If mutations are random, why do antibiotics 'cause' resistance?

There are many models for mutation accumulation (Liò and Goldman, 1998). The simplest model (Jukes and Cantor, 1969) assumes mutations to be a Poisson process. With a given mutation rate, the number of mutations accumulated will follow the Poisson distribution.

This basic model has been extended to include non-uniform mutation rate across the genome and different rates for different kinds of mutations. You can check out the link and the works it cites to have a better idea.

However, the answer to your question does not pertain to how mutations happen. Although there is some evidence that some antibiotic treatment can actually increase mutation rate (Long et al, 2016; Meouche and Dunlop, 2017, Windels et al., 2019), the main principle pertains to selection and not actually the mutations. Improper antibiotic treatment can lead to some cells with moderate resistance to survive, which in turn can evolve strong resistance. Here, we assume that the infecting bacterial pool already has enough variation (or develops during infection) some little resistance. Moreover, there is another phenomenon called persistence (ability to survive antibiotic, Brauner et al., 2016). Windels et al (2019) report that persistence can increase resistance.


Help explain multi alleles in terms of actual genetic code

I understand that someones genetic makeup at an allele is usually
  denoted as (AA,Aa,aa).

No. That's what you learn in high school, because it's easy, and because it's what Mendel worked out for the 7 traits he studied in pea plants.  Real life is a lot more complex.  Most phenotypic differences cannot be explained in terms of exactly two alleles, one of which is classically dominant to the other.

  That means that instead of an A-T pair you get a C-G pair on none, 1
  or 2 copies.

Not necessarily.  Two alleles might differ at many many points in their sequence.

And you seem to be a bit confused about how people write out DNA sequence.  Even though DNA is a double helix, when we talk about what the sequence is, we refer only to one strand, like this

GAGCCATGGGGCGCCATGTTGCCACCAGCTGCCACGTGGCCTGGCTTTTGGTGCTGATCT

A mutation might turn that last T into an A, but we don't say "oh, nothing happened, it's still an A-T pair" because it matters which strand has which letter.

  Now, what exactly happens when you have a tri-allele (as in blood
  type).

Well, blood type is more complicated that just ABO...but here's a pretty old paper with some helpful details

http://www.ncbi.nlm.nih.gov/pubmed/2333095

"Here we present a molecular basis for the ABO genotypes. The A and B genes differ in a few single-base substitutions, changing four amino-acid residues that may cause differences in A and B transferase specificity.  A critical single-base deletion was found in the O gene, which results in an entirely different, inactive protein incapable of modifying the H antigen."


From Sarah Hrdy (email):

A “fairy smile” is a reflexive smile that spontaneously and briefly flickers  across the face of a newborn baby.  Some years ago, Tetsoro Matsuzawa discovered that these occur even before birth, en utero in chimpanzees! (Long story, but Tetsoro was using laser probe with a camera on a highly habituated pregnant chimpanzee female, accustomed to working with him to learn this). So of course do humans en utero.  After birth, one may see a reflexive “smile” flicker across the face of a baby even while sleeping —no outside stimulus or engagement with another person needed, tho may occur in response to a sound. "Fairy smiles" are different from “social smiles” that emerge later, and occur in response to someone else speaking to or smiling at them, etc.

I grew up in the southern part of the U.S. and people around me used the term,  but now that you ask, am curious to know where this term to describe “reflexive, non-social smiles” in newborn babies comes from.


Chromosomal pair possible in metaphase - I

The correct answer is 8 as given by the formula 2n , where n is the number of chromosome in haploid cell.

Explanation:

During prophase 1, synapsis take place as a result of which bivalents are formed. Now each bivalent can arrange itself in two possible manner ( known as independent orientation). Since in this question there are 6 chromosomes which means 3 bivalents, the possible number of arrangement is 2 × 2 × 2 = 8

The photo here explain independent orientation in a cell having two chromosome pair. You can work this out for 3 chromosomal pair as well.

Your doubt:

As far as I can understand your doubt is that arrangement one is actually same as arrangement third ( with reference to the photo). Well, it might seem like this but if you look carefully the two non homologous chromosomes are arranged in different manner in them .. relative to each other and the homologous partner. And hence the whole arrangement is considered as different arrangements and not the same.

Thus, for 3 chromosomal pair, there are 8 possible arrangement of homologous chromosomes which could occur during metaphase-I.


Original vs. Adjusted

Adobe Camera Raw Temperature Adjustment +30 / Tint Adjustment +3

The fox has black skin and fur. The blue is just a problem with the White Balance of the photograph. See Adjustments made above.

This is similar to the Blue Dress / White Dress Meme this year.

  I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue. – Imprisoned Rhesus

The reason the legs look Bluer than the Nose is that the nose is mostly black with no white and the front part is in shadow. The top part, which is reflecting some of the sky appears blue in the original.

The reason the legs look more blue is

They are not in shadow
There is a good amount of white fur mixed in with the black

The white fur will look far bluer when the white balance is off and will trick your eyes into seeing the black as blue.


Whatever the diet, the food intake contains macronutrients: carbohydrate, fat and protein. When they are metabolised all of these molecules will end up, for the most part, as carbon dioxide, water, and ammonia, unless they are incorporated into components of the body.

These waste products are, of course, lost via breathing, and via the urine. That's where the "missing mass" goes.

A related question is here.


DNA complementarity against reverse complementarity

I agree that the definitions can be somewhat confusing when first encountered.
Each nucleotide has a complement A-T, C-G. But the DNA strand are reverse-complementary because when aligned from 5'->3' they are not (necessarily) complementary.
For example:
DNA strand 5'-ATCCGG-3'
complement 3'-TAGGCC-5'
reverse    5'-CCGGAT-3'
Since we want to write all sequences in the same direction we must call the strand reverse-complementary


How can a child be blood type AB, if both of the parents are blood type A?

Blood type A has a variety of subtypes, which have different features in terms of their antigens. This leads to people with different A subtypes having somewhat different kinds of antibodies in their blood (for a technical article, see here). I don't know the population prevalences well, but I read somewhere (can't find it now) that as many as 20% of blood type A people actually have one of the subtypes. And these are themselves going through their own mutations. It is possible that you have an A subtype of some kind.

Testing blood types usually consists of testing which antigens and antibodies are present in your blood (see e.g. here). So if you have some kind of A subtype that didn't fit well into the blood test's expectations, you might have shown up as AB. I'm not a hematologist or physician, so I'm not sure how plausible that is.

But if you are really interested, you might consider getting a DNA test that will identify which type/sub-type you have, as this will add a different source of information on top of the standard blood test. In the jargon, the standard blood test is for "phenotype" (what are your blood cells actually doing), whereas DNA tests are for "genotype" (what is your DNA sequence). Often genotype and phenotype have less to do with each other than you might expect, or they don't fit in all that well with the cut-and-dried tests. In particular, a lot of medically underserved populations have variation that isn't really accounted for by standard medical typology.

Hope that helps.


Why is glycerol kinase absent from adipocytes but present in the liver?

The short answer to this question is given in the Wikipedia article on glycerol kinase:

  Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation. This glycerol is instead shuttled to the liver via the blood where it is: phosphorylated by glycerol kinase to glycerol phosphate and/or converted to dihydroxyacetone phosphate which can participate in [glycolysis or] gluconeogenesis.

[My de-emphasis of glycolysis]

To understand this requires one to consider the different functions of liver and adipose tissue and how they should respond to the fed and fasted state. Then one can appreciate that the differences in enzyme complement are one of the ways by which this is achieved. (The other is their differential responses to hormones.)

The role of the adipose tissue is to store fat (triglycerides) in the fed state and make it available for the other tissues in the body in the fasted state.

The role of the liver is to divert metabolism to the synthesis of fat in the fed state (at the appropriate stage) and to ensure that there is a supply of glucose in the fasted state for those tissues that depend on it (brain, erythrocytes) or a supply of ketone bodies for the brain.

The substrates for triglyceride synthesis are L-glycerol phosphate and fatty acids. There are two enzymes that can catalyse its production, glycerokinase (glycerol kinase) in the liver and glycerol 3-phosphate dehydrogenase in both liver and adipose tissue, as shown in my diagram below:

Fed State

The liver has surplus glucose so it can switch to fatty acid production from acetyl CoA (from pyruvate) and generate L-glycerol phosphate from the dihydroxyacetone phosphate intermediate of glycolysis, catalysed by glycerol 3-P dehydrogenase. This allows the synthesis of triglyceride, which is exported as lipoprotein.

When the triglyceride reaches the adipose tissue it is broken down to fatty acids and glycerol by the hormone-sensitive lipase. The glycerol cannot be used by the adipose tissue, but adipose tissue can synthesize L-glycerol phosphate itself in the same way as liver as there is glucose available for glycolysis in the adipose tissue. Hence the triglyceride can be resynthesized and stored.

Fasted State

The hormone of starvation, glucagon, initiates the breakdown of triglyceride in the adipose tissue. As already stated, the glycerol produced cannot be used to synthesize L-glycerol phosphate as the tissue lacks phosphoglycerate kinase. In starvation uptake of glucose is prevented hormonally, so that there is no glucose for glycolysis and hence no hydroxyacetone phosphate as a source of L-glycerol phosphate. Hence the fatty acids cannot be re-esterified and are released into the blood for other tissues, i.e. the response of the adipose tissue to starvation is that required.

The glycerol diffuses to the liver where it can be converted to L-glycerol phosphate because of the presence of glycerol kinase. What is the fate of this? It is not converted into triglyceride, it is converted to dihydroxyacetone phosphate by the reverse of the reaction shown. This is not glycolysed, but converted to glucose by gluconeogenesis, the enzymes for which are present in the liver. The glucose is released into the blood where it can be utilized by the brain, i.e. the response of the liver to starvation is that required.

References

This answer is based on lectures I delivered to undergraduates some years ago, which were drawn from various sources. The problem is that most biochemical texts tend to be organism-agnostic, and any discussion of mammalian tissues tends to be limited. Thus, I can’t find much useful to refer to in Berg et al. on line, except for support in section 16.3 for my assertion that glycerol returned to the liver in starvation is used for gluconeogenesis. I’ll update this later if I find anything more useful.


Which strains of C. diphteria are causing Diphteria toxin?

Real simple: Beta!  Often called "phage beta" b-prophage is a more modern way to write it.  I knew that one off the top of my head, but I like to refer the general public interested in bacteriology to Tadar's online text.

It's nicely done, and I wish that it had been around when I was studying bacteriology.

Specific to your question:

  Hence, Corynebacterium diphtheriae can only produce the toxin
  responsible for the disease if it carries a temperate virus called
  phage beta. Only lysogenized streptococci  produce the erythrogenic
  toxin (pyrogenic exotoxin) which causes the skin rash of scarlet
  fever; and some  botulinum toxins are synthesized only by lysogenized
  strains of C. botulinum.


When consuming carbohydrates and fats together, why are the fats caloric?

To expand on my comments:

Just like you mentioned in your question, carbohydrates (mostly glucose) is used as the primary source of energy when available to satisfy metabolic needs in human cells, however lipids and even proteins will be used if required, in order to produce energy. Since all these biomolecules (carbs, lipids and proteins) can actually be used to sustain the metabolic activity of cells, that means all of them store energy to a greater or lesser extent (which we can quantify in a practical way as food calories). Other things that we eat or drink such as vitamins, cofactors, water, etc. are not accounted for in the calorie count because they can't be broken down to produce energy for metabolism.

Dietary carbohydrates are easily digested into smaller blocks (mostly glucose) and absorbed directly into the bloodstream, afterwards glucose is taken rapidly from the bloodstream by human cells and processed via glycolysis and lactic acid fermentation or the citric acid cycle (all these are metabolic pathways for glucose in humans). Each gram consumed of carbs yields approximately 4 calories of energy.

Lipids on the other hand undergo a more complex process of usage after their slower digestion compared to carbs since after their absorption they have to be transported in special molecules across the lymph, then into the bloodstream and then they can be taken by various kinds of cells. Considering just this, we can start seeing why lipids aren't a fast source of energy (they take long to be available as potential energy sources). Furthermore, the main destination of dietary lipids is the adipose tissue which constitutes a special tissue in which fatty acids can be stored for latter usage. Fatty acids not being used immediately to provide metabolic energy doesn't mean they lose their stored energy (doesn't mean they have no caloric intake value), its just "quiescent" for when its needed (when exercising or when fasting for example).

Each gram of consumed fat yields approximately 9 calories of energy, this quantity is higher compared to that of glucose because the metabolic pathway that breaks down fatty acids (beta-oxidation) in combination with the citric acid cycle produces more metabolic energy (ATP) compared to glycolysis in combination with the same citric acid cycle. However such amounts of energy are not usually required in rest.

It is important to mention that glucose can also be stored in the form of glycogen or even fat since it will be converted to these molecules if there is more glucose available compared to what the cell needs in a given moment. This glucose converted to glycogen or fat also has to be accounted for in the calorie count because its still a potential energy source (just not used right now).

References:

Dietary Carbohydrates - National Agricultural Library

Dietary Lipids - National Agricultural Library

Insights into digestion and absorption of major nutrients in humans - Goodman, B. E.

Food calories per gram of biomolecule - National Agricultural Library


What makes synaptic vesicle release probabilistic?

From the source you provided, the answers seem to be outlined well from the authors' sentence that states:

  The Pr [release probability] of SVs [synaptic vesicles] at the AZ [active zone] is set by a complex interplay of different presynaptic properties including the availability of release-ready SVs, the location of the SVs relative to the voltage-gated calcium channels (VGCCs) at the AZ, the magnitude of calcium influx upon arrival of the AP, the buffering of calcium ions as well as the identity and sensitivity of the calcium sensor. These properties are not only interconnected, but can also be regulated dynamically to match the requirements of activity patterns mediated by the synapse.

Below, I use an analogy to provide a framework for understanding how these factors come together to mediate Pr as a whole, but you can read a scientific review on that here:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059705/.  However, the actual molecular/proteinaceous machinery that underlie these phenomena are pretty well explained in your source (particularly in the sections "SV Proteins Regulating Pr" and "Recruitment of Calcium Channels to the AZ").

To use an analogy, think about the presynatpic terminal as the 100 meter dash at the Olympics.  The track only has so much space, so not everyone can run the race at the same time.  That's why there are multiple heats of the race.  The first point from the authors is availability of release-ready SVs, which your source discusses as part of the readily releasable pool (RRP) of vesicles.  Think of those SVs as the runners in a heat, lined up in the start position waiting for the gun to go off.  Their equipment is ready (starting blocks set, shoes tied, proper uniform and tag on, etc.). They're all in position, awaiting the signal, and they will take off as soon as they get that signal.  Therefore, the more SVs you have in that position with equipment/molecular machinery prepared to "go" in response to a signal, the more likely you are to have SV release.  The second point is location of the SVs relative to VGCCs.  In our example, this would be equivalent to having a lane closer to the person shooting the start pistol.  The closer a runner is to that, the more likely they are to hear the pistol go off and start the race.  Conversely if the person with the start pistol is at the finish line, it's possible less runners will hear it go off and miss their cue to start running. Since SVs require calcium to undergo membrane fusion and release their contents into the extracellular space, the closer these vesicles are to calcium channels the more likely they are to get that necessary substance for fusion/release. Third, the magnitude of calcium influx upon arrival of the AP, which we can think of as the volume of the start pistol.  If the start pistol is loud (a high volume of calcium comes into the cell), it's more likely the runners will hear the shot go off and start running (SVs will fuse to the membrane).  However, a very quiet start pistol (low influx of calcium) is less likely to be heard by the runners (less likely to bind SV proteins important for fusion). Lastly, they list buffering of calcium ions as well as the identity of the calcium sensor.  What's important to remember about the process of SV fusion is that it requires free calcium that can bind to the necessary vesicle proteins, so any other proteins (calmodulin, calbindin, the list goes on forever) that bind free calcium and make it unavailable to the vesicle will decrease the likelihood of successful vesicle fusion and neurotransmitter release.  This would be like someone giving the runners ear plugs before the race, which dampens the sound of the start pistol and decreases the likelihood of runners hearing their cue to start.  Again, there are nuances not covered in this analogy, but I'd recommend going through your source again with this framework in mind to pick up where those nuances come in.


What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?

Mendelian segregation is defined on the Nature site, and I quote:

The Principle of Segregation describes how pairs of gene variants are separated into reproductive cells. The segregation of gene variants, called alleles, and their corresponding traits was first observed by Gregor Mendel in 1865. Mendel was studying genetics by performing mating crosses in pea plants. He crossed two heterozygous pea plants, which means that each plant had two different alleles at a particular genetic position He discovered that the traits in the offspring of his crosses did not always match the traits in the parental plants. This meant that the pair of alleles encoding the traits in each parental plant had separated or segregated from one another during the formation of the reproductive cells. [...] We now know that the segregation of genes occurs during meiosis in eukaryotes, which is a process that produces reproductive cells called gametes.

Likewise, the Hardy-Weinberg equilibrium is explained on Nature's website:

The Hardy-Weinberg equilibrium is a principle stating that the genetic variation in a population will remain constant from one generation to the next in the absence of disturbing factors.

So in case of Mendell's experiments, his pea plants showed no disturbance and quite perfect ratios, for example 3:1 green:yellow seed pods:

The Nature site continues on the Hardy-Weinberg principle:

When mating is random in a large population with no disruptive circumstances, the law predicts that both genotype and allele frequencies will remain constant because they are in equilibrium.
The Hardy-Weinberg equilibrium can be disturbed by a number of forces, including mutations, natural selection, nonrandom mating, genetic drift, and gene flow. [...]. This occurs because certain alleles help or harm the reproductive success of the organisms that carry them. [...]. Because [...] of these disruptive forces [...] the Hardy-Weinberg equilibrium rarely applies in reality. Therefore, the Hardy-Weinberg equilibrium describes an idealized state [...].

So to get back to your question on the relation between Mendelian segregation and the Hardy-Weinberg equilibrium: The Hardy-Weinberg equilibrium is necessary for the Mendelian segregation to become phenotypically apparent. So in Mendell's controlled experiments the 3:1 green:yellow pods became nicely apparent as both phenotypes had equal chance of survival.
And to continue the seed pod example, if there were to be introduced a disturbing factor, such as a pest that wrecks havoc in plants with yellow pods, but not in green, the Hardy-Weinberg equilibrium (i.e., Mendell's 3:1 green:yellow) would be disturbed and Mendelian segregation would become less apparent as aberrant phenotpyic ratios would emerge (>3 : <1).


How to determine the primary Uniprot accession number from a list of accession numbers?

I think there is an issue with the terminology. The "primary" accession number, is the first accession number in cases where an entry has more than one accession number, as described in http://www.uniprot.org/help/accession_numbers:

  Entries can have more than one accession number. This can be due to
  two distinct mechanisms:

a) When two or more entries are merged, the accession numbers from all entries are kept. The first accession number is referred to as the

  ‘Primary (citable) accession number’, while the others are referred to
  as ‘Secondary accession numbers’. These are listed in alphanumerical
  order.

b) If an existing entry is split into two or more entries (‘demerged’), new ‘primary’ accession numbers are attributed to all

  the split entries while all original accession numbers are retained as
  ‘secondary’ accession numbers.

  Example: P29358 which has been ‘demerged’ into P68250 and P68251.

Both reviewed and unreviewed entries can have primary accession numbers.

What you probably mean, as previous posters understood, are accession numbers of reviewed entries as opposed to unreviewed ones.

In that case, you can indeed add "reviewed:yes" to your query, e.g. when you are using the UniProt ID mapping, http://www.uniprot.org/help/uploadlists


Explaining the simpson's diversity index

That's an estimator for Simpson index,
$$ \sum_i p_i^2 $$
where $p_i$ is the probability that $i$-th species is sampled.
This is sum of the probability that two independent samples are from the same species.
There are multiple ways of estimating this quantity from observations $n_i$.

When $n_i$ is small,
$$\hat{p} = \frac{n_i}{N}$$
is unbiased but has high variance, and plugging it in $\hat{p}$ to the definition would also have high variance. (Note that this is equivalent to sampling with replacement.)

If one uses sampling without replacement formula,
$$\hat{p^2} = \frac{n_i}{N} \cdot \frac{n_i-1}{N-1}$$
then, the resulting estimator is
$$ \sum_i  \frac{n_i \cdot (n_i - 1)}{N \cdot (N - 1)}$$

Note that both estimators converge to Simpson index for $N \to \infty$.
But of course, there aren't infinite number of samples, usually.


Yes, there are many early examples of ceratopsians before Triceratops. The oldest clear member of the lineage is Liaoceratops: "the oldest ceratopsian ever found ... was about the size of a large dog. It had a blunt beak and a dainty neck frill. ... Liaoceratops was a puny forebear of the feisty Triceratops. Size, horns and spectacular frills came later in ceratopsian evolution."  Here's a reconstruction:

Protoceratops is very well known, and is a pretty obvious intermediate between famous ceratopsians like Triceratops and early ones like Liaceratops:

This cladogram shows a number of steps in ceratopsian evolution (right side of the diagram):

Note the steps it describes: Starting with early forms that have a vaguely frill-like structure, we see added: Rostral bone with "horns" that are barely visible; Frill, with jugal "horns"; Enlarged frill and skull; Postorbital horns; Nasal horn.


Why can't humans use dietary citric or acetic acid as a primary source of energy?

Why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?

No reason it can't. Citric Acid technically contains 2.5kcal/g -- which is almost half of protein/carbohydrates, almost a third of alcohol, and a fourth of fat.

So if someone needed 2500kcal/day, they'd need 1kg of straight Citric Acid. There's about 47g/L of Citric Acid in citrus fruit juice. So if you wanted it all from "natural" sources you'd need to drink 21.3L of your favorite citrus juice, though that's a bit comical.

In terms of being more efficient since Citric Acid bypasses the first two enzymatic reactions,the part where Citric Acid is processed into alpha-ketoglutarate via Isocitrate Dehydrogenase is the rate limiting step of the entire cycle. You wouldn't be saving any time by flooding your system just before the bottleneck.

Interesting question, though!


When did the most recent common ancestor of all living domestic dogs live?

From the wikipedia article you linked:

  The origin of the domestic dog (Canis lupus familiaris or Canis familiaris) is not clear. Whole genome sequencing indicates that the dog, the gray wolf, and the extinct Taymyr wolf diverged at around the same time 27,000–40,000 years before present.

They cite Skoglund et al. 2015.

It seems that divergence between the grey wolf and the dog started at Taymyr (northern Russia) about 27,000–40,000 years ago. Therefore, the MRCA of all dogs and grey wolf today would have lived about 27,000–40,000 years ago. Tito et al. 2013 estimated canids fossils found in Europe were 39,000 years old. We currently don't have a better accuracy and we are not able to date the MRCA of all dogs with more accuracy than the MRCA of grey wolves and dogs.


What is this black shelled insect found in Western Arkansas?

Looks like the larvae of a carrion or burrowing beetle (i.e. some beetle species of the family Silphidae). Not sure on the species yet.

Wikipedia provides a good introduction to this family of insects.

Here's a picture:

And another:
Silphidae larvae

Did you see (or more likely smell) any dead carcasses around your property?


Validated Protein-Protein interaction database for cancer

One of the most popular databases of PPI data is STRING. It is not only for cancer though, but since many research is done in the field of cancer, you will find a lot of data derived from cancer research.


Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?

1)

a. Decorticate posturing means rubrospinal tract is the dominant output to the motor neurons of the body... maybe dominant is the wrong word, I am not all that knowledgable on this subject, but it is certainly altering the standard reticulospinal tract based extensor posturing.

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

It is responsible for the strange flexion of upper limbs (aka arms). I say strange because when you think coma you think extension, not flexion. The lower limbs (aka legs), as always is extensor. Why the upper limb but not the lower limb? The red nucleus may play an additional role in controlling muscles of the shoulder and upper arm via projections of its magnocellular part.

b. In decerebrate posturing the rubrospinal tract is also cut, since the lesion is below the red nucleus. In this scenario the reticular activating system (aka reticulospinal tract) is the dominant output to the motor neurons of the body. Here you get the classic extensor pose, for both upper and lower limbs...

The point is: Rubrospinal tract was what you were missing. The red nucleus is the specific part of the basal ganglia that is involved...

2)
the difference between spasticity vs rigidity:

spasticity is an increased resistance to the passive movement of a
joint due to abnormally high muscle tone (hypertonus) which varies
with the amplitude and speed of displacement of a joint.
rigidity is an increased resistance to the passive movement of a joint which is
constant throughout the range of joint displacement and not related
to the speed of joint movement.

your supposed to test this out on patients to get a feel for what's the difference.

spaciticity is the case for upper motor neurons lesions (ex. stroke), since the spinal reflexes are not being inhibited from above...

an example of rigidity in neurology is Parkinson's disease, which is the loss of the substantial nigra, which like the red nucleus is also in the midbrain... while the the substantial nigra and basal ganglia loop do influence the motor control of the body... they are not upper motor neurons. Upper motor neuron is specific to the corticospianl tract, it is the neuron going from cortex to anterior horn of spinal cord. Basal ganglia does influence the motor cortex but it isn't part of the corticospinal tract, hence not an upper motor neuron lesion.

3)
Role of muscle spindles in spasticity from upper motor neuron lesions:

I am using this website for this part of my answer:

http://www.d.umn.edu
it's from university of minnisota, which is funny because their acronym is UMN

  high resistance to stretch occurs when the spindles are overactive
  (usually due to high rate of gamma motor neuron discharge) -->
  HYPERTONIC (SPASTIC)

  removing inhibitory inputs to the gamma motor
  neurons increases their discharge rate, and increases spindle output

  this can happen when there is an UPPER MOTOR NEURON lesion

It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes are intact so the a/g-motor neurons should relax, since only UMN damaged and not any part of the reflex arc. I seem to be missing something here.

I'm calling for back up, someone please help!


Does every gland type have stem cells for regeneration?

Stem cells are not all 'unipotent' - they cannot necessarily differentiate into any type of cell. For instance, resident stem cells in tissues such as muscle - myo-satellite cells - are partially differentiated and during cell division one daughter differentiates further to become a myocyte (for example), and the other daughter the replacement myosatellite cell. As far as I'm aware, the majority of tissues have resident stem cells in varying degrees of differentiation (exceptions might include neurons and cardiac muscle, where cells are not replaced over the lifespan of the organism).

Here is some evidence for resident stem cells in glands;

The adult pituitary gland shows stem/progenitor cell activation in response to injury and is capable of regeneration (Fu et al, 2012),
The pancreas has been heavily studied from the perspective of diabetes research, with many studies looking to implant stem cells from elsewhere (Rezania et al, 2012). However there is some evidence for resident stem cells of the pancreas that may turn out to be more promising as treatment strategies in the future (Xu et al, 2004, Venkatesan et al, 2011),
Sebaceous glands are found throughout the skin, and secrete 'sebum' which keeps the skin waxy and waterproof. There is plenty of evidence for epidermal stem cells (Eckert et al, 2012),
There is also recent evidence for the existence of thyroid stem cells too (Fierabracci, 2012, Malaguarnera et al, 2012),
Saliva is mainly produced by the submandibular glands also contain resident stem cells, with this paper stating that stem cells have been isolted from salivary glands in humans (Okumura et al, 2012),

Given the limited (and very recent) evidence for the above (relatively well characterizd) glands, it seems likely that other glands will also have resident stem cells that remain to be identified.

Ageing: The so-called stem-cell pool gets depleted over a lifetime, so tissues lose the regenerative potential. However rejuvenation medicine is becoming a heavily invested in area of research (see www.SENS.org).


How to perform a DNA structural alignment in pymol

Aligning in PyMol
PDB ID 1h9t contains a structure of both a DNA and a protein. It starts as one object.
Before we perform an alignment, we need to separate your DNA from the protein.

Show sequence (click the S at the bottom right).

Highlight all the "residues" from the chains X and Y (these chains contain each strand of your DNA) in the sequence bar at the top.

Use the GUI to extract selection to new object (it's a faff doing this by terminal I find).

Rename new object (automatically named obj01 probably) to DNA1, or whatever you prefer.

Load your new, unaligned piece of DNA (I used fetch 1BNA).

Pymol uses the CEalign algorithm to align structures in 3D space. You can call it using the following command:
cealign DNA1, 1BNA, object=aln

Output:

Another 3D alignment software I really like is the Dali server.
Haddock
Haddock doesn't care if two molecules are aligned pre-analysis assuming you are submitting each DNA separately alongside a protein for binding analysis. This is because it tries a huge variety of orientations. Here is a list of things that you do need to do to your pdb before submitting to HADDOCK


Why do provitamins-A do not cause Vitamin-A toxicity?

Since, you didn't state whether you were referring to a concentrate or not, i'm assuming the following forms of Vitamin A were obtained via pill or topical suspension - except for the Carotenoid.

α-carotene and β-carotene are (primary) precursors to Vitamin A. Likewise with, Retinal, Retinol but not with Retinoic Acid (irreversibly metabolized/end point) however, i'm assuming that these first generation Retinoids are produced via ex situ (a facility) metabolism and hence, they do not contain the carotenoid component that cause yellowing of the skin due to the absence of lipid soluble orange/yellow pigments (Xanthaemia). Albeit, the color of the aforementioned FG retinoids when in a concentrated solid state are all yellow still due to molecular structure - explained in midsection.

For example:
Retinal:  Otherwise known as Retinaldehyde, is ingested via meat (as a single/complete molecule) or produced by ingestion of carotenoid containing food-stuff (e.g. carots). The pigment causing the color are, Carotenes. Carotene is a component of the Carotenoid molecule; α-carotene and β-carotene.
Alternatively, Retinal can be produced from the metabolism of β-cryptoxanthin, a Xanthophyll containing compound. Xanthophyll and Carotene are similar in terms of molecular structure, however, a Xanthophyll molecule contains Hydroxyl groups and hence, Oxygen atoms - Carotenes are hydrocarbons.

On that note, hypervitaminosis A can be caused by an over ingestion of α-carotene and β-carotene sources e.g. Carrots, due to the process of metabolism; over an extended period of time.

Generally;
Retinyl ester <=> Retinol <=>  Retinal => Retinoic acid

What causes Xanthemia in this context?

α-carotene and β-carotene, are absorbed via (passive) diffusion within the gastrointestinal tract. From there, they are metabolized (not fully/partially) at the the mucousal layer of the intestine for the substance to be transported into the liver. Next, the metabolite is diffused into the peripheral tissues by the blood plasma. This is were the "issue" is: Excretion. Carotenoids are excreted via bowel movements (gastrointestinal secretions), Urination, through the secretion of sebum and by sweating.

If very high levels of Carotenoids are being ingested, the pigment tends to show itself when a "build up" occurs, in the sweet glands of our dermis and more noticeably, in areas of which there are a large amount of sweat glands e.g. nasolabial folds.

The orange color is defined is due to the classification of what Carotenoids are. All carotenoids are tetraterpenoids: essentially being tetraterpenes that have been modified by chemical transformations such as oxidation or cyclization. Furtherly, tetraterpenoids are made up 40 carbon atoms and contain 8 isoprene molecules. α-carotene and β-carotene, are bicylcic tetraterpenoids. This molecular classification may have an affect on the amount of energy that the molecule can absorb, and more formally, the colour. Albeit, the greatest majority of reasoning in regards to the orange color, is in favor of the long conjugated chain'ed structure of the molecule.

Carotenoids absorb light in the blue-green and violet region and reflect the longer yellow, red, and orange wavelengths; these pigments also dispose excess energy out of the cell.

Conclusion

Retinal and Retinal are preformed retinoids and are not obtained by means of carotenoid metabolism so, they won't contain the the yellow/orange dark pigment that is found within some plant-based food (Carotene).

Retinoic Acid, is a retinoid although it's function is as a cell signalling molecule. The difference between it and the other retinoids is the functional group present of the tail of the carbon-carbon backbone

Theoretically, speaking, and due to retinoids having a shorter/less extended  conjugated system with less unsaturated (multiple) bonds in the molecules it will have shifted the absorption to shorter wavelengths (The two carotene precursors have 11 conjugated bonds and the latter retinoids contain 5).

Furtherly, I don't think that the carboxyl group attached to the Retinoic acid molecule could be classed as an Auxochrome although the remainder of the retinoic acids carbon-carbon chain is still the molecules Chromophore - likewise with the other retinoids.  For example, this would mean that there is possibility that the retinoic acid molecule will be more inclined to absorb shorter wavelengths and hence, less orange/yellow. This is relevant as, you will often find retinoic acid in topical preparations that are used to treat certain dermatological conditions.

I don't think that there is a 100% correct answer for this question as there is no evidence to prove that it would be true in this particular case.

So, you are susceptible to toxicity at lower levels in regards to retinol, retinal and retinoic acid because, of the fact that they are metabolites/concentrates and you need ingest less in order to get to the same point of toxicity. Carotenoids are "raw" in contrast to the preformed retinoids   and require breakdown. Look at the image below to get an idea of how much the molecular mass will have reduced when the carotenoid is metabolized into a useful form of Vitamin A.

Another example would be, you needing to eat more daffodil bulbs to get the required dose of Galantamine hydrobromide (used in Alzheimer's disease treatment) - that's a bit different though, to be fair.


Epinephrine is a hormone that works systemically and will activate any and all cells that express a hormone receptor with specificity for epinephrine.

As stated in the wikipedia article "It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar. Epinephrine does this by its effects on alpha and beta receptors."


How do tumor cells 'gravitate' towards each other?

It is reported that 99 genes are significantly upregulated in presence of normal gravity, whereas in absence of gravitational force no gene expression is seen in case of T cell activation. Research article attached concluded  that gravity is important for regulating various essential T-cell activation signalling pathways, which play key role in cell proliferation and apoptosis.

Transcription factors like NF-kB, CREB, ELK, AP-1, and STAT are responsible for tumor cell development. And NF-kB and CREB showed gravity-mediated gene expression. As, the PKA
signaling pathway regulates expression of these transcription factor, so it means that gravitational force moderates PKA signalling. And PKA signalling also mediates tumorigenesis. So, by regulating various cell signalling pathways, gravity controls the tumor cells.

Gravity also modulates the activity of Epidermal growth factor, which are implicated in tumor progression. (Via: https://www.ncbi.nlm.nih.gov/pubmed/7757250)


Possible to remove accumulated haze on fluorescence interference filters?

Its probably not from heat.  Filters are basically a glass substrate with some ionic compound deposited in thin layers.  These won't oxidize at reasonable temperatures, and furthermore since you have it on the emission filter as well, its even less likely to be from the source.

More likely its just accumulated organic material from the environment.  7 years is a long time, and microscopes are exposed to a lot of chemicals and other substances which can gradually build up on optical surfaces.

Most vendors have a recommended way of cleaning their optics, but usually it involves lens paper or lint free swabs and methanol (or sometimes acetone for more durable stains).  You must be very careful though, as you do not want to scratch the filter.

Semrock for instance has a detailed guide here:

http://www.semrock.com/cleaning-optical-filters.aspx


Is it hydrogen atoms or electrons that are passed along an electron transport chain?

As explained on the Wikipedia page of the electron transport chain:

  An electron transport chain (ETC) is a series of complexes that transfer electrons from electron donors to electron acceptors via redox (both reduction and oxidation occurring simultaneously) reactions, and couples this electron transfer with the transfer of protons (H+ ions) across a membrane.

Electron are thus transfered from the electron donor (NADH, H$^+$ produced by the TCA) to the electron acceptor (O$_2$) through the successive enzymatic complexes of the electron transport chain.

Complexes I, III and IV are proton (H$^+$) pumps: they use the energy gained thank to the electron transport in order to translocate protons across the membrane.


What can you tell about a person, having only their whole genome as information?

I've had a little encounter with this question in the past few months so I'm updating here...

The overall answer is 'really a lot about some things, but not as much as you'd like to think about others.'    There is a scientific genome interpretation 'contest' that has been going on for the past few years called CAGI (Critical Assessment of Genome Interpretation).  This is meant to be a cutting edge set of challenges and its worth looking them over.  Last year there was in particular one challenge - answering questions about ten individuals given only a list of traits and their genome sequences.

It was not so easy it turns out - simply looking up variants and cross referencing them to the literature led to poor predictions.  Glaucoma, asthma, migrane, irritable bowel syndrome, color blindness, lupus, lactose intolerance are examples from a list of 40-odd contest questions.  If you register onto the site you can get some of the results or there is a paper reporting the results, only four labs tried the challenge and the accuracies were sometimes not great, topping off with Rachel Karchin's lab with an AUC of 90%.  Even some of the phenotypes you think are easy are not a simple lookup.  Genetics is not as pre-determined as we think.

While we are good at inferring our history and geneology on the other hand.  A reasonable example of this is the 23andme analysis.  They have a lot less information about you than a complete genome sequence, but they do seem to make the most of the 0.0001% of the genome that they do have.

They have a nice lookup of some of the hereditary disease data that is available.  "Increased risk of skin cancer" or for Alzheimers are only chances and its never clear how much your actual lifestyle has impact on 44 outcomes, but its there.

What they also have is your ancestral analysis which is crazy interesting. it shows where your maternal and paternal lineages come from and how strong.  they have a very pretty heatmap of the continents for this.  National Geographic's DB is probably more sophisticated and ancestry.com also does this.  This is pretty cool.

Also included things like curly hair, color of skin eyes and hair.

Like SimaPro says they are described in OMIM.  OMIM stands for 'online mendelian inheritance in man' and all the straightforward directly inheritable traits we know of are listed there.  its worth taking a look. There are not a lot of known single mutation genetically inheritable conditions.

If the genome sequence includes methylation, then some other traits which are epigenetic, not genetic but would also be determined from a genome sequence.  Most famous example of this is MEST which will give an indicator of whether you are a doting parent or not.


What is the best file format to store gel images?

Always keep the raw data files! This is always a good idea for scientific data, and the only exception should be if the raw data is prohibitively large and it is not feasible to store it completely. This is not the case for gel images, so I would always keep the originals, and then use a cropped and edited copy in a suitable format for documents.

The original image has the full amount of data, any conversion can potentially destroy data. For example, some imaging systems produce images with more than 8 bit color depth. Converting to another format will in many cases reduce the color depth to 8 bit as many programs and some image formats like JPEG don't support higher color depths.

JPEG is lossy compression, I would always prefer PNG. You might have to use JPEG at some point because of the file size, but that should be at the latest point possible.


What evolutionary advantages are provided by ovoviviparity?

Reading this website (www.sharks-world.com/shark_reproduction) it seems that for most sharks the eggs develop inside the mother (ovoviviparity), and the young sharks ("pups") are born fully functional, but this is not true for all sharks (as you mention in your question).

This persons blog (morgana249/modern reptiles give birth to live young) discusses evolution of ovoviviparity in some reptiles, but not others. In some species this seems to have gone back and forth in their evolutionary history, which suggests that changing conditions favour one then the other at different times, possibly influenced by temperature, among other things.

  The researchers stated, "These results suggest that parity mode is a labile trait that shifts frequently in response to ecological conditions."

This could be similar for sharks, although I could not find an article postulating this.

Alternatively, this could be because the mother does no "parenting"; the pups are immediately independent. Because sharks do not have many eggs at a time (according to the sharks-world website) each individual egg/pup has a higher "value" than each individual offspring in other fish species, which often lay many hundreds of eggs at once outside their body (oviparity). Therefore sharks that evolved this trait may have been selected because the offspring are more likely to survive if they are protected until fully functional within the parent.

No doubt there are other possible explanations, but as with all these questions along the lines of "What are the evolutionary reasons..." we cannot ever actually know, only suggest.


Check out the muscle relaxant article on Wikipedia, it's pretty straight forward.  In short, there are two main types: Neuromuscular blockers, than act at the junction between the neuron and the muscle; and spasmolytics/antispasmodics, which (mainly) act on the central nervous system to reduce excitation or increase inhibition.  Most of the ones I've heard of, such as diazepam, are in the latter category.


Time required to evolve advanced chromatophores in octopuses and squid?

Here is a print screen from oneZoom.org.

Coleoida include decapods and octopods, both of which have chromatphores, so their MRCA (which lived 330 millions years ago) probably did as well. Coleoida is a sister group to the nautiloids. They branched +400 millions years ago. Together they form the group of cephalopods. As nautiloids do not have chromatophores, the evolution of chromatophores probably occurred in between these two nodes (between MRCA of cephalopods and MRCA of coleoida). In other words, it occurred at some point during a period of about +70 millions years.


A non human adaptive behaviour with a spandrel

One of the first example of spandrel that has been suggested by Gould was the genitalia of hyenas. At the time the term was created, behavioural consequences of having a big brain was a common example and of course, this does not concern only humans but many other animals.

The riddles on the knuckles is another example (that is not specific to humans only either). Those riddles are a by-product of the need the make movement with your fingers.

I am personally not a big fan of the term spandrel as used in evolutionary biology. This term easily leads to limit cases and it depends on how you define the phenotypic traits and the functions they serve.


It is not really slowing down. The graph that you see in that link is semi-log. So the exponentiality of the growth has reduced. It is not surprising because we have much more data than what we had 10 years back but the rate is not going to increase at the same rate (10 to 1000 is a great change but 1000 to 5000 is not despite the fact the the number of new sequences is greater in the latter). However, new data is being continuously added and the linear growth has not saturated yet.

See these graphs that I replotted from the data in your link.

Nonetheless, the number of new sequences will also slow down in future because we would be approaching the maximum.


Is the mesenterium a synonym for the mesocolon?

Mesentery is the name of a whole set of tissues attaching the intestines to the abdominal wall.

In human anatomy, there are three different portions of the mesentery:

Mesenterium sensu strictu, also called Meso
Mesocolon transversum
Mesocolon sigmoideum, also called Mesosigmoideum

Two smaller mesenteries can be found at the appendix (Mesoappendix), and at the cranial part of the rectum (Mesorectum)

So... Mesocolon is a part of the mesentery, but no synonym.


Possible reasons for DNA getting stuck in well

There is one simple reason for that, your agarose gel is most likely too dense. Depending in the type of agarose, I would prepare a 0.5-0.6% gel at maximum.

Synbio gives this list for "standard" agarose, which fits pretty good with my experiences. If you use low melting agarose, this table looks a bit different, as the gel matrix is not a dense. The disadvantage is that the gel is much more prone to get damaged while handling.


Do body lotions enter into bloodstream of people? And how do they do it?

Lotions, like any other drug, can effectively enter the blood system. However, the fraction of the applied lotion that actually enters is really small, and it only achieves a significant concentration in the zone near the application. The skin, if healthy, offers a very high resistance to the passage of substances. Moreover, the bloodstream actually dilutes even more the little fraction it achieves to enter, further reducing its effects. If the skin is damaged the penetration is greater, though you'll never be able to get drunk by dropping booze in an injury.


In which of the following diseases structure of haemoglobin produced is normal but their amount reduced?

You are correct, Thalassemia is the wrong answer.

In Thalassemia and Sickle Cell Anemia, the structure of Hemoglobin is altered.

Chronic Blood Loss: Here the hemoglobin and packed cell values will be low, however there is no alteration in structure of either RBC or Hemoglobin
Hemolytic Anemia: This is a host of conditions which can cause hemolytic anemia. Some mechanisms where Hemoglobin structure remain normal would be:

The structure of RBC membrane is altered, this will make RBCs less maleable and cause early destruction - Example: Spherocytosis
G6PD Deficieny - In this the deficiency of G6PD will decrease the ability of Red Blood Cells to handle oxidative stress and when subjected to sudden oxidative stress, hemolysis will occur. Here the structure of both RBC membrane and Hemoglobin are normal.

Transfusion reaction (I am talking about only hemolytic transfusion reaction, there are other transfusion reactions too): Here the problem is the host reaction to transfused Red Cells. The host was initially severly anemic (Therefore low Hb) for which transfusion was done, now the host immunity is reacting against transfused RBCs which have normal Hemoglobin, resulting in reduced RBC counts and Hemoglobin. So this too can be taken as a correct answer as the end-result will be severe normochromic normocytic anemia.


Why don't individuals with sickle cell trait suffer from sickle cell anemia?

This could be a very long answer, but I'll try to keep it brief.

The first thing to understand is what causes the anaemia. I'm going to refer to defective haemoglobin found in a sickle cell patient as HbS and normal haemoglobin as HbA. Under certain circumstances (low O2 concentrations) the HbS protein is prone to aggregating into long filaments. Here is an image of a lysed erythrocyte releasing some of these filaments.

The presence of these filaments in the erythrocytes causes them to become misshapen (sickle-shaped) and this in turn causes them to get filtered out for destruction in the spleen which is continuously monitoring for defective erythrocytes (which could cause blockages in the circulation). This causes the anaemia (specifically a haemolytic anaemia, due to erythrocyte destruction, and nothing to do with a lack of iron).

The appearance of the ability to form filaments is due to a single Glu>Val mutation in the two β subunits of the haemoglobin tetramer. The new amino acid can fit into a pre-existing hydrophobic pocket on the surface of another subunit and so the molecules can daisy-chain to form the filaments.

The normal HbA can also bind on to a growing filament (it has the binding pocket) but that terminates the filament (because HbA doesn't have the Val residue). In this way people with sickle cell trait are protected from the anaemia by their normal haemoglobin.


Why I cannot find dendritic cells in blood smear?

The dendritic cells are antigen presenting cells that process and present pathogens to the T Cells.
As such they are present in interfaces where foreign organisms are frequently present. Eg: Skin.
When these cells get activated i.e. come in contact with pathogens, they process them and move to lymph nodes to present the processed antigen.
Thus these immune cells do not circulate in blood once they reach the target tissue but reside in the tissues and found in lymph nodes on activation.
Further, from Kuby's Immunology:

Dendritic cells can be difficult to isolate because the conventional procedures for cell isolation tend to damage their long extensions. The development of isolation techniques that employ enzymes and gentler dispersion has facilitated isolation of these cells for study in vitro. - Kuby Immunology 5Ed. P.42
Since blood is the most accessible tissue for clinical studies, we set out to extend the findings that were reported in mouse blood to humans. However, when we tried to induce DC growth by adding GM-CSF to human blood, we identified actively proliferating DC aggregates only infrequently -
Proliferating Dendritic Cell Progenitors in Human Blood
By Nikolaus Romani, Stefan Gruner, et.al.


What does 'virus prototype strain' mean?

A prototype virus may or may not be the first isolated virus of a group. It's essentially the same as a "reference" virus -- in fact, the International Committee on Taxonomy of Viruses
(ICTV) uses the terms interchangeably, as in the  Hepeviridae Study Group which has a column entitled "Prototype/Reference Strain".

In many cases the reference virus is the first isolate, but it isn't necessarily the case. The ICTV is the official body that determines reference strains, and they may choose a different virus as the reference/prototype. For example the first isolate may turn out to be unusual or an outlier in same way, so that a more typical strain may be chosen as a reference or prototype (I don't know offhand of examples of this though).

"Prototype" is often used in a broader sense as well, where a group of viruses can act as prototypes for a still broader group.  For example, "The genomic structure of Pencillium chrysogenum virus (PcV), the prototype of the genus Chrysovirus ... " (pdf link) uses "prototype" to refer to all the viruses in the Pencillium chrysogenum group, as compared to the broader genus.


What is the evolutionary advantage of having pubic hair?

Many consider pubic hair to be a sort of protection or warmth, however this can only hold true for the vagina, since pubic hair doesn't offer any additional protective advantages to the male urethra. The most prevailing theory is that simply it is one of the odor producing parts of the body and humans (like most life forms in general) are simply aroused by strong smells. Also most odour producing parts are usually accompanied by hair in order to "catch" pheromones. It is notable that those odours are not the direct product of glandular secretions, as those secrations are in fact odorless. It is their combination with bacteria that gives every person a unique smell. This unique smell gives a lot of important information to the canditate sexual partner. Here is an interesting study about odour importance in sexual reproduction as well as the role of MHC(Major Histocompatibility Complex)

If you are interested you can read further for for the Importance of smell in sexual production


Is this modification of Livak's 2-delta delta CT method valid?

PCR efficiency is not usually expressed as percentage (or per-unit). Its bounds are [0 2] i.e the maximum efficiency is 2 and the minimum is 0. (Ruijter et al. 2009; also see this post for calculation of efficiency.)

However, I just noticed that some people do express efficiency as percentage or per-unit. In that case your formula would be correct. I realize that there may be a confusion within the community; so you should know what you are calculating. For avoiding confusion lets just call this measure as amplification factor (denoted by E), which would be 1 + per-unit efficiency (as you mentioned).

When the primers have different efficiencies then you can't really use the $\Delta\Delta CT$ method. You'll end up with this formula (pretty much similar to what you have mentioned):

$$\large\text{Fold Change}=\frac{\left[E_\text{GOI}^{-CT^\text{condition}_\text{GOI}}\right]\bigg/\left[E_\text{Ref}^{-CT^\text{condition}_\text{Ref}}\right]} {\left[E_\text{GOI}^{-CT^\text{control}_\text{GOI}}\right]\bigg/\left[E_\text{Ref}^{-CT^\text{control}_\text{Ref}}\right]}=\frac{E_\text{GOI}^{-\Delta CT}}{E_\text{Ref}^{-\Delta CT}}$$

Where:

$CT^\text{condition}_\text{GOI}$ means CT value of the gene of interest (GOI) in a given condition (other than control), and $E_\text{GOI}$ means the efficiency of the primers for your GOI.  Similarly for the reference (Ref).

See this post too.


Why is cisplatin a very potent antineoplastic for testicular cancer, but not necessarily for other cancers?

From the dedicated cisplatin website and Drugbank it appears its use is quite diverse and not confined to testicular cancers. Further, your linked (Siddick, 2003) paper mentions on the first line of its abstract that cisplatin has clinical activity against a wide variety of solid tumors.

Cisplatin.org mentions that cisplatin finds use as chemotherapy against a range of cancers:

  Cisplatin is a chemotherapy drug which is used to treat cancers including: sarcoma, small cell lung cancer, germ cell tumors, lymphoma, and ovarian cancer. [I]t can be a valuable part of a combination chemotherapy regimen. Look at the regimens given to patients and you will often see cisplatin as one of the drugs.

Moreover, cisplatin is explicitly used to treat ovarian cancer:

  Treatment of ovarian cancer involves putting the cisplatin into the peritoneal cavity rather than a blood vessel. The type and extent of a cancer determines the exact dose and schedule of administering the drug.

As to your comment that cisplatin has "magical powers" I can say that it does not. The article that your linked cisplatin wikipedia page refers to (Einhorn, 1990) is a review paper that describes the efficacy of  combination therapies with cisplatin. The high cure rate of 75% was reached when cisplatin was used in combination with etoposide plus bleomycin. The last 10% was theorized to be achievable with 'salvage chemotherapy'. Hence, it is not cisplatin on its own.

In general, it is common practice to use various chemotherapeutic agents in consort, preferably with differing modes of action to reduce the dose of each and hence lessening the side effects.

References
- Einhorn, JCO (1990); 8(11): 1777-81
- Siddick, Oncogene (2003); 22: 7265–79


How much damage is caused by smoking 2-3 cigarettes on a healthy body?

http://tobaccocontrol.bmj.com/content/14/5/315

2-3 cigarettes could make difference absolutely.  It deals 5 points of damage exactly; just kidding.  Hopefully this study provides some insight.


Are there electron or proton receptors in our nose?

Chloride (Cl2) carries 34 protons and electrons.

A common example of a relatively heavy odorless gas is CO2, carrying 22 protons and electrons.

All noble gases are odorless. The heaviest, naturally occurring noble gas is Radon, which has a proton count of 86. Ununoctium, an exotic artificial element with atomic number 118, is a noble gas too. However, with a half life of approximately 0.9 ms it's difficult to sniff out whether it's really oderless.

Sulfur hexafluoride is odorless too, with a proton count of 72.

Hence, the atomic number per se is not the determining factor reason for generating the sensation of odor.

What determines whether a compound generates the sensation of odor I am unsure of, but the above compounds mentioned are all chemically inert. Note that Ununoctium decays rapidly, it doesn't react with anything. I have not been able to verify whether inertness always means odorless, but with the above examples I am inclined to believe it holds true. However, the reverse is definitely not true, as carbon monoxide is odorless, but reactive.


How do cells relocate transmembrane proteins from one side of the cell to the other? Is it possible?

The breakdown and reassembly of proteins is a ubiquitous process within cells, and yes this is expensive but transport is expensive, too, and recycling has the added benefit of dealing with proteins that become misfolded or otherwise damaged as well as allowing for transcription and translation to regulate overall protein levels. The Toyoma & Hetzer 2013 review (see references below) cites estimates of the median protein half-life in a non-dividing mammalian cell to be about 43 hours, though they discuss some exceptions that do last much longer.

However, it is possible to relocate transmembrane proteins via vesicles.

Essentially the same way proteins are put in the plasma membrane in the first place, but in reverse. Endocytosis is often taught as a way that cells (often macrophages are used as an example) take in materials from the outside world, but it is just as applicable to internalizing chunks of membrane. Nature has an entire 'web focus' on entocytosis reviews.

One situation where this happens is in synaptic plasticity; receptors can be internalized or trafficked to the membrane to decrease or increase the potency of that synapse, respectively (see Carroll et al., 2001), but similar processes occur all over (and some proteins constantly cycle back and forth; see Trowbridge et al. 1993 for a more general review, though a bit dated).

However, to your specific question, I don't know specifically of examples where transmembrane proteins are literally cycled from one side of the cytosol to the other. There may be examples I am not aware of, but my understanding is that it is more typical to think of a "store" of certain proteins in endosomes, from which they can be trafficked to the membrane and reinserted via exocytosis. Probabilistically, some will be transported from one place to another, but not so much in a stepwise fashion.

Toyama, B. H., & Hetzer, M. W. (2013). Protein homeostasis: live long, won't prosper. Nature Reviews Molecular Cell Biology, 14(1), 55.

Carroll, R. C., Beattie, E. C., von Zastrow, M., & Malenka, R. C. (2001). Role of AMPA receptor endocytosis in synaptic plasticity. Nature Reviews Neuroscience, 2(5), 315.

Trowbridge, I. S., Collawn, J. F., & Hopkins, C. R. (1993). Signal-dependent membrane protein trafficking in the endocytic pathway. Annual review of cell biology, 9(1), 129-161.


I think that the rest of the paragraph that you left out of your quotation helps to clarify. The CHO have 21 chromosomes, while the somatic lung cells have 23.

Neither case is exact for Chinese Hamsters, 2n = 22. So they have almost the complement of chromosomes that a diploid Chinese hamster somatic cell would have but they are missing one or have one extra. For the most part they will behave like normal somatic cells in culture, but it is an important fact to note as you can have cases where dosage dependence of a missing chromosome in a pair or an additional chromosome (trisomy) can affect the outcomes of research.

In the back of your mind you always need to be thinking how does the missing/extra chromosome affect the data I am collecting.

This Nature article may also be of interest.


A Study by Lee & Shirreffs addresses this question.  Unfortunately I only have the abstract, but it's enough to summarise from:

Method

Three groups exercised by  cycling before being given water at either 10°C, 37°C or 50°C.
They then continued to exercise until exhausted.
Mean skin temperature, core body temperature and heart rate were measured throughout.

Results

Mean skin temperature was highest in the hot drink category - half a degree warmer than in the cold group.
There was a heat difference between the two outlying groups of 33kJ.

Irritatingly the pre-drink temperatures are not included in the abstract so it's hard to compare the effect that the drinks have had.  Certainly the hot drink has warmed skin temperature above the thermoneutral group but I suppose that could be due to increased vasodilation leading to better core heat dissipation (as you suggest).

In absolute terms, you are warmer than you would have been after having a neutral or cold drink, however it could be that you feel cooler as your hotter skin loses heat energy at an increased rate due to the greater gradient.

References

 Lee JKW, Shirreffs SM. 2007. The influence of drink temperature on thermoregulatory responses during prolonged exercise in a moderate environment. Journal of Sports Sciences 25: 975–985.


Flow cytometric counting of apoptotic adhering cells

Here some resources,

Cell harvesting effects on Annexin V staining.
Protocol for apoptotic analysis using Annexin V.
Quite a long discussion about this issue.
Another protocol.

Cheers,

Pedro


H is the set of all possible Diplotypes that are consistent with genotype data

Disclaimer: Like the OP, I know very little about genetics and I suppose other people in the site can give better answers than me. Anyway, since the question has been unanswered for months I'm posting my answer. Hopefully someone will improve it.

Just beware that "possible" in this context doesn't mean all haplotypes that we can imagine. As the paper says, "$\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$" and that is an additional restriction that allows just some diplotypes - the seven ones listed, not the 32 we can imagine.

Furthermore, please notice that sum of frequencies in the table equals 1, therefore there can be no more haplotypes in the set.

However, it would help if you linked the source where you got those data and quotes.


What is the formal terminology for two species that are "close" to each other in a phylogenetic tree?

Are you looking for something like "sister lineage" (or "sister taxon" or "sister group")

This term may be more specific than what you're looking for, and to use it correctly you'd want to be a little careful – I guess in this case you might have to say something like:

  "the lineage that includes chimpanzees and bonobos is sister to the
  lineage of which humans are the only extant species"

or

  "the lineage that includes chimpanzees and bonobos and the lineage of
  which humans are the only extant species are sister lineages"

both referring to this phylogeny.

It's also possible that explaining exactly what you mean by 'close', or what it entails, would be appropriate, be it Ilan's suggestion of % genetic similarity (or maybe genomic similarity?), # of nodes between your two taxa (again, this would have to be in reference to a specific phylogeny), or if you have a dated phylogeny you could refer to the time since divergence, as in "coding DNA divergencies ...place the most recent common ancestor of humans and chimpanzees at between 5 and 6 million years ago."(Wildman et al 2003).


Why do most breast cancers occur in women?

Yes, this is mostly about estrogen. Most breast cancers rely on endogenous estrogen to sustain proliferation.

Some general reading: Cancer Medicine, Chapter 18

More in-depth reading: Endogenous Hormones as a Major Factor in Human Cancer

Requested summary of mentioned readings:

First of all, there is an established link between breast cancer cell proliferation and concentration of estrogens and progesterone, which is logical, because normal breast cells divide in response to those hormones (e.g. puberty, pregnancy, even luteal phase of the menstrual cycle). Secondly, the incidence of breast cancer in women correlates with major changes in their hormonal profile - girls and elderly women (i.e. women with lower levels of sex hormones) don't get breast cancer.

Many factors, that influence the risk of developing breast cancer are in fact tightly connected to the hormones' levels. For example - early age of menarche (or, more importantly, first ovulation, because physical activity at young age disturbs ovulation AND is protective against breast cancer) and Hormone Replacement Therapy raise the risk, early age of first full-term pregnancy or any form of artificial menopause (such as preventive oophorectomy for women with mutations in BRCA1 or 2) reduce the risk.

The first table from the book chapter lists known risk and preventive factors. The review article explains the same ideas, but connects them to other types of cancer (e.g. ovarian cancer) and suggests mechanisms, which might be the cause of those risk changes.


PBST vs. TBST buffer in western blotting

I used to work for a company well-known for its modification state-specific antibodies, including phospho-specific ones, and they actually performed extensive in-house testing of PBST vs. TBST in Western blotting. Part of the reason the company chose to recommend the use of Tris-buffered saline over phosphate-buffered saline based buffers was the clearly-demonstrated fact that some phospho-specific antibodies just didn't work as well in PBST as they did in TBST, for whatever reason. As I recall (it's been quite a while since the testing was performed), some of the antibodies tested gave weaker signals, with more background, and one in particular just didn't work at all in PBST - no signal whatsoever. For that reason, the company chose to standardize its recommended Western blotting protocol with TBST, and it's been that way ever since.

That being said, I'm sure that the majority of antibodies out there would work just fine in either buffer. However, to be on the safe side, if a company states one buffer or other in their protocol, it would be best to use the recommended one.


How does a stonefish get oxygen out of water?

I have been trying to find an answer to this question, but until now, no one seems to have really analyzed why this is possible. The only hint I found comes from this paper:

A study of the distribution, habitat, behaviour, venom apparatus and
venom of the stonefish.

They state:

  At periods of low water, stone-fish are often left partially exposed
  by the retreating tide. At such times they may be surrounded only by a
  small quantity of water which fills the depression in which each lies
  and the main mass of water may be a considerable distance away. They
  can survive long periods (at least 24 hours) out of water providing
  their surroundings are kept moist.

Obviously the fish only needs minimal moisture to get enough oxygen. I would further speculate that the fish turns down its metabolism during this time to minimize the need for oxygen. This paper is widely cited as a source for this survival time, but there seems to be no follow up on it. What is widely analyzed is the toxin of the stonefish.


For an organism (think single-celled) living in just the right kind of environment, it might just be possible to survive using only facilitated diffusion, at least as far as small molecules are concerned. This kind of organism would have to maintain exactly the right concentration of the molecules it wants to keep or get rid of, based on the external concentration of those molecules.

For example, if an organism was living in a glucose-rich environment, it might be able to fulfill its glucose requirements by (1) making the membrane itself tightly impermeable to glucose and (2) tightly controlling the number of passive glucose transporters.

It would be nigh-impossible to achieve this for every solute in the environment, especially those that are able to permeate the membrane.

If there were such a thing, it might be found in organisms that live in very low energy aquatic regimes such as anaerobic methane oxidizers, where the solute concentration in the environment doesn't really change in small time scales.

Even in such environments, the number of small ions in the environment is likely to be high enough that some active transport would be required to maintain the osmotic balance within the cell.


How is (Insect) population control through male sterilization effective

Sterile insects are typically produced by radiation. A sufficient dose is used to cause substantial DNA damage in the gametes of the males. However, this doesn't mean the sperm are completely non-functional.

In fact, it is important that the sperm are functional and simply contain dominant-lethal mutations at a sufficient probability (Robinson, 2005 describes this in detail as well as the dosing strategies to optimize the desired outcome).

The males still mate and fertilize the eggs of the female; it is only later that the eggs will eventually fail to develop, but there is no way for the females to be aware of this (nor much that can be done even if they were - once the eggs are fertilized they cannot be fertilized again).

It is also important to release a sufficient population of sterile males to impact the population. Depending on the species, it may or may not be necessary to completely overwhelm the existing population, but a typical goal seems to be 10-100x the native population. By raising males in laboratory conditions, it may be possible to produce a larger population than would typically survive to mating age in the wild.

References:

Cockburn, A. F., Howells, A. J., & Whitten, M. J. (1984). Recombinant DNA technology and genetic control of pest insects. Biotechnology and genetic engineering reviews, 2(1), 68-99.

Klassen, W., & Curtis, C. F. (2005). History of the sterile insect technique. In Sterile insect technique (pp. 3-36). Springer Netherlands.

Robinson, A. S. (2005). Genetic basis of the sterile insect technique. In Sterile Insect Technique (pp. 95-114). Springer, Dordrecht.


In biology phosphorylation marks the addition of inorganic phosphate groups to proteins or other organic molecules. The phospho-group usually comes from ATP which is converted into ADP in this process.

In the context of the Calvin Cycle there are two positions where molecules get phosphorylated. The first is the phosphorylation of 3-phosphogylcerate to 1,3-bisphosphoglyerate, the other is the phosphorylation of Ribulose 5-phosphate to Ribulose 1,5-bisphosphate.

See the image (from here):


Workspace preparation and cleanup for DNA work

From the comment section:

Mostly segregation of PCR-amplified DNA from non-amplified DNA. Typically no DNA or sample should ever enter a specific room designed to prepare the MasterMix for PCR (this is true for diagnostic labs, in the research one I never saw that). For the rest, following good laboratory practices (google that) should be enough.


Can people be bred for tameness in a similar way to Russian foxes?

Setting aside the eugenic implications of what are you suggesting (short answer: yes it is theoretically possible, but no it is practically impossible), a more interesting observation is that evolutionary anthropologists think that humans might have "self-domesticated" during our evolutionary history.

There is a wide literature on this topic, but a recent paper summarizes the main ideas and addresses the question from a genomic point of view. Theofanopoulou and coauthors find credible genomic evidence for similar patterns of genetic evolution in humans and other domesticated animals.


What you've circled is not a heteroduplex. A better name for it would be "crossover" or "junction". Instead, the two duplexes at the bottom of your diagram are what should be labeled heteroduplexes. Your diagram shows one process by which you could generate heteroduplexes starting from homoduplexes.

Here's a better picture from the NCI Dictionary of Genetics Terms that more clearly shows the difference between homo- and heteroduplexes:

The two strands in a heteroduplex still have to have a high degree of sequence identity or they won't be able to form into a duplex in the first place. However, because they come from different sources there's likely to be many short subsequences in which one or more base pair is mismatched, causing a deformation as shown.


Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS?

CNS consists of brain and spinal cord, and PNS consists of everything else

That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system) and the peripheral (nervous system): that is, the most important part is that together they are parts of the nervous system, rather than being distinct systems; the central/peripheral difference is fairly minor, especially if you are thinking primarily of the somatic part of the peripheral nervous system (that is, not the autonomic part) relative to the associated part of the CNS.

The peripheral part of the nervous system is not protected by the bones of the skull and spine, does not have the protection of the blood-brain barrier (specialized endothelial cells and astrocytes that limit transmission of molecules between CNS and the blood circulation moreso than in other tissues), and myelination is mediated by cells with a different morphology: Schwann cells in the periphery vs. oligodendrocytes in the central. That's about it.


How does a prophage leave the host cell's genome?

This is explained reasonably well at the Wikipedia entry for phage λ, which is the prototype lysogenic phage. Basically, integration occurs by site-specific recombination between the attP region on the phage genome and the attB region in the host genome. This means that in the prophage form the phage DNA is flanked by direct repeats. Excision involves the reverse process - recombination between these direct repeats. Excision is promoted by the phage-encoded Xis and Int proteins in combination with the host protein Ihf. The regulatory cascade which links cellular stress to this recombination event is detailed at the linked page.


Your "grieving bird" is a video of a peregrine falcon (Falco peregrinus) and its (nearly?) dead chick on a hot summer day in Phoenix, Arizona (USA) in 2016.

 Photo credit: Arizona Game And Fish Department

The video is from a nest camera webcam set up in the Maricopa County building in Phoenix, Arizona by the Arizona Game and Fish Department.(See this video for more information). The camera was active in 2016, but according to here the falcons did not return to the nest in 2017. Your video shows one of the adult birds with the only chick that hatched (out of 4 eggs) in 2016. That chick died from a combination of heat and an 8-story fall in June 2016 [Source]. Your video is an edited and audioless version of a video capture of the live stream that can be seen on Youtube. The information for this video indicates that the adult bird in view is the father.

The adult falcon in the video is not wimpering, crying, or grieving. Instead, the bird is trying to cool down on a hot day. He is displaying a familiar temperature regulatory behavior: panting.

From Bartholomew et al. (1968):

  Most birds pant when subjected to heat stress...

In fact, in the more complete video I link to above (with audio), you can clearly hear the bird making panting sounds while breathing heavily.
The falcon also spreads out its wings to better help cool himself down toward the end of the video as it cares to its injured chick.

You can see another video of a panting falcon in New Hampshire (USA) here, and you can find more information about panting, gular fluttering, and other thermoregulatory behaviors in birds here, here, and here.


ID of a pair of similar-looking birds in NT, Australia

I think these are most likely nankeen night heron (Nycticorax caledonicus). The only that does not fit is your size estimation. See the images (from here):

I think the first image shows a bird which still has parts of its juvenile feathers, which look pretty different (from here):

A lot of information about these birds can be found here and here.


How to correlate the pattern by which CAP activator from E.coli binds to DNA and its mechanism of action?

I found a great article that might help. To summarize the contents of the article, there are two classes of CAP dependent promoters/genes, and the distance of the CAP bindings site in these classes are different. Also the actions in which CAP is involved are different in the two classes of promoters. In the first class it does not overlap with the promoter region and is only involved in RNAP recruitment. In the second class it overlaps with -35 element of the core promoter and is involved in multiple interactions.
So the binding distance of the CAP is determines what interactions is it involved.

You can see the difference between the two classes on the picture below (taken from the article i linked). And I think this answers your question on why the patterns are multiples of ten - because this is the space needed for alpha-CTD to make a bridge between the protein complexes, or the CAP to interact with the RANP complex.

I only took a glance at the paper I linked and quickly extracted the info, but I hope it still helps


Consequences of abnormal blood pressure unrelated to cardiac output?

Blood pressure, as you noted, is just a means to an end: the flow of blood through tissues. The trouble is, many of the body's regulatory systems use blood pressure (rather than flow) as an index of cardiovascular status. A key example is the baroreceptor system, which senses changes in blood pressure and tries to correct them by effects on the heart, blood vessels and kidneys.
In sepsis with decreased blood pressure, baroreceptor firing increases in an attempt to increase cardiac output $^1$. This increased demand on the heart can be counterproductive and cause the heart to fail. But this phenomenon is not unique to sepsis. There are many other conditions where a hyperdynamic circulation leads to heart failure: such as anaemia, thyrotoxicosis and thiamine deficiency $^2$.
All of these examples highlight a basic principle in pathophysiology: adaptations can sometimes turn maladaptive.
Note: The effects of sepsis on the cardiovascular system are complex and go beyond vasodilation. For more details, you could read a textbook of pathophysiology/medicine. Or go through any of the review articles on this topic, such as the one by Lelubre & Vincent $^3$.

References:

Gattinoni L, Carlesso E. Supporting hemodynamics: what should we target? What treatments should we use? Crit Care [Internet]. 2013 Mar 12 [cited 2020 Aug 24]:17(Suppl 1):Article S4 [8 p.]. Available from: https://ccforum.biomedcentral.com/articles/10.1186/cc11502
Mehta PA, Dubrey SW. High output heart failure. QJM. 2009 Apr;102(4):235–41. https://doi.org/10.1093/qjmed/hcn147
Lelubre C, Vincent J. Mechanisms and treatment of organ failure in sepsis. Nat Rev Nephrol. 2018;147(7):417–27. https://doi.org/10.1038/s41581-018-0005-7


You will likely need a tool to "map" the reads on the reference genome.
You may find such a reference genome, together with annotations, here:
ftp://ussd-ftp.illumina.com/.

Mapping tools such as bowtie2 or bwa take fastq files and reference genomes and output mapping results in a format called sam.

You then have a lot of options to estimate gene expression.

You can write your own algorithm to parse sam format and estimate normalized read counts on each gene.
You can combine more or less low-level tools such as samtools, pysam, htseq with some scripting to do this.
You can use tools that do the counting (like bedtools ot htseq-count) and differential expression analysis (like deseq2).

In the last case, I would advice to start from the documentation of the final tool to find out what are the tools you need to generate the output of the preceding step.

It is very likely you will use some R or Python, or use the web platform galaxy for some of the steps.

Edits

As mentioned by @scribaniwannabe in this answer, the paper about the Tuxedo suite of tools gives a good example of the steps to carry out an RNA-seq analysis using recent tools (as of October 2016).

As @Student T reminds in this answer, RNA-seq data contain reads that can come from exon-exon junctions, so the read mapper has to be set up in such a way as not to discard reads not mapping continuously on all their length on the genome. To my knowledge, HISAT2 and CRAC do this by default. Bowtie2 needs special settings.


When did vision evolve for the first time?

"To me, it also makes sense that the evolution of sight would have accompanied the evolution of advanced brain functions in almost every case."

Not necessarily! For instance, think of phototropism: the plant detects the presence of light and uses it to grow towards the light, but that's a very simple process regulated by auxins. Or the light-sensitivity (phototaxis) shown by Euglena, a single-celled protist, which reorients its entire body towards a light source. Really simple vision (is there a light, and if so, where is it?) can help organisms absorb more energy than rivals, giving them an evolutionary advantage.


Why would a plant evolve to produce an addictive chemical?

It's a matter of perspective. Most of the chemicals that are addictive to us humans (particularly alkaloids), and may be addictive for some other animals as well, are also insecticides. Lots of plants that we consider poisonous are good food for other species, and lots of plants that insects would consider poisonous are treats for us.

This is a great example of the aimless nature of evolution. The plants that could successfully defend themselves against insects stabilize on a solution that happens to be bad for them in certain ways. Although, you would be hard pressed to find a better way to guarantee reproduction than being addictive to humans.

Background reference

Plant-insect coevolution and inhibition of acetylcholinesterase
The defensive role of alkaloids in insects and plants
Exploration of nature's chemodiversity: the role of secondary metabolites as leads in drug development

Also of interest

Bees prefer foods containing neonicotinoid pesticides


Why are diseases generally specific to a particular species

The pathogens which are responsible for certain diseases have adapted to their hosts. Viruses need to attach to structures on their cells they invade to replicate. These structures usually consist of proteins and are unique for the respective species (e.g. the ACE2 receptor in the case of Covid-19). During an infection, there will be billions of viruses released and some carry mutations, which are just mishaps in the replication process. In most cases, these errors are leading to a virus that is not viable or cannot infect, i.e. the mutated virus can't replicate and the mutation gets lost, but sometimes it can infect the host better and thus will have a higher chance to propagate.
If this happens with a zoonotic pathogen after it has spread to a human, a new disease has emerged.


Does DNA replication in 5' to 3' (leading strand) need RNA primase?

The DNA polymerase also needs a RNA primer on the leading strand to be able to start polymerization. Afterwards this is not needed anymore, since the replication goes on without a break. On the lagging strand polymerization replication can only work between the replication fork and the next region of double-stranded DNA. See the figure (from here):

The reason for the need for RNA primers is located in the function of the enzymes. While the DNA polymerase can only work on a double stranded template (add nucleotides to the 3'OH-end of the strand) the DNA Primase (actually an RNA polymerase) can work on single stranded targets and thus add the RNA primer there.


Can drinking caffeine, alcohol and other diuretics be part of a good drinking regime?

A PlOS One study notes drinking moderate amounts of coffee (aka moderate caffeine intake) doesn't necessarily lead to dehydration. They note coffee has hydrating qualities akin to water. Further empirical studies found no substantial fluid loss in caffeinated beverages.

EDIT: Make note we're talking normal doses and moderate intake, though source 2 goes into diminishing effect of caffeine-mediated fluid loss in heavy/prolonged uptake.

The issue therein is with alcohol, which tends to inhibit vasopressin and the kidneys are constantly permeable to fluids.


What type of immersion oil should I buy?

For the best image (where you lose the fewest photons and get less refraction), you want the immersion oil to have a refractive index as close to the refractive index of the coverslip you intend to use.  In my experience, this is not much of a consideration on the oil-side, but rather on the coverslip-side.

There is little difference between type A and B oil, although for other types of oil see here.  If I were you, I would just use some type A.

For a lesson on the impact of immersion oil on optics, see this Zeiss website (similar sites for Nikon and other scope manufacturers exist too I'm sure!)


How to determine the relationship of competition or cooperation?

Species interactions

Generalities

Species interact. Species actually interact a lot. One can classify species interactions into categories based on the effect that the interaction has on their fitness (≈ reproductive success). Here is a table of possible biological interactions (comes from [wiki][1]), where a + indicates "beneficial", a - indicates "detrimental" and a 0 indicates it has no effect on fitness.

Different terms exist for a given relationship. Typically, antagonism is often called parasitism.

Note about symbiosis

Different authors use the word symbiosis differently. From wikipedia:

  The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any type of persistent biological interaction (i.e. mutualistic, commensalistic, or parasitic).[6] After 130+ years of debate,[7] current biology and ecology textbooks now use the latter "de Bary" definition or an even broader definition (i.e. symbiosis = all species interactions), with the restrictive definition no longer used (i.e. symbiosis = mutualism)

Blurry limits

Generalities

It may seem pretty obvious that two species should have either one type or another type of interaction. However, the reality is often more complicated than that. An interaction might fall in one category under one set of environmental conditions and fall under another category under another set of environmental conditions. In addition to that, it is not uncommon that due to selection on the host genes due to the presence of a parasite, the host evolve so to tolerate the presence of the parasite up to the point of actually having a lower fitness in the absence of the parasite.

Example of environment-dependent interaction type

Consider an animal that is host to an algea. The host is providing shelter to the algea while the algea is providing sugar (produced through photosynthesis). If there is no light or if the enviroment is loaded with sugar, then the host has no gain of hosting the algea. In such case, the algea may even be parasitic. If, however, there plenty of light and there is few nutrients in the environment, then the algea and the host have a mutualist relationship.

Example of the evolution of a parasitic interaction

Consider for example a snail which is infected by a parasite. Let's assume (I think it is a real world example but I am too lazy to find out a reference) that the parasite need the snail to be eaten in order to reproduce in the body of the predator. In order to improve the chance of its host to be eaten the parasite is selected so to diminish the thickness of the snail's shell. In response to that, there is selection (which intensity depend also on the proportion of infected snails in the population) for having thicker shells. But now, snails that are not infected have shells that are so thick that the can't move as fast as they'd need to forage. So, by the end infected snails may have a higher fitness than non-infected snails. And therefore the interaction between the snail and its parasite is not a parasitic interaction anymore but a mutualistic interaction.