrence in a given array compared to what you would obtain in a randomized array of same components (expecting at random).

[Here i use the term array to mean an arranged set such as a genome (array of nucleotides with their position in the sequence) or a protein structure (array of amino acids with their vector positions). A randomized array with same components is generated by shuffling the elements and their values; for e.g. assign the same collection of nucleotides to random positions]

RSS nonamers/heptamers are called a motif because they are a pattern of sequence which a) has more than one occurrence b) the occurrence is significantly higher than a random expectation. Generally in sequence motifs randomization is not usually done because the genome size is too huge. In such conditions if your sequence has >= 2 occurrences throughout the genome it may be considered a motif. Lets assume a 10bp sequence. Its random probability = 1/4¹⁰. Therefore in 1048576 bp (1Gb) there is a likelihood of finding one instance of that sequence on random. So I assumed that if that sequence has >=2 instances it can be called a motif. However, I am not sure about this.

RSS is not a motif because the entire RSS is not conserved; the conserved 'motifs' are interrupted by sequences. This is analogous to lets say a promoter which is a functional region of the DNA. Promoter can have binding sites for different transcription factors and these operator sites (TFBS) can constitute a motif (if they are conserved) but not the entire promoter.


Are there any neurotransmitters that trigger all neurons?

There is no such  promiscuous neurotransmitter. There is always some difference between central and peripheral nervous system w.r.t neurotransmitter usage.

Glutamate is one neurotransmitter which acts as an excitatory agonist in most neurons (but still.. not ALL neurons)


Are human chromosomes connected or separate molecules?

Each chromosome is a pair of distinct, separate DNA molecules.  A chromosome of an eukaryotic cell nucleus is a (long) helix of two linear molecules and so has two ends, which are called telomeres.  DNA naturally forms a double helix with its complementary DNA molecule, and the double helix can further curl in what are called supercoils.

In humans, the chromosomes occur in 23 pairs (totaling 46). Except for the sex chromosome pair, each member of the pair is identical in appearance in a karyotype (picture) and each such pair has a number assigned from 1 to 22; the numbering generally follows the size of the chromosome, with chromosome 1 being the longest.  In mammals, the sex chromosomes in a male are quite different in size and are labelled X and Y; a female has two identical X chromosomes.


That looks very much like a brown color morph of the Box tree moth (Cydalima perspectalis), which has been seen in the UK since 2008. The size is about right (around 4.0-4.5 cm wingspan).
This species is an invasive pest outside of its native range (Asia).

By Nagy Sándor (NagySandor.EU) CC BY 3.0, Link
According to the Royal Horticultural Society this species has been invading the UK from the southeast with London a likely place to find them.


That is a Moth Fly, also known as a Drain Fly. It is in the order, Diptera, family Psychodidae. https://en.wikipedia.org/wiki/Drain_fly


What species of wasp is this? And how to get rid of them?

These are European paper wasps.

(They look very similar to yellowjacket wasps but you can notice the antennae; they are brown here whereas they are black in case of yellowjackets. There are other subtle differences too.)

See this post on Gardening & Landscaping stackexchange about getting rid of wasps.

(This part is probably not really on-topic here and I don't want to copy-paste an existing answer in another stackexchange site.)

If you are upvoting this post then please also upvote the original one in G&L SE


Your answer to a) is correct (standard Hardy-Weinberg equation).

For b) you have to consider that you are calculating proportions of the population, which should sum to 1. Since 30% of the AA individuals and all SS individuals die, this is not the case after selection, which is why you should divide the frequencies by the total proportion that survive (also for the AS genotype), such as:

$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq before} & w_{survival} & \text{freq after selection} & \text{corrected freq}\\
&\text{selection}&&&\text{after selection}\\
\hline
AA & 0.64 & 0.7 & f(AA)\cdot w_{AA}=0.45 & 0.58\\
AS & 0.32 & 1 & f(AS)\cdot w_{AS}=0.32 & 0.42 \\
SS & 0.04 & 0 & f(SS)\cdot w_{SS}=0.0 & 0.0\\
\text{sum} & 1 & & 0.768 & 1
\end{array}
$$

here $w$ is the fitness of genotypes. And for your comment on why you didn't have to divide by the sum of freqencies in a): you could do this, but since the sum of genotype frequencies is 1 it doesn't make a difference.

For c) you use the standard formula for calculating allele frequencies from genotypes, so that $f(A)=f(AA)+f(AS)/2= 0.79$ and $f(S)=f(SS)+f(AS)/2= 0.21$.


Why are some genes dominant over others? What is the mechanism behind it?

One version or allele of the gene for eye color may encode instructions to make the brown pigment, while the blue allele makes no pigment. Alternatively, it is possible, logically speaking, that the blue allele blocks the productions of brown pigment, but this is not the case.

Now, brown vs blue is not a case of one gene and two alleles. After producing pigment, it must be transported, deposited and such. Many processes are involved. So, the pigment deposition process may be functional or not, but as above, it is often found that a non-functional version is simply non-functioning and not actively inhibiting the process. There are numerous cases where an aberrant form of a protein, encoded by a variant allele, acts as an active inhibitor of a given biological or biochemical process.

The key to your question as written is blue eye color is a lack of pigmentation.


What roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?

I just took a quick look.

These classes of enzymes are important to a family of lipid based molecules which perform intra and intercellular signalling with a lot of medical importance.

Epoxygenases can create epoxides of arachidonic acid,  which can modulate cell proliferation.  Arachidonic acid is a well known second messenger in many tissues in the cell, so these enzymes clearly would affect many signalling pathways.

Cyclooxygenases (COX) enzymes are such important mediators of inflammation signalling that they are the primary targets of aspirin and other Non steroidal anti-inflammatory drugs.

Lipoxygenases oxygenate compounds such as prostaglandins which are downstream from aranchidonic acid (as does COX).


Why does contracting the iris allow less intense light to go in?

Imagine the iris like a shutter in front of a focussing lens (which, in fact, it is; see the diagram).

This means that any light going through the iris will be focussed on a very small point on the retina, and your eye is wonderfully developed in a way that this exact spot is the fovea, the only spot in the retina that allows you to see colour and high-resolution.

The iris does not modify the focussing function, it merely changes the amount of light going through into the lens to then be focussed onto the fovea. Imagine that every single object in your field of view reflects/radiates light in every possible direction - narrowing the shutter won't exclude parts of the field of vision, it will only exclude some of the rays coming in at very flat angles and thereby reduce intensity.

Only if your lens is deformed, focussing (adaptation) will malfunction (directing the gathered light to the wrong spot; or focussing the incoming light in front of or behind the retina) and blur your vision.


Finding a template/oligo combination for my first PCR experiment

You need a genome that isn't too complex, which suggests something microbial. You also need a genome that is well-characterised : either fully- sequenced, or with lots of sequenced genes to allow you to design primers. And finally you need a readily accessible source of material for DNA extraction.

I would suggest either dried yeast, as a source of Saccharomyces cerevisiae DNA, or live yoghurt as a source of DNA from Lactobacilli. You could even try culturing something from yoghurt to get pure bacterial colonies: since these would be from a food source there should be minimal risk.

You might be tempted by one of the traditional plant sources of DNA (e.g. onions) , but it can be tricky to avoid copurifying polysaccharides which inhibit DNA-related enzymes.

Finally, if you do culture some bacteria, or even if you use dried yeast, you probably wouldn't need to actually prepare DNA at all. PCR direct from bacterial cells is widely used - the 95 C step will release sufficient DNA.

added later in response to comment by OP

I chose to follow up on Lactobacillus delbrueckii subsp. bulgaricus because I found this coming up over and over again with reference to yoghurt. If you were to test a range of yoghurts I think you could be fairly confident that this would be present.

There are 5 published genomes for different strains of the species Lactobacillus delbrueckii including subspecies bulgaricus (various strains) and lactis. How different are they? I decided to look at one gene, and lactate dehydrogenase seemed like a logical choice (it produces the lactic acid).

The complete nucleotide sequence for the lactate dehydrogenase gene from Lactobacillus delbrueckii subsp. bulgaricus ATCC 11842 is here. If you run a BLAST from that page limiting the search to Lactobacilli (taxid 1578) you do indeed find hits to the gene from several other genomes. Here is a representative selection from the sequence alignment to the least similar of the hits:

Query  99766   CCTTCCACGCTTCTGGAGGTACTGAATTCGCCCTGGCTCAACTGGGCAACGATGCCGGTA  99825
               ||||||||||||||| ||||||||||||||||||||| ||||||||||||||||||||||
Sbjct  90616   CCTTCCACGCTTCTGAAGGTACTGAATTCGCCCTGGCCCAACTGGGCAACGATGCCGGTA  90675

Query  99826   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATGTAAAAAAGCACCAGGCTTTTAA  99885
               ||||||||||||||||||||||||||||||||||||| |||||||||||||| |||||||
Sbjct  90676   TGTACGGTGCCGTTAAGATGGTTCTGTAATTTTGAATATAAAAAAGCACCAGACTTTTAA  90735

Query  99886   AGTCTGGTGCtttttttGTTTATCCTAAAGAGTCCAGGGTTGCCTTTATCGTCGCGGCTG  99945
               |||||||||||| |||||||||| |||||||||||||||||||||| |||||||||||||
Sbjct  90736   AGTCTGGTGCTTATTTTGTTTATTCTAAAGAGTCCAGGGTTGCCTTCATCGTCGCGGCTG  90795

Query  99946   AGGCCCGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGTACGTGGCTGATCC  100005
               ||||| |||||||||||||||||||||||||||||||||||||||| ||||||||||| |
Sbjct  90796   AGGCCTGCATCTTGGCCAATTCGCTGTCATTTAACGGCAATTCCAGCACGTGGCTGATTC  90855

Query  100006  CTTGTCCGTTGATGATGGCCAGGGTGCCCAGGTAGATCTCATCCTTGATCCCGTATTCCC  100065
               |||| |||||||||||||||||||||||||| ||||||||||||||||||||||||||||
Sbjct  90856   CTTGCCCGTTGATGATGGCCAGGGTGCCCAGATAGATCTCATCCTTGATCCCGTATTCCC  90915

Query  100066  CGTGCAATGGTGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGTCACGA  100125
               |||||||||| ||||||||||||||||||||||||||||||||||||||||||| |||||
Sbjct  90916   CGTGCAATGGCGCGGAAAGAGGCAGGGCCAGGTCGTTGTTTTCCAAAATGGCCGCCACGA  90975

Query  100126  TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTTGCGCCCTTTTTGACGATAATCTCGC  100185
               |||||||||||||||||||||||||||||||||| |||||||||||| |||| |||||||
Sbjct  90976   TCTTGGCCAGCATCATGGCCACGCCATAGTAGGTCGCGCCCTTTTTGCCGATGATCTCGC  91035

As you can see, there are some differences, but there should be no problem designing primers matching both (again - this is just one part of the gene). Obviously you might wish to make an alignment for all 5 sequences, but I got the impression that at least some of the others were identical to the query, even though they are from different subspecies. These are very closely-related organisms.

In terms of your experiment, I suggest that you plan to use a range of yoghurts and/or starters as the source of template. You could even mix them, if there are constraints on your set-up.


What is the genetic reason that this flower has petals of two different colors?

This can be a result of a somatic mutation, especially if the other flowers on the same plant don't have the same color pattern. Somatic mutations are not inherited for parent organisms but occur spontaneously in one of the cells in the body. If that cell then proliferates all of its descendants will have the mutation and new phenotype associated with it.

Look for example at Fig. 1 (c, d) in this article. Those peach flowers have similar coloration to the one on your photo.


what is the margarine metabolism in our body?

As pointed to by @Chris the Wikipedia link for margarine explains that these are formulated upon vegetable oil-based fats. Their melting points and other properties are adjusted by industrial hydrogenation of the unsaturated fatty acids in the vegetable oil.

Most unsaturated fatty acids present in nature are in the cis conformation at the double bonds. The hydrogenation process, if it is not carried to completion, produces the trans isomers of fatty acids. These so-called trans-fats are blamed for the undesirable side effects of consuming margarine, or other foods containing hydrogenated oils.

Most of the fatty acids present in margarine (i.e. cis unsaturated and saturated fatty acids) are metabolised by the normal route (β oxidation).


Ideally amplification happens between the two primer pairs and results in one product. However, complicated secondary structures, the depletion of some of the reagents may cause pauses and fall off of the polymerase. This happens often later in the reaction and results in shorter products. This final amplification step is introduced to finish all these shorter products.
A pair means the combination of a forward and a backward primer (see the image below from here). Bothg primers are added in a concentration high enough that both are not depleted and enable long PCR runs. No primers (or other reagents) are added during a standard PCR reaction.

The temperature of the PCR reaction is changed through 1 reaction cycle: First you start with the denaturation of the DNA at 94°C, then cool down to anneal the primers (typically between 50 and 60°C, depending on the primers), followed by the amplification step at 72°C (it'S length depends on the length of the amplified DNA piece, Taq polymerase processes about 1kb/min) (see figure below from here). This is one cycle and you know where you are, because the PCR machine counts this cycles.


Cnidarian life cycle, a case of ontogenetic polymorphism?

Sure it would.  I would usually use holometabolous insects as an example of this (egg, larva, pupa, adult), but Cnidarians certainly fulfill the basic requirements encapsulated by the phrase "ontogenic polymorphism." It appears that the pressures of finding/establishing food sources and escaping predation in competitive environments has driven both Cnidaria and Insecta toward this evolutionary strategy, though that is a field of active study still (at least in insects).


How does formaldehyde/PBS or methanol fixation of cells affect lysosomal pH?

In my opinion, cell fixation shouldn't change the pH. However unbuffered formalin will oxidize and lower the pH, but using PBS should buffer around pH 7.
Maybe Glutaraldehyde fixation would also be an option, if the others are not working...

I found this website by leica very useful, maybe it will also help you:

  http://www.leicabiosystems.com/pathologyleaders/fixation-and-fixatives-2-factors-influencing-chemical-fixation-formaldehyde-and-glutaraldehyde/


The tRNA anticodons are both complementary and anti-parallel. That means for $5'-\text{AUG}-3'$, the tRNA anticodon would be $3'-\text{UAC}-5'$.

The image has the mRNA oriented with the $5'$ end on the right end. It shows both, complementarity and anti-parallel configuration. The reference you cite might have cited the anticodons $3'\rightarrow 5'$ and mRNA codons $5'\rightarrow 3'$. In general, we usually cite the codes from $5'\rightarrow 3'$ but it doesn't matter until it is explicitly specified or unambiguous.


What is the name of this plant which is located in Hyderabad city of Telangana State,India?

From the twisted overlapping appearance of the petals it is a member of the Apocynaceae family.  So I searched for "Apocyanaceae india" and found images consistent with your picture.  Good chance it is Allamanda blanchetii or Purple Allamanda.  Here is a picture comparable to yours (source/CC0).

Here's a bit about the plant and Wikipedia has a short page.


anyone can help identify this aquatic microganisms?

It's a Rotifer, commonly called wheel animal It uses the hooks to attach itself to the fish's gills.
https://www.google.com/search?tbm=isch&sa=1&ei=1t4qXJS_Jaiu0gLYppCYBw&q=rotifer+under+microscope&oq=rotifer+&gs_l=img.1.1.0l10.83680.92883..95716...0.0..0.181.993.1j7......0....1..gws-wiz-img.......0i67j0i10i67.8Yg5stvFiH4

https://l450v.alamy.com/450v/k42bdt/rotifer-lapadella-apsida-female-free-swimming-microscope-freshwater-k42bdt.jpg
I hope this helps


Will amylase inhibitors affect the colorigenic reaction between starch and iodine?

To measure your amylase activity, you will monitor the disappearance of amylase’s substrate, starch.
Starch reacts with iodine (which is yellow) to form a blue compound (Amax 620 nm). This reaction is
the basis of a colorimetric assay for amylase activity. You should be very careful about the volume of the final solutions so it won't effect your results. For example you will add inhibitor to one of them and you won't add that to the other but you should add water instead of the inhibitor so dansity won't be a problem. (final volumes should be same since starch amount at the beginning will be same) You can use some acid like HCL to stop enzyme activity so it won't change the colour and won't effect your results. After the acid stops the enzymatic reaction and the iodine
reacts with the starch to produce the blue color. Any starch that has not yet been hydrolyzed by the
 amylase will turn blue color being proportional to the amount of starch
remaining. The intensity of the blue color can be by measured by its absorbance at 620 nm. The greater the change in absorbance between a sample containing the initial
amount of starch (without enzyme) and the hydrolyzed mixture containing the enzyme, the greater the
amount of starch degraded by the enzyme, therefore the greater the activity of the enzyme being
measured. Make sure you give the enzyme enough time and heat to catalyse the reaction. Sorry for grammar errors. I hope this was helpful!

Edit:you asked if inhibitor effects the experiment. I did say it above. If you use a colorless substance to denature or inhibit the enzyme it won't effect your results. If you can't do this you may add the inhibitor after the reaction is over so it won't effect the reaction but you may eliminate possible differences in color


How can enzymes be immobilised on glass?

Glass can be functionalized by organosilanization so that biomolecules can be covalently attached via some cross-linker. As an example, one might aminosilanize the glass and then cross-link their enzyme of interest with glutaraldehyde.

For what it’s worth, urease activity can be measured in solution.


Are serotonin levels in humans affected by light?

I'm not sure about humans, but this is true of many vertebrate's retinas. There is experimental evidence showing light-inhibited production of serotonin. This article reviews how serotonin is regulated in response to day lenght (as well as fasting/feeding cycles). The authors suggest a mechanism in which serotonin and ghrelin integrate signals from fasting/feeding and night/day together.

Nowak JZ, Z Urawska E, Zawilska J. Melatonin and its generating system in vertebrate retina: circadian rhythm, effect of environmental lighting and interaction with dopamine. Neurochem Int. 1989;14(4):397-406.
Kirsz K, Zieba DA. A review on the effect of the photoperiod and melatonin on interactions between ghrelin and serotonin. Gen Comp Endocrinol. 2012 Nov 1;179(2):248-53. doi: 10.1016/j.ygcen.2012.08.025. Epub 2012 Sep 5.


How were (many) dinosaurs' brains so small?

I don't think there is a concrete answer, because we don't really know the minimum size of a vertebrate brain in relation to body size. Many vertebrates, including many fish, get along fine with tiny brains in large bodies.

For many decades, scientists speculated for this very reason of small brain size, that dinosaurs seemed to have an extra brain, or ganglion, at the hip. Especially sauropods and thyreophorans appear to have had a widening of the spinal cord cavity around the sacral area suggesting this possibility. This pelvic ganglion or "hip brain" was then presumed to be responsible for running the hind legs and tails. However, this idea has not gained any further evidence or traction in the scientific community and is generally dismissed.


Are the antibodies developed by differing vaccines still the same?

Due to the nature of the immune system, even people who receive the same vaccine will have a different set of antibodies.
Our immune systems generate a vast number of essentially random recognition combinations, unique to every individual. This leads to a polyclonal response to both infections and vaccines, involving multiple antibodies and the fine details of those antibodies differ based on the specific antibodies in the "library" that the person's body has generated.
Now, different antigens do result in different antibodies being selected for, so one might expect there to be additional differences due to getting an mRNA coding for a SARS-CoV-2 spike protein vs. getting a whole inactivated virus. There's a reason that the spike protein is the preferred target, however, in that its position on the outside of the virus leads it to be a focal point for the response to an inactivated virus.
Bottom line: the responses will differ, but will likely always have a varied set of antibodies targeting the spike protein in any case.


Why is proteinase K digestion performed at 50 °C?

In your linked wiki article: "An elevation of the reaction temperature from 37 °C to 50 - 60 °C may increase the activity (of Proteinase K) several times." The enzyme works faster at 50°C.


There are several twin studies showing, that the tendency to be religious has a genetic component. Not which religion you choose, because that is a cultural thing, but how serious you are abot it. I am lazy for a detailed report, but this blog can lead you to the studies: http://www.scilogs.eu/en/blog/biology-of-religion/2011-03-12/religiosity-genes-again-confirmed-by-another-twin-study

Also this article: http://www.popsci.com/science/article/2013-08/what-twins-reveal-about-god-gene

EDIT after a few years - I was informed one link is broken and the other contains no citation. So I checked for new material today and wikipedia has a cool passage how genes and environment affect religion. Wikipedia saves the old version, so this is from March 8 2018, article Religiosity.

"
The contributions of genes and environment to religiosity have been quantified in studies of twins (Bouchard et al., 1999; Kirk et al., 1999) and sociological studies of welfare, availability, and legal regulations [15] (state religions, etc.).

Koenig et al. (2005) report that the contribution of genes to variation in religiosity (called heritability) increases from 12% to 44% and the contribution of shared (family) effects decreases from 56% to 18% between adolescence and adulthood.[16] "

15 Nolan, P., & Lenski, G. E. (2010). Human societies: Introduction to macrosociology. Boulder, CO: Paradigm Publisher.

16 L. B. Koenig, M. McGue, R. F. Krueger and T. J. Bouchard, Jr. (2005). Genetic and environmental influences on religiousness: findings for retrospective and current religiousness ratings. Journal of Personality, 73, 471-88

https://en.m.wikipedia.org/wiki/Religiosity#Genes_and_environment


Why aren't genetic triplets roughly evenly found in DNA?


Comparison of gene expression time series in vitro and in vivo

Direct comparison of the course would be difficult between tissues and cultured cells. In stead of time scale, you might want to use markers.
For example, Kislinger et al. show the expression peak of SIX1 is 2 days after differentiation; SMAD3, 4 days. I am not a right person who can tell which markers are good, but I believe you could find more information by literature search.

http://www.mcponline.org/content/4/7/887.full


Why does the apex of the human heart usually point to the left?

From a quick look at the paper @ChinmayKanchi links to (Palmer, 2004) it seems that:

  All living vertebrates possess a heart that is conspicuously asymmetrical and normally displaced toward the left (Fishman & Chien, 1997).

So the heart orientation seems to be evolutionary conserved in vertebrates (as are many fundamental traits), and no specific explanation is needed for humans.

This is said with the reservation that human anatomy is not my subject field, and the refered paper also digs deeper into the molecular basis for the orientation/symmetry of organisms. For instance, it also says that:

  Second, the molecular pathway directing hearts leftward—the nodal cascade—varies considerably among vertebrates (homology of form does not require homology of development) and was possibly co-opted from a preexisting asymmetrical chordate organ system.

so the molecular mechanisms governing this seems to differ between species. This could indicate that there is a selective pressure molding species into the same heart orientation. This is pure speculation on my part though.

I also want to mention that evolutionary outcomes doesn't have to have a "reason" (i.e. a selective advantage). Much depends on chance events and evolution can only act on what is present at the moment (i.e. is restricted by earlier evolutionary history).


Can someone provide resources on human electromagnetic frequencies?

For a start, you could learn about Bioelectromagnetics which is the study of the interaction between electromagnetic fields and biological entities (reference). Electro-magnetic fields are generated by the heart, brain, tissues and cells. These fields are in-turn affected by temperature and the overall mood of a person (reference).

There is a lot of research that is being conducted in the field. You can find a lot of papers relating to the field with a simple search on Google Scholar.

Well technically electromagnetic fields.

There are instruments to measure EMF which are detailed in the Wikipedia page. Here is an article on an instrument made to measure the electromagnetic field of the heart (reference).

Generally, if you have measured the electromagnetic fields in different parts of the body (eg: this article states that the electric field of the heart is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m) then it shouldn't be too hard to generate them seeing that EMF generated is a low value (reference).


Is 100% antibacterial resistance possible?

This is a theoretical question, which I can't answer, because genetics is not my favorite topic. In practice we only have about a dozen antibiotic classes. There are already panresistant bacterias, which are resistant (as far as I know) all of these classes of antibiotics, so we have already lost.

The causes of our defeat is more interesting I think:

Pharmaceutical industry does not have enough interest in the antibiotics research, since it is not as profitable as for example cholesterol reducers. Antibiotics are cheap, and you usually heal after the first treatment, while the research and the clinical trials are really expensive, it is hard to find working chemicals, which do not have severe side effects.

  “We  need  to  shift  from  the  concept  of  the  pharmacy  as  a
  ‘shop’  and  build  a  culture  of  pharmaceutical services. This is
  already happening  in some countries, but we need to make it  the
  rule  everywhere,”  says  Zsuzsanna  Jakab,  WHO  Reg ional  Director
  for  Europe.  “As  pharmacists  dispense  medicines  to  patients,they
  are   important  allies  in  our  fight  against  antibiotic
  resistance.  As  such,  they  need  to  be  ena bled  to  deliver
  accurate  information  and  counselling on proper antibiotic use.”

  Over  40%  of  antibiotic  prescriptions  are  inappropri ate,  recent
  studies  found.  This  relates  especiallyto antibiotics prescribed
  for the common  cold and sore throat; these most oftenresult  from
  viral infections,on  which antibiotics have no  effect. Further, in
  some countries, there is  atendency towards self-medication.
  Inappropriate an tibiotic use is the major driver of growing
  antibiotic resistance.

Pharmacists have decisive role in combating antibiotic resistance, says new WHO European survey
People with Mycobacter infections does not always do the treatment long enough, so Mycobacters can become resistant to antibiotics.

  Most people with TB are cured by a strictly followed, six-month drug
  regimen that is provided to patients with support and supervision.
  Inappropriate or incorrect use of antimicrobial drugs, or use of
  ineffective formulations of drugs (e.g. use of single drugs, poor
  quality medicines or bad storage conditions), and premature treatment
  interruption can cause drug resistance, which can then be transmitted,
  especially in crowded settings such as prisons and hospitals.

http://www.who.int/features/qa/79/en/
There is no global regulation of how to use antibiotics, so in some countries you can buy them without consulting a doctor and get a prescription. On top of this you can buy antibiotics without prescription on the internet if you want. This leads to overuse of antibiotics, and overusage leads to resistance.

  Self-medication is more common in developing countries due to factors
  such as ready availability of antibiotics without prescription, the
  unrestricted access to antibiotics,lack of regulation over drugs, and
  physicians and pharmacists prescribing and dispensing antibiotics
  without regard to the cause of infection

http://article.sapub.org/10.5923.j.cmd.20110101.02.html#Sec3.3.4

  We found 138 unique vendors selling antibiotics without a
  prescription. Of those vendors, 36.2% sold antibiotics without a
  prescription, and 63.8% provided an online prescription. Penicillins
  were available on 94.2% of the sites, macrolides on 96.4%,
  fluoroquinolones on 61.6%, and cephalosporins on 56.5%. Nearly all,
  98.6%, ship to the United States.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746509/

  These results demonstrate that, although illegal, the sale of
  antibiotics without a prescription continues in Spain.

http://cid.oxfordjournals.org/content/48/10/1345.full
Some of the antibiocstics are used by agriculture industry, which leads to antibiotics resistance as well.

  They identified bacteria able to shrug off the drug of last resort -
  colistin - in patients and livestock in China.

  It is likely resistance emerged after colistin was overused in farm
  animals.

http://www.bbc.com/news/health-34857015

  Nutritive and therapeutic treatment of farm animals with antibiotics,
  amounting to half of the world's antibiotic output, has selected for
  resistant bacteria that may contaminate the food produced.
  Antibiotic-resistant enterococci and staphylococci from animals are
  found in food when they survive the production processes, as in raw
  cured sausages and raw milk cheeses1. The broad host ranges of some
  plasmids and the action of transposons in many bacteria allow
  antibiotic-resistance genes to be communicated by conjugation between
  different species and genera2,3. A multi-antibiotic resistance plasmid
  from a lactococcus found in cheese provides a historical record of
  such events.

http://www.nature.com/nature/journal/v389/n6653/abs/389801b0.html

  About 2/3 of the antibiotics are used in animals.

https://youtu.be/iLJAleLjJv8?t=3m47s

So the problem is with not enough motivation in development and the lack of proper regulation of usage. Regulation is the business of the politicians, so its their fault as always. :D


Which ingested allergens can be transferred to a partner via bodily fluids?

It depends on several factors: what's the biochemical nature of the allergen? Is it a protein? What's its size?

In short, the answer seems to be yes, to some particular cases. For instance, this paper deals with allergens from Brazil nuts transmited by the semen:

http://www.jiaci.org/issues/vol17issue03/10.pdf

According to the paper:

  We report the case of a 20-year-old woman with
  documented Brazil nut allergy who developed widespread urticaria and mild dyspnea after intercourse with her boyfriend who had earlier
  consumed Brazil nuts.

Of course, there is no general rule, and each case has to be individually analysed. This makes very hard, if not impossible, to answer your second question ("I would like to know in particular intake of which allergens should be avoided to prevent allergic reaction of a partner due to contact with bodily fluids"), because it depends on the case in question: the allergy, the allergen, the people involved etc.

This Scientific American blog post makes a good overview of the matter:

http://blogs.scientificamerican.com/food-matters/sexually-transmitted-food-allergens/


How best to count bees entering and leaving a hive to measure hive activity?

One thing that's certain is that the activity of bees varies according to time of day, so more important than how long you record for is probably at what time you record. If you always record at the same time of day, this should allow a reasonable comparison between results of different days. For example, recording from time 14:30 to 14:35 every day could be fine. You could then record conditions at this time each day (temperature, weather, etc.) along with this.

As for the exact length of your recordings: Of course, the longer they are, the better. More samples usually increases reliability and representativeness of your results. However, more importantly you want a practically useful time as well. This really depends on the actual number of bees entering into the hive within different time frames, as well as the baseline variability between days irrespective of the conditions you are investigating. I don't know anything about either of these :)

You want the number of entrances in your recording to be at a level where you will notice if there is a meaningful difference between days, and the only way of going about this is usually to start with a guess and then change if you notice that you can't really make sense of your results.


Why can a gene lack of a binding site be expressed in skin cells?

You understand this wrong: All present enhancers of a gene must be bound by a enhancing factor, not all factors of a certain cell types have to be bound. So when skin cells contain activators for B, D and E they can activate gene 2 and 4 of your example, but not gene 3 since the activators for A and C are missing.
So when you have a gene containing any combination of B, D and E, its activation in skin cells is possible according to this model. The same is true for any combination of A, C and E for liver cells. The special case would be a gene having E as the only enhancer as this could be activated in both, liver and skin cells.


How much weight/volume do microbes occupy within the human body?

@AlanBoyd's calculations are reasonable, I think the estimate is off though.  The human microbome includes other bacteria which are not necessarily E.coli equivalent.

The human microbome projects give estimates that microbes are 1-3% total body mass.  i.e. several pounds of bacteria.

The GI tract alone has most of the microbome mass - faeces is ~60% intestinal flora/fauna by dry weight, which for many adults alone must be hundreds of grams at any given moment.


Why does increasing the space constant increase conduction velocity in myelinated neurons if nodes of Ranvier are constantly spaced?

I think the simplest answer to your question is that you're correct in thinking passive flow would be what changes, but the reason behind it is important to understand.
I'd recommend looking at UT Health's neuroscience online resource where they break down action potential propagation in an understandable way. The main takeaway is that the space constant is determined by a number of different physical characteristics of the neuron/axon. You can find these characteristics at the link I provided, but the three parameters that define the length constant are diameter of the axon (d), membrane resistance (Rm), and axial resistance (Ra).
Starting with Rm (because you allude to myelin in the question), this is dramatically affected by myelination. An internode (the myelinated portion of an axon in between nodes of Ranvier) has an excessively high Rm, which just means that current doesn't readily flow across the membrane, so current doesn't "leak out" while it's passively flowing down the axon here. Therefore, increasing Rm by lengthening internodes would help increase the distance across which current can passively flow in the axon (which increases the space constant). Shortening internodes would have the opposite effect. However, you seem to be asking "All things with myelin remaining the same, why would a higher space constant increase conduction velocity?"  That's where d and Ra come in. I explain these below:
The values of d and Ra are somewhat linked. Basically, a high the value of d allows passive current to flow more easily along the axon, meaning it has a low value of Ra. So in the context of your question, if you had an axon and theoretically doubled the axon diameter (so from d to 2d), Ra is cut in half (so from Ra to Ra/2) and passive conduction can speed up. This would increase the space constant by its effect on passive conduction. The converse is true if you shrink the axon diameter. However, it's important to realize that Ra can also be affected by other factors like the contents of the cytoplasm in the axon. That is why both are used to calculate the space constant even though they relate to one another.


Is it possible to process electrical signals from the brain and interpret the results as exact thoughts?

The brain activity is electric and chemical. The male adult human brain contains about 86 billion neurons (Azevedo et al). There is about 100 trillion connections between them. Solving a puzzle like that is not easy..

  what sort of breakthroughs would be necessary to intercept these signals and interpret them as exact thoughts?

What you are referring to would be called solving the neural code in neuroscience. With today's methods, it is probably not possible.

Consider electroencephalography (EEG). It records the electrical activity of the brain. Ag/AgCl sensors are placed along the scalp (typically 64-256 in research settings). When about 50,000 parallel neurons fire simultaneously, a change in a recorded signal can be seen. While the time resolution is about 1 ms for EEG, the spatial resolution is several centimeters (it is not easy to find which areas produced the recorded signals; it is an inverse problem). A newer technique, called magnetoencephalography (MEG), is becoming more and more used but is expensive. It records the magnetic fields related to the electrical activity and allows better localization.

Is there other complications? Well... lot's of them. Blink your eyes during the recording and there will be a major artefact masking the brain signals in most channels (10-100x greater in amplitude than the brain signals).

Anyway, you would probably be interested in the new research involving the use of machine learning techniques: it has been possible to decode the contents of dreams, reconstruct what a subject is seeing, etc. The best papers have been published by Science, Nature, and PNAS, so using their search engines with the keywords decoding and brain should allow you to explore the topic easily.

PS. I did not have time discuss fMRI; someone else can may be do that..


what will be the effect of cockroach bite?

I have reared cockroaches by the thousands, for years. Three species, but mainly the infamous Periplaneta americana which I am sure everyone has at least heard about (see picture at the end).

First of all: Cockroaches do bite, and they have powerful mandibles. This is in the paper below:

https://doi.org/10.1371/journal.pone.0141226

Many people think they won't bite because they have never handled cockroaches. In fact, cockroaches are amongst the most common insects scavenging dead bodies, and they'll pester sleeping individuals when they're starving (e.g. in crowded infested buildings or ships).

In the case of large P. americana, males are way more prone to biting than females, especially when they're flying around. I have been bit three times by these cockroaches, and it hurts. Once I was wearing latex gloves and seized a large male, and it bit me through the glove. Because of the pinch, I pulled it off with my other hand, and the glove teared open. Last time, I was bit about 1.5 year ago on the shoulder in my sleep by an adult female P. australasiae. The pinch was enough to wake me up (so I could kill the bloody roach) and left a red mark that lasted for 2 days.

There are numerous reports of cockroach bites going infected, specially around lips. Linked paper is referenced as: http://dx.doi.org/10.1590/S1413-86702006000100006

Finally, they're not poisonous neither venomous insects, as they produce no relevant toxins. However they may carry many pathogenic microbes, so laster effects from contact with cockroaches may develop.

Hope this was clear enough!


Can antimicrobial peptides be called antibiotics?

Antibiotic peptides are definitely antibiotics.  They are often referred to more specifically as peptides because the fact implies that they are less toxic and conveys some important understanding of how they work.  Not sure if they all form pores in the target cell, but that's how magainins work.


Why can't cats run longer distances like dogs?

Cats, both domestic and wild are, for the most part, ambush predators that catch their prey with bursts of speed. Lions and cheetahs do run down their prey, but not over long distances. Wolves chase their prey over long distances, sometimes for hours. This is a classic case of trade-offs. Humans have modified the behavior of domestic cats and dogs, but both still rely on the characteristics of their ancestors. You can build cat muscles with exercise, but you can't make them "dogs".


Helicos stopped shipping reagents around 2010-2011, as they couldn't compete with Illumina. For now it seems that reverse transcription -> Illumina-sequenced cDNA is so much cheaper than any other option, that's the method that is dominant.

Oxford Nanopore has discussed direct RNA profiling, but unfortunately their first product still hasn't shipped (for DNA or otherwise), and they haven't even released data, it may be a little while longer.


Quick answer: we don't really know.
As WYSIWYG said, splice sites do have a sequence signature. The image below (taken from [1]) shows the consensus for human acceptor and donor sites:

In the images above, the size of a nucleotide represents its frequency at that location. As you can see, there is a clear signal around the splice sites and this signal is used by various programs that do splice site prediction. What is not quite clear yet is how the cell recognizes these signals. Sometimes a "perfect" (identical to the consensus) splice site is ignored by the cell in preference to one that we would consider "worse". This is further complicated by the presence of various downstream and upstream signals such as splicing enhancers, silencers and structural elements (loops, hairpins etc) in the mRNA molecule.
So, to answer your question yes there are start/end markers for introns/exons but they are far more complex than the simple START and STOP codons of transcription. We know know a lot about it but we still don't fully understand the details of splicing.

References
Brent MR, Guigó R., Recent advances in gene structure prediction, Curr Opin Struct Biol. 2004 Jun;14(3):264-72.


Oxygen balence from growing plants for food

If oxygen and respiration were carbon and oxygen neutral, there wouldn't be free oxygen at all. Plants would just respire all the oxygen they produce.

The extra carbon goes into the plants themselves. It isn't just what they use for energy, it is also what they are made of.

See also this question:

Are plants really oxygen neutral?

Plants are oxygen neutral when we take into account the decomposition of the plant, i.e. take the long-term view where the carbon making up the plant gets back to being CO2.


Which species of bee or wasp are in this photo?

Looks like the family Halictidae to me. Known as a sweat bee. Maybe Lasioglossum zephyrus?


Why upper surface of leaves is more green and shiny than the lower one?

You can find two chlorophylls in most plant leaves, chlorophyll a and b. We'll use as a reference Leaf characteristics and chlorophyll concentration of Schyzolobium
parahybum and Hymenaea stilbocarpa seedlings grown in different
light regimes. The most important observation is that in shade-tolerant leaves, chlorophyll b dominates chlorophyll a. And the opposite is true of shade-intolerant leaves. I'll argue now that the portion of a given leaf that must tolerate more shade will have the darker green pigment due to the presence of more cholorphyll b, and that the side of the leaf that must tolerate lots of light will have the lighter pigment due to the presence of more chlorophyll a.

The light-tolerant side of the leaf is also shiny, and this is because of a thick waxy cuticle. The shade-tolerant side of the leaf also has a cuticle but if we follow it logically, the light-tolerant side of the leaf needs more protection from heat evaporation because it's always being hit by light.

So what I'd do, instead of thinking of the leaf as having a top or bottom, think of them as having a side that must tolerate excessive shade, and a side that must tolerate excessive light.


How far into a pregnancy is it before visible signs of it is apparent and risk of physical trauma increases

Around the second trimester.  That's an article from WedMD, which says quite a few things.  To summarize, by the end of the first trimester:

  You may be noticing some of the first physical signs of pregnancy: breasts that are sore or tingle at the slightest touch, skin that's drier or oilier than usual, and "morning sickness" -- which may or may not restrict itself to the morning hours. As many as 70% to 80% of pregnant women have it, but not feeling morning sickness doesn't mean there's anything wrong with the baby.

In the second trimester:

  Most pregnant women begin to "show" during the second trimester. You likely gained less than 5 pounds during your first trimester, but now the number on the scale is edging relentlessly upward. As your second trimester proceeds, you'll gain an average of 1 to 2 pounds per week.

The exact time and rate of "showing" can vary, including whether or not this is your first pregnancy.  By the third trimester, the infant is rapidly becoming more and more capable of surviving on its own.


How did giraffes develop their rete mirabile failsafe?

I think what leads to the confusion here is the assumption that the neck was evolved before the rete mirabile.  Giraffes evolved from creatures with shorter necks.  As evolution occurred nature was selecting for longer neck creatures (being able to eat more leaves) but at the same time creatures with longer necks had problems with blood pressure.
At this point this would also not be lethal because we are talking about animals with much shorter necks, just in some way disadvantageous to the animal.
So over time necks got bigger, blood pressure went up, and blood vessels developed that could better and better deal with the change of pressure. Rete mirabile also occur in other animals, so they are not a rare evolutionary phenomenon of giraffes.


Trees growing around objects vs pushing them away. Where is the threshold?

Since you asked for the science I'll try to give a scientific but simple explanation.
Trees (and plants) become wider and taller over time. This growth is due to cell division and cell elongation from meristematic cells (analog to stem cells in animals).
The stem (upper part of a plant) becomes wider because is it constantly creating new vascular tissue from the cambium. The cambium creates xylem to the center of the tree and phloem to the outer parts. The bark that peels off is the phloem and other tissues irrelevant for the explanation. Here you can find a good illustration.
Since the tree adds new xylem all the time the, cambium gets further away from the center of the tree.
When the tree pushes against a wire, the wire cuts and kills the phloem cells and after that the cambium cells. But the plant has mechanism to regenerate the cambium ring and that's why the tree continues to grow there. In the photo the wire is already in the xylem section.
When the tree pushes against a wall there is a barrier in the whole section. Either the wall collapses (or, more commonly seen, the sidewalk rises) or growth in that sections stops.
I saw graphs of cells having up to 3MPa of turgur pressure but the actual pressure you should check is that of the bark which can be higher or lower. It changes between plants species, sections of plants and plants itself so the best is to simply check.
I wouldn't hang a weight from a tall tree. Trees get diseases and many times you only see that they are rotten from the inside when it is too late.


What is allele-specific gene expression?

There are a few well known examples of allelic exclusion (which is what you've described):

In females (human and probably other mammals too) one of the two X-chromosomes is silenced (shut down) during embryo development. This means that some cells have one allele (from maternal X) active, while other cells have the other one (from paternal X) active. The actual mechanism behind this is quite complex, but ultimately results in the complete epigenetically-controlled prevention of gene expression from one X-chromosome. This is necessary because otherwise females would produce twice the amount of all proteins on the X-chromosome compared to males.

Another well known example relates to the genes that lead to the building of the B-cell receptors and antibodies. During maturation of the B-cells different segments of these genes are rearranged in a process call VDJ recombination. In order to make sure that the cells produce only one kind of B-cell receptor/antibody one of the two alleles for these genes is silenced after a certain rearrangement step has taken place.


What is the substance that tumors release that stimulates growth of blood vessels but suppresses its release from other tumors?

One very important signal for angiogenesis are the Vascular endothelial growth factors (VEGF)  (a small group of ~5 similar proteins). They generally promote generation of new blood vessels & migration of these towards the source of VEGF expression.
Blocking VEGF signalling (mostly be blocking the receptors with antibodies) has been a pretty good strategy in cancer treatment, since tumors can't grow over a certain size without blood supply by new grown vessels.

However, I am not aware of any blood-vessel specific signalling mechanism that stops it's own expression at a secondary site. (This may be possible though, especially for specific signals)


It seems like your question might contain two separate and linked issues, both of which are perhaps equally confusing and equally interesting. They're both really discussion questions in a sense, but they've also both been dealt with in the literature in thoughtful ways, so here's a stab at an "answer".

Issue One: how does your species concept deal with polymorphism?

This may depend on which species concept you're using. And, to some extent, the choice of which species concept you use depends on what kind of organism you're dealing with (for instance, organisms that reproduce asexually have a whole different set of issues and challenge several species concepts).

Various papers by Kevin de Queiroz deal very well with species concepts. In 'The General Lineage Concept of Species'  (which is also summarized on this page), he argues that although there are many different species concepts that can be better applied to different situations, they all share the basic tenet of defining a "segment of a population-level lineage". In other words, each concept is attempting to put a continuum into slightly different categorical bins, but they all recognize the existence of the same continuum (the lineage). (Also see his 'Species Concepts and Species Delimitation'.)

I think most species concepts have no trouble dealing with polymorphism because the different morphs are all part of the same lineage, that is, "a series of entities forming a single line of direct ancestry and descent" (de Queiroz 1999).

Issue Two: how does your concept of the individual organism deal with colonialism?

In 'Does Biology Need an Organism Concept?'  Pepper and Herron make a similar point to that of de Queiroz. They argue that multiple definitions (concepts) exist, and that these concepts all attempt to categorically bin what is in fact a continuum. Like de Quieroz, they argue that most definitions recognize the same underlying continuum, and that the difference is in the categorical bins.

In the case of the organism concept, this continuum is based on two criteria: increasing genetic homogeneity, and increasing physiological integration.

So, for instance you could have two organism concepts (in the picture below, lighter yellow and darker yellow) that agree that Physalia falls in the same location along these axes, but disagree on exactly where to draw the boundary between their "multiple organisms / colony" zone (yellow), and their "individual organism" zone (white).

I'll finally get to my point, paraphrasing both de Queiroz and Pepper and Herron. For both concepts of the species and of the organism, arguing about whether one concept is better than another is endless (especially on a site that aims at answers rather than discussion). However, recognizing that there are different concepts, understanding that what these concepts do is to bin the same continuum in different ways, and being clear about which concept you decide to use is very useful.


Why do Lapidaria margaretae look like stones?

"Teleology is like a mistress to a biologist: he cannot live without her but he's unwilling to be seen with her in public." - J.B.S. Haldane (1892 - 1964)

I can't tell you why Lapidaria margaretae looks like 'stones'. But I can deduce something from the way this plant looks.

First and foremost, I can say this plant probably evolved in an arid region, possibly a desert (less than 10 inches of water per year), because it is a succulent, with a shape that comes pretty close to minimizing it's surface to volume area (decreased evaporation, decreased transpiration). Seeing as it's a dwarf and shaped as it is, I might hazard that it's windy and sandy where this plant evolved, also because of it's shape - low to the ground, sturdy, low surface area, able to resist the wind. Finally, the light color of the plant suggests a lot of bright sun (reflects sunlight more than some darker colors).

None of that is foolproof, but in this case, it turns out to be right; the plant comes from southern Namibia, and is commonly called the "Karoo rose".

This is one image of the Karoo region:

Stones come in all kinds of shapes and sizes, also influenced by water, wind and other environmental influences. That this plant looks like stones is mostly coincidental.


How do viruses provide selective advantage

See the instances of "selective advantage / pressure" from the source provided by Jonathan, emphasis mine:

Persistent infection with HPV leads to an environment of genomic instability and local immune suppression, which can lead to both the accumulation of genomic alterations in the host cell, as well as to the integration of the viral genome into the host genome. When these additional alterations provide a selective growth advantage to the cell, carcinogenesis may ensue.

Furthermore, the integrated viral transcripts confer stronger transforming capacity than those derived from episomes, due to longer half-life of transcripts (32). This promotes immortalization and transformation of these cells and provides a selective growth advantage (3, 8, 30, 33). Integration may, however, confer a selective growth advantage to the host cells not only through its effects on the viral genome (i.e., enhanced/deregulated expression of viral oncoproteins), but also through its effects on the host genome (i.e., by affecting key cellular genes).

Several mechanisms by which HPV integration may confer a selective advantage have been described (Fig. 3).

This environment is also amenable to accumulation of genetic alterations and viral integration, and subsequent tumor formation. Integration affects both the viral genome and the host genome, likely conferring additional neoplastic selective pressure, by one or more of the following mechanisms: (i) enhanced expression of viral oncoproteins, (ii) alteration of critical cellular genes (leading to increased expression of oncogenic proteins, decreased expression of tumor suppressor proteins, altered DNA repair mechanisms, or modulation of the immune system), and (iii) changes in global promoter methylation and transcription.

In biology, "selection" often refers to natural selection -- in short, genetic diversity in a population manifests as different traits in individuals, which result in differences in relative fitness in a given environment that, through time, result in evolution.  The quoted excerpts refer not to the environment acting on different traits but rather to the (potential) enhanced growth characteristics of HPV-infected cells, relative to non-infected cells.  So, the use of "selective" here is misleading.  Yes, viral integration may lead to enhanced growth of a cell population by disruption of certain cell cycle checkpoint genes, but the organism on the whole will certainly be less fit when that unrestricted growth leads to cancer.
In my opinion, the text could read "growth advantage" or "enhanced growth" in all instances and do away with "selective" entirely.


What is the largest animal that has no hard parts?

Please forgive me for plagiarizing the open source wikipedia, here are some species of large soft bodied animals. I honestly don't think I could re-write this more clearly for any logical reason:

Citation:

The lion's mane jellyfish (Cyanea capillata) is the largest cnidaria species, of the class Scyphozoa. The largest known specimen of this giant, found washed up on the shore of Massachusetts Bay in 1870, had a bell diameter of 2.5 m (8.2 ft), a weight of 150 kg (330 lb). The tentacles of this specimens were as long as 37 m (121 ft) and were projected to have a tentacular spread of about 75 m (246 ft) making it one of the longest extant animals

The largest roundworm, Placentonema gigantissima,[174] is a parasite found in the placentas of sperm whales which can reach up to 9 m (30 ft) in length

The largest nemertean is the bootlace worm, Lineus longissimus. A specimen found washed ashore on a beach in St. Andrews, Scotland in 1864 was recorded at a length of 55 m (180 ft).[183]

There are a couple of animals that are of interest but they are not technically soft bodied:

The colossal squid (Mesonychoteuthis hamiltoni) is projected to be the largest invertebrate. Current estimates put its maximum size at 12 to 14 m (39 to 46 ft) long and 750 kg (1,650 lb),[185] based on analysis of smaller specimens. In 2007, authorities in New Zealand announced the capture of the largest known colossal squid specimen. It was initially thought to be 10 m (33 ft) and 450 kg (990 lb). It was later measured at 4.2 m (14 ft) long and 495 kg (1,091 lb) in weight

The largest known species of sea sponge is the giant barrel sponge, Xestospongia muta. These massively built sponges can reach 2.4 m (8 ft) in height, 80 kg and can be of about the same number of feet across at the thickest part of the "body". Some of these creatures have been estimated to be over 2,400 years of age.

https://en.wikipedia.org/wiki/Largest_organisms#Invertebrates


At which end does polymerization of microtubules occur?

From my Campbell's Biology textbook (Ninth Edition):

  Because of the orientation of tubulin dimers, the two ends of a microtubule are slightly different. One end can accumulate or release tubulin dimers at a much higher rate than the other, thus growing and shrinking significantly during cellular activities. (This is called the "plus end", not because it can only add tubulin proteins but because it's the end where both "on" and "off" rates are much higher.)

So in summary: polymerization and depolymerization occur on both the + and - ends. The "+" and "-" merely designate the speed/efficiency of polymerization and depolymerization.


What is "integrated spindle activity" in plain English?

Integrated spindle activity is just this paper's measure of the intensity of spindles. It isn't really a term of art, there is no defined thing "integrated spindle activity," it is just a description for their method of quantifying spindles, or in other words operationalizing their definition of spindle activity.

Spindles are brief bouts of (relatively) high-frequency oscillatory activity that occur occasionally during sleep - often they are called "sleep spindles."

Figure 1 of the paper you link shows their method for detecting and measuring these spindles.

Ferrarelli, F., Huber, R., Peterson, M. J., Massimini, M., Murphy, M., Riedner, B. A., ... & Tononi, G. (2007). Reduced sleep spindle activity in schizophrenia patients. American Journal of Psychiatry, 164(3), 483-492.

In summary, the top trace is a raw EEG trace. Spindles are present in this trace, but the authors want to quantify spindle activity in some way. By filtering between 12-15Hz, the spindles become more obvious (middle): they are the high-amplitude things bracketed by vertical lines.

On the bottom, they have rectified and smoothed the signal to approximate the amplitude of the spindles (that is, they aren't interested in the area under the curve in the middle plot, which has negative and positive going components, they just want a measure of the whole event).

They are defining the integrated spindle activity as the integral (i.e., the area under the curve, just like in calculus) of bouts of activity that exceed some threshold, indicated by the area shaded blue.

In summary, to answer your question, there isn't really a better or simpler English way to say "integrated spindle activity" without losing information for the reader - they are indeed referring to mathematical integration. You could say something like "total spindle activity" but then it is much less clear how exactly you are quantifying spindle activity. Probably the best plain English description of integration is the 'area under the curve' of a function or measurement, though this isn't a perfect mathematical description.

As someone who is familiar with general methods for analyzing electrophysiological data, it was pretty clear to me what they meant by "integrated spindle activity" before opening the paper - this is a fairly common way to report the amplitude of oscillatory activity, because it captures both average amplitude and duration in a sensible way.


Does Usnea (Old Mans Beard) have negative effects on the respiratory system?

According to the Institute for Traditional Medicine and the Gale Encyclopedia of Alternative Medicine:

Usnea (aka Songluo or "Old Man's Beard") is a fruiticose lichen (not a fungus).
Used in traditional medicine worldwide, including historically in China, Europe and by native Americans, as well as globally today.

"Uses": topical antiseptic; therapuetic agent; medicinal herb; anti-cancer
It has traditionally been used in the treatment of bronchitis, in the treatment of tuberculosis, to ease coughing, to cleanse lungs and as an expectorant (i.e, to resolve phlegm).

Contains a secondary metabolite, usnic acid, which is claimed to be an effective inhibitor of gram positive bacteria-including tuberculosis, staphylococcus, streptococcus, and pneumococcus

So Usnea is often used for the lungs. In fact, today, supporters of traditional medicine still use it rather regularly as an expectorant. I could find no sources that claimed that this was unsafe or had any negative effects on the respiratory system. I would think that if you were to inhale any usnea, its effects would simply rid your body of any particulates during expectoration.

However, a number of sources (e.g., see Sanchez
et al., 2006, here , here and here) mention that usneic acid can cause liver damage (and failure).

Disclaimer: I did not find any reputable source acknowledging usnea to be effective at treating any of the aforementioned ailments. Use at your own risk.

Citations

Sanchez, W.T., Maple, T.J., Burgart, L.J. & Kamath, P.S. (2006). Usnic acidhepatotoxicity. Mayo Clinic Proceedings 81: 541-544


Why are fatty acids synthesized in two carbon units?

The answer to this question lies in the chemistry of fatty acid synthesis — specifically the chemical energetics of the reactions. For those new to the biochemistry there is a basic concept that must be understood: that a reaction can occur spontaneously only if it involves a negative change in Gibbs Free Energy. This is discussed, among other places, in my answer to another question.
As regards long-chain fatty acid synthesis, the answer can be found in Section 22.4 of Berg et al. Biochemistry some of which I summarize here.
The reactants in fatty acid synthesis are linked to a protein during the cycle of reactions — acyl-carrier protein, ACP:
malonyl CoA + ACP ⇌ malonyl ACP + CoA
The first condensation reaction of a malonyl constituent in the elongation cycle of reactions is shown below.

The key point to note is that in this step the malonyl carboxylic acid
group is released as carbon dioxide with a substantial decrease in
free energy that makes the reaction favourable. Without it the
reaction would not proceed, which is why the synthesis of acetoacetyl
ACP from two molecules of acetyl ACP does not occur.

It is worth adding that this free energy is ultimately derived from ATP, which is needed to drive the reaction in which malonyl CoA is formed from acetyl CoA and carbon dioxide.