It depends how you define locomotion.

If you take it to mean moving from one place to another, then yes, almost all plants do this at some stage during their life cycle. Primarily seeds and pollen move around, and generally they do so by harnessing either natural forces like wind and rain, or by manipulating animals to do the leg-work, e.g.:

by recruiting pollinating insects
by having barbs which snag the fur of passing mammals
by producing tasty fruit so monkeys eat them, seeds included, and deposit them with a dollop of fertiliser somewhere else

If you take it to mean moving around under ones own propulsion, then yes, some plants do this. The example that springs to mind is the gametophyte generation of ferns:

The prothallus (i.e. the gametophyte) has rhizoids on the underside and uses them to slide around and find some space in which to start the next generation. I have seen this happen when fern spores are germinated on agar - when they reach the tiny prothallus stage, they start sliding around to avoid overlapping with one another. I can't find any references for this, but I'll keep looking.

Another example of self-directed locomotion in plants is the motile sperm of bryophytes. The male sex cells have flagella, which they use to propel themselves through water to the female sex cells (reviewed by Renzaglia & Garbary 2001).

Renzaglia, K.S. & Garbary, D.J. (2001) Motile Gametes of Land Plants: Diversity, Development, and Evolution. Critical Reviews in Plant Sciences. [Online] 20 (2), 107–213.


Do any cells change in size or mass as mammals grow?

I'm wondering if it is safe to assume that the approximate number of cells per unit mass in a mammal will remain fairly constant throughout its lifespan.

Not exactly.  When a tissue is put under stress, it can respond in four main ways:

Hypertrophy - individual cells get larger.  E.g. stressed muscle cells get bigger.
Atrophy - invidivual cells get smaller.  E.g. naturally in the thymus during development.
Hyperplasia - increased cell division to produce more cells.  E.g. mammary gland cells in pregnancy
Metaplasia - one type of specialised cell is replaced with another, usually more durable one, E.g. columnar epithelium in the respiratory tract of a smoker being replaced with squamous epithelium.

The first three responses to stress can change both cell size (auxetic response) and number (multiplicative response), meaning you can't really say that cells per unit mass stays constant throughout life.

Muscle tissue grows predominantly by hypertrophy, meaning that the muscle gains during puberty are likely to be more as a result of cells getting larger than the development of new ones.

Both auxetic and multiplicative growth occurs as the body develops.  In addition to this, accretionary growth also occurs - where connective tissues such as bone and cartilage increase in size.


Why/How do Cyanobacteria Produce Toxins?

This available paper has some ideas,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736421/
Search terms cyanotoxin and evolutionary give at least two more promising papers.

https://www.biorxiv.org/content/10.1101/615542v1.full
says:
i) photoprotection due to absorption of harmful ultra-violet radiation; (ii) facilitating the acquisition or more efficient use of available but limiting resources; (iii) impeding growth or resource use of competitors such as green algae or other cyanobacteria; and (iv) limiting predation by inducing toxicity in organisms predating on cyanobacteria. While the role of cyanobacterial metabolites in photoprotection, resource monopolization, and habitat dominance has been demonstrated experimentally, hypotheses regarding the anti-predation role are not entirely consistent


CFTR is the gene which encodes the "Cystic fibrosis transmembrane conductance regulator", which is a membrane protein. Its function is to transport chloride and other negatively charged ion like thiocyanate ions from the inside of the cell to the outside (into the extra cellular space). This happens along a gradient, meaning the ions flow from the place of high concentration (inside the cell) to the place of low concentration (outside the cell). Since this would mean that a negative charge would build up on the outside of the cell, positively charged sodium ions follow the chloride ions by passive diffusion. This ions are secreted into the mucus in the extra cellular space.

This leads to a higher concentrations of electrolytes (salts) outside of the cell, which causes water to leave the cell (following the higher concentration of electrolytes), which makes the mucus thinner.

When the CFTR gene is mutated, this function is impaired and ions cannot be transported across the membrane. This causes a higher electrolyte concentration inside the cell and water stays there. This causes the mucus to get thicker (due to less influx of water), which then can block fine channels of the lung. Additionally bacteria can grow in the thicker mucus, which can cause severe problems as pneumonia. The process functions as shown in the figure below (from here), the sodium ions are not shown here:

If you want to read further about cystic fibrosis, I recommend this website.

Regarding the immune system there are different functions affected. First, the reduced (or prevented) secretion if thiocyanate ions lead to a reduction in the production of Hypothiocyanite ions which kill bacteria. Then different cells which are of importance to a proper immune reaction are impaired in their function, as shown in the figure below (from the first reference):

The function of CFTR is impaired in all cell types, not only in epithelial cells in the lung (although these are the most obvious consequences). In the cells of the immune system (T-cells for example) the intracellular ion concentration is disturbed including Ca2+ which plays an important role in the regulation of other genes. Other observations show that the activation of the immune system itself is also affected.

Further informations can be found in the articles I linked below. They require some knowledge of immunology, but when there are question, ask.

References:

Immune Responses in Cystic Fibrosis
The innate immune system in cystic fibrosis lung disease


Hard to tell without a clearer picture, but the size and color pattern seem to match the description for the Plain-bellied Watersnake.
See for example the following picture from the Virginia Herpetological Society:

I assume from the location being in something called a swamp that the habitat (in and near slow moving bodies of water) also fits.


How Common are Paraneoplastic Syndromes in Cancer Patients?

The incidence of paraneoplastic syndromes appears to be variable and dependent on the kind of cancer. Estimates by Baijens and Manni (2006; Eur Arch Otorhinolaryngol 263: 32–36) are 1% to 7.4% of all cancer patients, however they are citing Gulya (1993; Laryngoscope 103: 754–761) and Zuffa et al. (1984; Neoplasma 31: 231–236) for the data.

Pelosof and Gerber (2010; Mayo Clin Proc 85: 838–854) make the particularly salient observation that

  As patients with cancer live longer, and as diagnostic methods
  improve, this prevalence will likely increase.


This is a cricket in the family Gryllidae. The two thin "strings" on the left are antennae, and the two sturdier "strings" on the right are cerci (though your image is not clear, and perhaps one of the extensions on the right is actually an ovipositor). See here for a clear image showing cricket anatomy.

An example cricket with wide geographic range that includes Egypt:

Gryllus bimaculatus

 Credit: Vlad Proklov

Without additional info, I'm not sure you'll get an accurate species ID on your specimen.


It's a Dutchman's Pipe (aka Calico Flower); the genus has over 500 species, but I'm pretty sure this is it.


What initiates primase to add an RNA primer to a DNA strand and what makes it stop?

Prokaryotic primases are activated by DNA helicase [1, 2] while the eukaryotic ones are triggered when they form a complex with DNA polymerase alpha and its accessory B subunit [2].

I couldn't find too much information about what exactly triggers activation, but according to De Falco M et al. (2004):

  [...] synthetic function (of the prokaryotic primase) is specifically activated by thymine-containing synthetic bubble structures that mimic early replication intermediates. [3]

It stops when it finishes reading a DNA template:

  The Sso DNA primase utilizes poly-pyrimidine single-stranded DNA templates with low efficiency for de novo synthesis of RNA primers [3].

References:

Wikipedia contributors, "Primase," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Primase&oldid=593928284 (accessed December 1, 2014).
David N. Frick, and Charles C. Richardson. DNA PRIMASES. Annual Review of Biochemistry. Vol. 70: 39-80 (Volume publication date July 2001). DOI: 10.1146/annurev.biochem.70.1.39
De Falco M, Fusco A, De Felice M, Rossi M, Pisani FM. The DNA primase of Sulfolobus solfataricus is activated by substrates containing a thymine-rich bubble and has a 3'-terminal nucleotidyl-transferase activity. Nucleic Acids Res. 2004 Sep 30;32(17):5223-30. Print 2004.


If we can make magic bullets that are basically artificial antibodies, why has a cure for cancer not yet been developed?

This is a good question.
The first answer is that there are antibody therapeutics for cancer.
These fall into two categories which I will call therapeutic and immunotherapy (this is not typical naming but, keeping it simple they will do).
Therapeutic antibodies are designed to bind to an enzyme or signalling protein that will weaken the tumor specifically.  An example is an antibody to nutrient intake receptors (cancers eat a lot more than other cells). HER2 is a receptor that is heavily populated on breast cancer tissue.  Antibodies that inhibit HER2 activity can slow the growth of breast cancer specifically with minimal toxic effects.
There are also antibodies to proteins found only on cancer cells.  These can be specific antibodies (monoclonal antibodies) to proteins from a mutation that only the cancer cell has.


How is Hypertonic Urine Produced in a Mammalian Kidney?

The process of urine concentration in mammals occurs due to the interaction of the loop of Henle and its nearby collecting tubule. When someone is dehydrated, the kidney will aim to a maximal water reabsorption.
To concentrate urine, a maximal amount of ions will be reabsorbed. This is to maximalize the concentration gradient for water. However, the main driving force for water reabsorption is the urea concentration gradient (created by the loop of Henle). Then aquaporins will allow water to flow from the collecting tubule to the nearby medulla because of the presence of the neighboring loop of Henle. It is this proximity between the loop of Henle and the collecting tubule that allows such a high efficiency for water reabsorption.

Concentrating urine is not about leaving more ions in the water, it is about reabsorbing a maximal amount of water.


What are the minimal chemical requirements for a food which we all can eat?

Considering the three basic biomolecules used by the body are carbohydrates, lipids, and proteins, you would need to consume these three molecules only. Now we can choose three substances.

Glucose, one of the most basic carbohydrates, is needed for ATP production, so that would be a food choice there.
Any oil or butter will provide lipids.
Protein comes from a variety of sources. Meat is typically though of as the best, but nuts are a pretty good source too.

Since nuts satisfy proteins and lipids, I'd say honey roasted peanuts are the most basic food you could live off of, if you replace pure glucose for the honey.


What are the brain structures directly on top of the brain stem?

You're looking at many structures in this area.

The region directly above the midbrain is the diencephalon (meaning "across + brain"). From inferior to superior it's composed of the hypothalamus, thalamus, and structures that developed from a developmental region referred to as the epithalamus that include the pineal gland, habenular trigone, and choroid plexus. Between the hemispheres of the thalamus/hypothalmus lies the third ventricle (which may be "bridged" by a structure called the interthalamic adhesion).

Of each of these structures, only the thalamus and hypothalamus are truly visible from your images -- with the hypothalamus articulating with the midbrain and the thalamus emerging superior and slightly lateral to he hypothalamus. The following structures are also visible in your image:

The most inferior structure you see is the pituitary gland, while the "X" shaped structure superior to it is the optic chiasm with cut optic nerves anteriorly and optic tracts continuing posteriorly out of view.
It's not entirely clear, but I believe the two protruding structures posterior to the pituitary are the paired oculomotor nerves.
Finally, the two long ribbon-like structures that extend anteriorly are the olfactory tracts of cranial nerve I that terminate anteriorly in optic bulbs.


Do all bacterial cells have a double membrane?

No. There are a number of bacterial membrane and cell wall structures. Some of them have a double membrane, some of them don't.

In microbiology, we often make the initial distinction between two groups of bacteria based on whether or not they take up an iodine based stain called a Gram stain. Gram negative bacteria have an inner membrane, a rigid cell wall, and an outer membrane around the cell wall, so they don't take up that stain. Gram positive bacteria have an inner membrane and a rigid cell wall, without the outer lipid membrane, so they do take up that stain.  There are other bacteria that don't stain well with either the Gram stain or its red counter stain (typically safranin), but most medically important species of bacteria fall into one of these two categories (gram positive: blue, no outer lipid envelope, or gram negative: red, has an outer lipid envelope).

You can read about gram-negative and gram-positive bacteria on Wikipedia, but it's surprisingly technical. This biologywise post might be a more approachable introduction.

  How does this compare to my general knowledge of bacterial cells having one plasma membrane surrounded by a cell wall?

When the concept of prokaryotes and eukaryotes is introduced, you're taught about key distinguishing features between the two. One of the key distinguishing features of (most) prokaryotes is a rigid cell wall. This is present in both gram negative and gram positive bacteria. They just didn't tell you about the outer lipid envelope in gram negative bacteria. At that point in your education, the idea is to introduce you to the concept of prokaryotes vs. eukaryotes, not to catalogue or understand all the different kinds of prokaryotes.

The more you learn, the more you'll see that life is quite varied. Many eukaryotic cells are coated in a layer of complex sugars and proteins that is in some ways similar to the cell wall of prokaryotes. It just doesn't provide rigidity against an osmotic challenge like prokaryotic cell walls. On the prokaryotic side, mycoplasma don't have rigid cell walls.


INTRODUCTION:

The basic process by which opening of stomata takes place is by endosmosis.Endosmosis causes an increase in turgidity in the guard cells thereby causing its opening.

The closing of stomata is achieved by exosmosis which makes the guard cells flaccid.

HOW DO THE REGULATION TAKES PLACE IN PLANTS:

If you read the theory proposed by Levitt from the given [link]
,in which the theory is explained in simple steps with diagrams, you will understand that $K^+$-$H^+$ pumps is the main driving force which regulates whether endosmosis or exosmosis would take place.

When the concentration of $K^+$ increases in the guard cells there is osmotic influx of water from the surrounding epidermal cells  and thus 'endosmosis' occurs causing opening of stomata.

Similarly when concentration of $K^+$ decreases there is osmotic loss of water from the guard cells to cause 'exosmosis' and thus closing of stomata.

WHY THE STOMATA CLOSE IN SALT WATER:

When the guard cells of the stomata are open it means they are turgid due to endosmosis.However when such a turgid plant cell is placed is  in salt water(hypertonic solution) the latter having a higher concentration of salt ions than the guard cells causes the loss of water from the guard cells.

Thus the salt water is inducing exosmosis to take place in the guard cells due to which they become flaccid and close.

REFERENCE:
[link]


How to determine the evolution of a dimension of fitness that has high variability of selection intensity?

It's complicated. The classic answer is from Dempster 1955 Cold Spring Harb Symp Quant Biol 1955. 20: 25-32 (doi:10.1101/SQB.1955.020.01.005), which has a whole section on "Selection Intensity Varying With Time".  Summarizing:

An example from Kimura (1954) with a mean selective coefficient of zero: "the variation of selection facilitates the loss or near loss of alleles thus tending, if anything, to decrease rather than maintain genetic heterogeneity".
An example with haploid populations (approximately equal to the diploid case for weak selection) with a time-varying selection coefficient of $s_k$ shows that the behaviour of allele frequencies over time depends on the mean value of $m=\left\langle x_k \right\rangle= \left\langle\ln(1/(1-s_k) \right\rangle$, i.e. the geometric mean of the relative fitness; in general, the geometric mean is smaller than the arithmetic mean (i.e. variation in time would lower the fitness advantage of the more-fit allele). I believe the bottom line here (although it takes quite a bit of work to understand the whole story) is as given in the last sentence of the paper: "Selection pressures variable in space or time could act to maintain genetic variance of fitness ..."

On the other hand, Tănase-Nicola and Nemenman (2011), "Fitness in time-dependent environments includes a geometric phase contribution" (DOI: 10.1098/rsif.2011.0695) say it's still more complex:

  the selection coefficient in infinitely slowly changing environments (we call this the adiabatic limit) is given by a time-average of static selection coefficients corresponding to each environment. This time-average is equivalent to the geometric mean result of Dempster [10]. It is independent of the order or the speed with which different environmental states are visited. However, for environments varying at a slow but finite rate, this time-average is not the whole story ...

All of the above is about the evolutionary dynamics of a single allele, not a comparison of the evolution multiple alleles/traits within the same genome.  Things could get (much) more complicated in that case, even in the absence of explicit pleiotropy, linkage, etc. (e.g the Hill-Robertson effect). I doubt there's a simple answer; I would suggest heuristic guesses based on independent dynamics of alleles based on the single-allele phenomena described above, followed by simulation ...


Does atrophy of the thymus not effect T-cell selection and tolerance?

T cells have a long half life (both naive and memory cells have halflives measured in years), especially when taking into account the fact that memory cells in particular can slowly proliferate and renew themselves.  An adult human therefore has 20-50 years' worth of accumulated T cells by the time they grow old, and those include both memory cells and naive cells that are potentially able to recognize new antigens. The thymus does continue to produce some new cells at a slow rate, but the backlog of previously produced cells are also able to monitor for pathogens.


I need some forearm bone motion pictures

Here is a basic image. Palm up is called supination and is the resting (anatomical) position. The radius and ulna sit parallel. When the forearm is in pronation, the radius crosses the ulna.

You can feel this yourself. Put your fingers on the ulna and move the palm into pronation and supination. You will not feel the ulna rotate. Only the radius pivots during this movement. The wrist is not involved in this movement.

The ulna is unable to rotate at all, because its olecranon process is locked into a groove on the distal end of the humerus. If you put you fingers on your bony "elbow" (olecranon process) and pronate/supinate your hand (without flexing/extending your elbow), you will not feel you ulna moving.


I think that changes in features that determine a node may happen in parallel or close together in a sequence. If the fossil record is not complete enough then the cladogram has to contain these stars. From a stochastic statistic point of view, although unlikely, it could actually happen that 2 or more  characteristics develop exactly during a similar time frame, so from a philosophical point of view, I disagree with yang.


As far as I know, edibility (wow, I'm surprised that passes the spell checker!) is not a strictly defined term, biologically or otherwise. Humans have been around eating and drinking stuff long before the scientific method was around to study this question rigorously, and before there were regulatory agencies charged with approving new products as "safe." As one might imagine, knowledge of what is and is not edible was likely passed down by oral tradition and personal experience.

Honestly, I'm not even sure designating a food (or a substance) as edible or inedible really makes much sense. Let's consider wild fruit, as mentioned in your question. If ingesting 5 or more berries of hypothetical fruit X causes your body to have a nasty reaction, then we could probably agree that fruit X is toxic and inedible (even if eating only 1 or 2 berries might not elicit the same reaction). On the other hand, ingesting berries of hypothetical fruit Y causes no reaction unless consumed in much larger quantities (maybe 100 or more berries). Although fruit Y does cause a reaction when ingested in excessive amounts, it would be a stretch to call it inedible. This principle applies to many foods that we typically consider edible but can be unhealthy or even dangerous when taken in excess.

So where do we draw the line? How much of a substance do you have to ingest without an adverse reaction to deem it edible? I don't think there is an objective answer to this question. It is complicated further by the vast amounts of variation in the human population: food allergies, differences in tolerance to certain substances, etc.


Yes, seizures can affect autonomic function including blood pressure. Such symptoms can even result in death. Note though that not all seizures are the same: there are many different types with many different causes, and they can affect different parts of the brain. There can also be different effects before, during, and post-seizure.

The effects described seem to be more related to overall discharge rates rather than synchronous firing in the periphery per se. The autonomic nervous system does not directly control heart rate, for example, but rather modulates the rate. The heart beat or vasculature would not entrain to any sort of seizure activity, for example, because the neurotransmitters involved in autonomic regulation of heart rate and blood pressure are comparatively slow-acting relative to the rate of seizure activity (essentially those functions are taking a moving average of neural input, rather than responding specifically to each impulse).

The relationship between autonomic function and seizures need not be unidirectional, either; circulatory changes can also be triggers for seizures.

References

Devinsky, O. (2004). Effects of seizures on autonomic and cardiovascular function. Epilepsy currents, 4(2), 43-46.

Nei, M. (2009). Cardiac effects of seizures. Epilepsy currents, 9(4), 91-95.

Penfield, W., von Sántha, K., & Cipriani, A. (1939). Cerebral blood flow during induced epileptiform seizures in animals and man. Journal of Neurophysiology, 2(4), 257-267.


The Eliava Institute in Tiflis (Georgia (a country)) has been at it since the 1930`s. A US company sells a phageproduct for desinfection of meat.

The risk of Phagetherapy is there, if the phage is ill choosen or contaminated with other phage it could introduce pathogenic genes to the target or other bacteria.

If those risks are eliminated there is very little risk in phage therapy aside from the fact that it may not work at all. Phagetherapy is most useful in regions where bacteria are normally found, in other places the immunesystem will make short work of it.

The faster and cheaper sequencing gets the more effective phagetherapy will become. Since a "bad" bacteria can quickly be isolated and a proper "phage cocktail" can be prepared. If we get to the point that we can sequence the whole microbiom of a person then i bet that Phagetherapy will be a very normal thing.

To your cancer question, i think its rather hard to apply it to cancer therapy except if u are looking to combat the cancer with a Intracellular bacteria...but then again. How u get the phage to it.

A excellent read on this topic is the Book "the bacteriophages".


Is this double stranded property the same as saying an organism is
  diploid?

No.  You are a diploid organism because you have two copies of every chromosome.*  You got one from your mother, and one from your father.  All your cells are also diploid, except for your gametes, each of which contains only one copy of every chromosome (due to crossing over, each chromosome is partially from your mother, partially from your father).

Bacteria just have one copy of their genome.  They duplicate it prior to cell division, and each resulting cell has one copy of each chromosome.

*Unless your sex chromosomes are XY, or are anuploidic.


What are the molecular mechanisms that make the turtle brain more resistant to hypoxia?

There is a bunch of literature on the topic. A good starting point is probably a short description with lots of references in this thesis (page 8), not to talk about other articles, which pop up in google scholar: 1, 2.

The mechanisms are multifaceted and involve principally decrease in oxygen and ATP demands: reduced neuronal activity, lower density of ion channels (but hyper-polarization of the membranes) and so on. Concerning blood flow: "Brain blood flow was continued or increased, and oxygen and creatine phosphate (PCr) stores offered some immediate protection. As PCr declined, turtle brain became increasingly reliant upon anaerobic glycolysis."


First I think that is a Western Spotted Dove (Spilopelia suratensis), now splitted from the Eastern spotted Dove (Spilopelia chinensis). In your area there should be both species but the red iris and eye-ring should indicate the Western. Sexes are alike so there are no signs you characteristics you can check (source, handbook of the bird of the world, which is the most updated and reliable source in many occasions). Males sing much more often than females (so you can observe this behaviour) and in many species, but I dunno about this one, is the male providing food to the female...so I think your guess is right!

All the best,

Have fun


Are tergo-sternal muscles of cockroach involved in blood circulation?

It is not the tergo sternal muscles that are involved in blood circulation in cockroaches. Tergo sternal muscles help in breathing. It is the Alary muscles that help in blood circulation. The alary muscles are associated with all the thireen chambers of cockroach's heart on either side of it. The alternate contraction and relaxation of these muscles help to pump the blood.

Sources which support my answer:

Tergo sternal muscles are involved in respiration, Look into the book "A Dictionary of Entomology" pg 4, link
Alary muscles help in blood circulation, link


Why is high fructose corn syrup unhealthy?

Besides a lot of propaganda there is not much evidence that high fructose corn syrup (HFCS) is more dangerous than normal sugar. Lets have a look at the sugar in detail:

HFCS is produced from corn and is originally a glucose syrup. Since fructose is obviously much sweeter, the glucose is converted enzymatically into fructose (see here for more details). Before the use in food production additional glucose is added to the syrup so that typical syrups contain 55% fructose and 42% glucose or 42% fructose and 53% glucose (the remaining % are water).

If you look at saccharose (which is our ordinary sugar) then this is a disaccherid which is build from one molecule of glucose and one molecule of fructose. The enzyme sucrase breaks this molecule up into one molecule of fructose and glucose each, so reaching a 50%:50% ratio between the sugars.

As the ratios are more or less the same, it doesn't matter for the human body, where the sugar come from meaning that in this context it is more too much sugar in the food than a problem with HFCS, as also this study suggests:

Straight talk about high-fructose corn syrup: what it is and what it
ain't.

Fructose itself is not without problems as this induces the production of fats in the liver, but again, it doesn't matter for the body, where this fructose comes from:

Fructose induced lipogenesis: from sugar to fat to insulin
resistance.

For further reading I can also recommend this article on Gizmodo:

Is High Fructose Corn Syrup Really Bad for You?


Fraction of channels open at equilibrium

The mechanism given by the OP is renowned in the world of pharmacology and drug-receptor interactions, and is due to Castillo and Katz (1957). A very readable review of the history and importance of this mechanism may be found in Colquhoun (2006), published in Trends in Pharmacological Sciences. (For more great papers from the Colquhoun lab, see here)

If A is the agonist, R the vacant receptor, AR an occupied but closed form of the receptor, and AR* the occupied but open form of the receptor, the situation where an agonist must bind before the channel can open may be represented as a three state receptor model (unoccupied, occupied-closed and occupied-open) as follows:

$$\ce{A + R <=>[$k$_1][$k$_{-1}] AR <=>[\beta][\alpha] AR{*} \tag{1}}$$

We need to be more specific here, and define exactly what is meant.  Let $A$ be the concentration of free agonist (ie agonist not bound to receptor), let $AR$ be the concentration of occupied closed receptor, and let  ${AR^*}$ be the concentration of open occupied receptor.  In addition, let $k_1$ be the second-order rate constant for the association of agonist with unoccupied receptor, and let $k_{-1}$ be the first-order rate constant for the dissociation of agonist from the occupied, closed receptor. Finally, let $\beta$ and $\alpha$ be first-order rate constants for the inter-conversion of the occupied receptor between closed and open states, respectively. Rate constants may be thought of simply as constants of proportionality arising from the law of mass action (see below).

The OP asks for a derivation of the following equation,

$$p_1^{(equil)} = \frac{({\chi}_a/{K_a})(\beta/\alpha)}{1 + ({\chi}_a/{K_a})(1+ \beta/\alpha)}\tag{2}$$

where $p_1^{equil}$ is the fraction of channels open at equilibrium, ${\chi}_a$ is the total agonist concentration, ${K_a}$ is the dissociation constant (not the association constant) for the binding of agonist to the closed receptor.

The situation is very nicely illustrated in the following diagram, taken from Colquhoun & Hawkes (1995)

Derivation

Although Eqn(2) looks daunting at first sight, the derivation is surprising simple.

Let $R_t$ be the total receptor concentration. An expression for $p_1^{equil}$ (the fraction of receptor channels open at equilibrium) may now be written as follows:

$$p_1^{(equil)} = \frac{AR^*}{R_t}\tag{3}$$

As

$$R_t = R + AR + AR^*$$

Eqn (3) may be rewritten as follows:

$$p_1^{equil} = \frac{AR^*}{R + AR + AR^*}\tag{4}$$

The problem with Eqn (3) & Eqn (4), of course, is that they are pretty close to useless. The total concentration of receptor is unlikely to be known, and obtaining reliable estimates for $AR$, $R$ and $AR^*$ present almost insurmountable experimental difficulties.

By the law of mass action, which holds that states that the rate of any reaction is proportional to the product of the reactant concentrations (and where rate constants may be considered constants of proportionality), the following may be written assuming the system described by Eqn. (1) is at  equilibrium.

$$ {k_1}. A. R = k_{-1}. AR \tag{5}$$

$$ {\beta}. AR = {\alpha}AR^* \tag{6}$$

Let  ${K_a}$ be the dissociation constant for the binding of agonist to the closed receptor. From Eqn (5), the following may be written.

$$ \frac{A. R}{AR} = \frac{k_{-1}}{k_1} = {K_a} \tag{7}$$

Therefore:

$$ R  = \frac{{K_a} AR}{A} \tag{8}$$

An equation for the total concentration of agonist, ${\chi}_a$, may be written as follows:

$$ {\chi}_a  = A + AR + AR^* \tag{9}$$

The problem with using Eqn (9) to obtain an expression for $A$ (the concentration of free agonist) is that it makes the resulting equations very difficult to solve. As regards the algebra, the situation is make a lot simpler by assuming that the total agonist concentration is equal to the free
agonist concentration, ie by assuming that Eqn (9) may be written as follows:

$$ {\chi}_a  \approx A  \tag{10}$$

When the concentration of agonist is very much greater than that of the receptor, this approximation is justified.

Eqn (8) may be re-written as follows:

$$ R  = \frac{{K_a} AR}{{\chi}_a} \tag{11}$$

From Eqn (6), an expression for $AR^*$ may be obtained.

$$ AR^* = \frac{{\beta}. AR}{{\alpha}}  \tag{12}$$

By substitution for $R$ (using Eqn 11) and  $AR^*$ (using Eqn 12) in Eqn (6), followed by cancellation of the common term ($AR$), the following expression may be obtained:

$$p_1^{(equil)} = \frac{\beta/\alpha}{1 + {\beta/\alpha} + K_a/{\chi_a}}\tag{13}$$

Multiplying Eqn (13) 'above-and-below' by ${\chi_a}/K_a$ gives Eqn (2), the equation requested by the OP.

Comment

Note that when $K_a$  = $\chi_a$ and $\beta/\alpha$ >> 1, almost all of the receptors are open as $p_1^{(equil)}$ is close to 1.  When $K_a$  = $\chi_a$ and $\beta/\alpha$ << 1, almost all of the receptors are closed, as $p_1^{(equil)}$ is very much less than 1.

Note also that $K_a$ is a dissociation constant and is the ratio of a first-order rate constant and a second-order rate constant, and will have dimensions of concentration.

Addendum

It may be of interest that Colquhoun's great book, Lectures on Biostatistics, is (legally) available free of charge (as a pdf) from here

DC's Improbable Science

A great site


How to derive Hill equation (one specific part)

In your second step $(K_d)^n$ should be $(K_A)^n$.

Where:

$K_d$ is the apparent dissociation constant and
$K_{A}$ is the ligand concentration that results in half occupation

See for example the relevant wikipedia article.


Why is 'Grudger' an evolutionary stable strategy?

Unfortunately it is not necessary to invoke group selection to answer this question.  This is one of the reasons that Dawkins likes this discussion so much - he does not believe in group selection and so the discussion in SG does not invoke group selection.  ESSs are described in the book as the product of direct competition or interaction between genes.

ESSs in this case, can be described in terms of game theory.  In the famous Prisoner's Dilemma experiment, Grudger is similar to tit for tat, which 'won' the competition in the original Axelrod contest.

To see how this works you make a simple win/loss game matrix:

     G        NG
G    win 1    win 3
NG   lose 3   lose 1

if you are groomed you win 1, if you are groomed, but you don't have to groom - even better win 3 (say)
If you groom but are not groomed, lose 3
If neither of you are groomed, you both lose 1

one might argue the exact proportions, but the point is that getting some thing for nothing is better than reciprocating, and getting nothing for your efforts and time are a loss, because you could have been getting groomed by someone else. As you can see cheaters end up in the top row all the time.  grudgers end up along the diagonal, and once in a while in the lower left, Suckers get stuck in the lower left a lot whenever there is a cheater around.

now run this encounter over and over.  A behavior which scores negative the more times you run is not stable - they are going to disappear from the population, at least if this disadvantage is real

It has more than one stable outcomes in populations, a population that is full of Grudgers will all groom each other as before you know everyone, you assume they will reciprocate.  Everyone wins!

Any invading Cheaters will quickly be at a disadvantage, in that they will not be groomed more than N times where N is the number of grudgers in the community.  Note that there is an equilibrium here - the Cheaters may exist in a small number - when N is large enough for a cheater to get enough grooming to make a 'living'.

Suckers can also exist within a population of grudgers, but a population of Suckers where Cheaters show up are quickly sucked dry by the cheaters over several generations where you tally up 'points' and give more, healthier offspring to high scorers.  They are not ESS stable.

Cheaters are also stable - nobody ever wins, but they don't lose big either and any invading grudgers can't get groomed.


What type of epithelium are the pancreatic Islets of Langerhans?

I think the image you've attached lacks clarity. If you see the image below, you could say that the epithelium is cuboidal with central rounded nucleus.

Unlike the oval nuclei of columnar epithelium, rounded nucleus suggests that they are cuboidal in shape.
The image is from https://webpath.med.utah.edu/HISTHTML/NORMAL/NORM010.html


Ipsilateral vs contralateral side of body

Yes. Ipsilateral and contralateral always have to be relative to something; ipsilateral means "same side" and contralateral means "other side" - you can't really be the same or other side of something unless you have a reference point.


There will always be a tradeoff in terms of resource allocation between reproduction and self maintenance. Since worker ants forego reproduction to perform other roles (gathering resources, caring for young etc.) within the colony, it makes sense that this would favour a longer lifespan. This idea works for most animals (i.e. higher reproduction = lower lifespan across species in general) and is well documented (Partridge et al. 1987, Gems & Riddle 1996 (PDF link), Westendorp & Kirkwood 1998 - to name a few). However the relationship is reversed in eusocial animals: the queens of ants, some bees and naked mole rats (which are all eusocial) tend to be longer lived than their sterile workers (Hartmann & Heinze 2003). Aging patterns within ants and other eusocial organisms are a very popular research topic at the moment, but the mechanisms causing differences between social castes are not fully understood.

Eusociality is strongly associated with increased lifespan, indeed many studies on the evolution of aging have focussed on eusocial animals which have appeared to overcome aging effects to an extent (Keller & Genoud, 1999, Buffenstein 2005). The naked mole rat is one of very few species of eusocial mammals and the relationship between its lifespan and body mass is very dissimilar to that of other rodents (ignore the bat points):

Image from Buffenstein & Pinto (2009).

If a queen has a longer reproductive lifespan then over the course of its life it will create a higher number of offspring. This will cause their increased longevity genes to be more prevalent in the gene pool over time - as long as they are able to reach the limit of their reproductive lifespan and are not killed by externalities (accident or attack) in the meantime. Therefore this trait (longer reproductive lifespan) will be selected for as long as the queen is protected.

Within eusocial colonies, there is often a protective environment (Buffenstein & Jarvis 2002): there is usually a physical structure (nest or burrow); symbiotic bacteria and/or fungi creating a more hygienic microflora; and queens are also protected by other castes. This gives queens a lower incidence of death due to accident or attack which (from the reasoning in the previous paragraph) supports the selection of a longer reproductive life. This is likely to lead to longer lived workers since they share the same genes.

However queens do tend to live much longer than their workers (O'Donnell & Jeanne 1995). This is probably due to their reproductive role. All the ants in the colony are investing in reproduction (whether by physically giving birth to young or by providing it with food and protection) therefore the normal relationship (reproduction and lifespan tradeoff) mentioned at the start is not relevant, but since the queen is the only individual reproducing, it will be the only one for whom lengthened lifespan is beneficial evolutionarily.

A mean lifespan of 20 years has been observed in Formica exsecta, and a maximum lifespan of 28.5 years observed in Lasius niger. Pogonomyrmex owyheei has an observed maximum of 30 years, and mean of 17 years. These (and many more) figures were obtained from a review by Keller (1998).

Other references on this subject include (Svensson & Sheldon 1998), (Keller & Genoud 1997) (PDF link), (Calabi & Porter 1989), and (Amdam & Omholt 2002).

References

Amdam, G.V. & Omholt, S.W. (2002) The Regulatory Anatomy of Honeybee Lifespan. Journal of Theoretical Biology, 216, 209–228.
Buffenstein, R. (2005) The naked mole-rat: a new long-living model for human aging research. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 60, 1369–1377.
Buffenstein, R. & Jarvis, J.U.M. (2002) The Naked Mole Rat--A New Record for the Oldest Living Rodent. Sci. Aging Knowl. Environ., 2002, pe7.
Buffenstein, R. & Pinto, M. (2009) Endocrine function in naturally long-living small mammals. Molecular and cellular endocrinology, 299, 101–111.
Calabi, P. & Porter, S.D. (1989) Worker longevity in the fire ant Solenopsis invicta: Ergonomic considerations of correlations between temperature, size and metabolic rates. Journal of Insect Physiology, 35, 643–649.
Hartmann, A. & Heinze, J. (2003) Lay eggs, live longer: division of labor and life span in a clonal ant species. Evolution, 57, 2424–2429.
Keller, L. (1998) Queen lifespan and colony characteristics in ants and termites. Insectes Sociaux, 45, 235–246.
Keller, L. & Genoud, M. (1997) Extraordinary lifespans in ants: a test of evolutionary theories of ageing. Nature, 389, 958–960.
Keller, L. & Genoud, M. (1999) Evolutionary Theories of Aging. Gerontology, 45, 336–338.
O’Donnell, S. & Jeanne, R.L. (1995) Implications of senescence patterns for the evolution of age polyethism in eusocial insects. Behavioral Ecology, 6, 269–273.
Svensson, E. & Sheldon, B.C. (1998) The social context of life evolution history. Oikos, 83, 466–477.


Is Rheumatic fever more Chronic than acute?

the inflammatory response it autoimmune reaction, thus it occurs 4 weeks after the Strep infection.

please, look at the picture from the "Nature" -


Yep, the soma-soma synapse in that paper appears to be a chemical synapse between two cell bodies. There are no axons or dendrites in that preparation so the synapse must be between the somas. They are using two snail neurons that are far from each other (in different ganglia) in vivo, but which are known to synapse. This in vivo synapse is long-range and so must be mediated by an axon. In the dish, they can encourage the  synapse to form even without encouraging axons and dendrites to grow.

Note that this is an artificial in vitro preparation and they are, in some sense, forcing a synapse to occur in an unusual way in a cell culture dish. They do this because it makes it easy to study certain aspects of the signalling mechanisms for generating synapses. In your paper, they appear to be using it as an easy preparation for a proof of principle for the interface between a biological neuron and a non-biological semiconductor substrate.

The paper you cited references this paper that outlines the soma-soma preparation with a pretty picture to make things clear: http://www.jneurosci.org/content/19/21/9306


In biosynthesis of cysteine and methionine, where does the sulfur come from?

Microorganisms (and plants) make cysteine from serine using H2S as the sulphur source. Condensation of these two directly gives cysteine in some bacteria, but most often the reaction sequence is:

serine + acetyl-CoA >>> O-acetylserine + CoA-SH
O-acetylserine + H2S >>> cysteine + acetate + H2O

As you say, in terms of the sulphur, cysteine and methionine are interconvertible.
Animals rely upon their diet for methionine, and can make cysteine from that methionine.


At what rate do chromosomal rearrangements occur?

Obviously, there won't be a single number for this.
The phenomenon is fairly well understood in yeast. Unfortunately, most studies tend to focus on the rate of formation of specific well-understood rearrangements, and then use that as a baseline. I am having trouble finding a measurement of overall rearrangement rate, although the system is ideal for this.
There has been some work on characterizing rates of rearrangement (and its evolution) across evolutionary history, I don't know if that is directly relevant.
This paper has a decent breakdown of the incidences in humans across different kinds of translocations. For example:

Additional studies (5, 6) followed and the incidence of balanced translocations was ultimately determined to be 1 in 500 in the general population.

Studies using cleavage stage biopsy for reciprocal translocation PGD have reported proportions of unbalanced embryos as high as 82% (57).

There is good reason to expect that it varies significantly across species and across chromosomes. For example, the Drosophila Y is a hotspot.
And (first paper):

Rearrangements involving chromosomes 13 and 14 (der(13;14)(q10;q10)) account for 75% of Robertsonian translocations (12).

For an early paper looking at a large population, you can see here.
Note that most of these human numbers are indicative of population incidence rather than rate of occurrence. Others have attempted to study effects on the translocation rate directly.
The best citation that I found for directly measuring translocation rate is here. However, the data are apparently for somatic translocations and are rather unevenly sampled so I am unsure of how generalizable it is. I looked at WYSIWYG's papers and they might provide some specific examples but they don't seem to address translocation rate directly either.
Take-home, it's hard to directly measure rearrangement rate in humans due to inviability of many/most aneuploidies early after fertilization. Somatic is easier to estimate but may not be representative of rearrangements in the gametes.


In my opinion wearing gloves during cell culture is a good idea. It works both ways as a protection: For your cells since you are not loosing small danders from your hand and for you since you are not getting media or chemicals used in cell culture on your skin when you are uncautious.

I usually prefer nitrile gloves over latex, since nitrile gloves are ways more stable and pose no risk for allergies (I am not allergic, but minimizing risks is always a good idea). The downside of nitrile is, that they are a bit more expensive (thats the point where you need to argue with some coordinators about what to buy).

I never had problems with desinfectants and gloves, but this is my personal experience and probably not more than an anecdote. I desinfect my gloves, since I touch different things with them, but I usually don't spray everything which comes around with alcohol since this is usually pointless. To be useful, it needs to reach all points of a surface and also needs to stay there for a while. What I make sure is that all the stuff, which goes into the hood is either very clean or packaged sterile anyway.

After my experiences some data, this PDF has quite a lot of information. The list below is taken from the PDF:

Nitrile gloves:

Acetone - fair
Ethanol - excellent
Isobutyl - alcohol excellent
Isopropyl - alcohol excellent
Methanol - fair

Latex gloves:

Acetone - good
Ethanol - excellent
Isobutyl - alcohol poor
Isopropyl - alcohol excellent
Methanol - fair


Why is it important to have a restriction point? (G1-S phase control)

The reason you want a check point in the transition from the G1 phase of mitosis to the S phase of mitosis, is that the cell needs to make sure that it synthesized all of the necessary proteins, and accumulated the necessary compounds with which to have DNA synthesis begin AND complete.

The transition from G1 to S is a point of commitment for the cell. There is no turning back at that point. It either needs to faithfully replicate the entire genome or it should die. An incompletely replicated genome would be disastrous for the cell.

If it tried to arrest and go backwards it would likely have too many copies of certain genes and those gene products would likely cause lethality to the cell. You would end up with all sorts of errors and breaks where replication forks collapsed. It would basically be death for the cell. What would be even worse would be if this cell was actually able to avoid the death signals, and at some point enter the cell cycle with all of these damaged chromosomes and you are looking at the possibilities of cancer.

If it arrested and then proceed to G2 and M and somehow got through those checkpoints, then you will have two daughter cells with incomplete genomes. Again if they could survive at all, then likely end up becoming good candidates to proceed down the road to cancer.

That is why G1 needs to be completed properly before the cell commits to replication. It is a point of no return and needs to be tightly regulated for the benefit of the multicellular organism.


How some virus are able to reach the CNS?

some viruses like rabies get into the peripheral nerves, and travel through those to the spine , unimpeded by any obstacle.


Evidence of condition-dependent sex-allocation in regards to humans

I am not aware of any such evidence in humans but I know little about this literature. If you happen to have data showing that, then it would probably be a relatively big thing! Below is a series of comments that might be of interest.

Evidence from Hyena

The evolution of the sex-ratio variation in hyena have been quite extensively studied. This very short article (not peer-reviewed) cite a number of key papers on the subject.

Logic behind the second assumption

In case clarification is needed. The variance in fitness is indeed often higher in males than in females. The reason is that females (by definition) produce the larger gametes, the one that don't leave the body and therefore often pay a much higher cost when reproducing than males do. As such, females are the limiting factors. As a consequence, males compete a lot to access females and "good males" receive a lot of mating opportunities while "bad males" receive little mating opportunity causing the higher variance in fitness among males than among females.

Statistics

IMHO, there is a tradition of horrible statistics when dealing with human sex-ratio data. It is particularly the case as these papers are often published in journals where reviewer have little knowledge in statistics (e.g. medicine). Typically, "windowing" data is generally a very bad idea and previous papers in the field have reported very bad interpretation from data due to cherry picking specific ways to classify observations. Please be cautious in your statistical analysis!

About the post

The formulation of the hypothesis is clear enough but some sentences are misleading

  it makes "natural selection" sense for females to vary sex ratio`

This sentence sounds very wrong. You should rather say "females that are able to vary the sex-ratio among their offspring will be have a higher fitness".

Note that I said "among their offspring" because while this would cause variation in sex-ratio in the population, genotypes are selected based on their ability to vary the sex-ratio among their offspring and not in the population. In fact, any given individual, would appreciate if all the other would produce the exact opposite sex-ratio than the one they actually produce among their offspring.

  better chance of reproductive success

This sentence a little clumsy as well and should be replaced with higher fitness


Chlorine is a reactive substance and an oxidizing agent. It can cause damage to surfaces exposed to it such as eyes, skin etc but it cannot penetrate deeper. Chlorine can damage your hair by oxidation — hair becomes rough and brittle. This is not same as hair loss — chlorine doesn't cause hair to fall out because it cannot penetrate to the follicles. See here

EPA has set maximum residual disinfectant level for chlorine (as Cl2 and other chlorinating agents such as chloramine [NH2Cl] and chlorine dioxide [Cl2O]) beyond which it is considered unsafe.

Chloramine       :  4.0 mg/L or 4 ppm
Chlorine         :  4.0 mg/L or 4 ppm
Chlorine Dioxide :  0.8 mg/L or 800 ppb


Could an "overactive" brain increase the chances of Alzheimer's Disease?

I think the article that quoted(1) is different to what the link shows now(2). However, both the article quoted and the one in the link are relevant to the question.
Alzheimer's Disease : In a nutshell, AD is the most common form of dementia. Although the exact cause is still under investigation, several genes have been implicated in the development of AD. One of the things you see in the brain with disease progression is beta amyloid plaque deposition which disrupts brain activity.
Brain Activity : While the brain consumes around 20% of our body's energy at a baseline, an increase in brain activity only increases this consumption by around 5%. Hans Berger, the first to record an EEG stated that "mental work, as I explained elsewhere, adds only a small increment to the cortical work which is going on continuously and not only in the waking state".(2)
However, there are a few 'intrinsic' networks or regions that perform functions such as "information processing for interpreting, responding to and predicting environmental demands". One of the areas active in this state of the brain is referred to as the 'default mode network' (DMN). It's thought that DMN is the main target of the amyloid plaques responsible for Alzheimer's Disease.(2)
However, there are other multimodal regions of the brain that perform processing of various types of information. It's now suggested that "regions vulnerable to Ab deposition do not simply involve the DMN, but rather comprise multimodal brain regions that are highly interconnected, plastic, and capable of rapid ATP generation"(1).
So it's a variation of activity in these particular areas - not all - that are implicated with Alzheimer's Disease. When you are performing a task, activity in these areas diminish.
Why keep the brain intentionally active : The reason for the hypothesis that actively engaging in challenging activity may reduce the risk of AD is that individuals with a high cognitive reserve have been shown to cope with the pathological changes such as beta amyloid deposition better. Cognitive reserve has been linked to a bunch of factors including "education, occupation, socioeconomic status, social networks and lifelong participation in cognitive and physical activity" and reflects "lifelong patterns of behaviors, endogenous factors (including genetics) and exposure to environmental factors"(1).
Moreover, it's suggested that perhaps higher cognitive reserve increases neuronal efficiency which has been shown to reduce plaque deposition.(1).
So InquilineKea's question and jp89's answer aren't really contradictory.

August, et al. Lifespan brain activity, β-amyloid, and Alzheimer's disease.
Trends in Cognitive Sciences. 2011. 15(11):520-526.

Raiche. Two views of the brain.
Trends in Cognitive Sciences. 2010. 14(4):180-190.

Hafkemeijer, et al. Imaging the default mode network in aging and dementia.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 2012. 1822(3):431-441.

Harrison's Principles of Internal Medicine. 16th Ed. McGraw Hill.


Indirect pathway of movement and Parkinson's?

The dopaminergic neurons of the substantia nigra pars compacta are a part of neither the direct nor the indirect pathway. The dopaminergic system rather acts as a modulator between those two pathways. More dopamine steers the system towards the direct pathway, less dopamine towards the indirect pathway.

One of the best explanations of the basal ganglia that I've ever seen were video lectures by Dr. Najeeb on youtube.

explanation of the basal ganglia pathways

pathologies involving the basal ganglia

At the beginning of the second video there is a short review of the pathways he explains in the first one. At 5:06 he starts talking about Parkinson's disease.

A paper about the topic:

Functional organization of the basal ganglia: Therapeutic implications for Parkinson's disease (Obeso et al. (2008)


By what mechanism is Streptococcus bovis acting as a risk factor for colorectal cancer?

As you probably know, there is a lot of literature on the correlation between Streptococcus bovis and colorectal cancer, but very little on possible mechanisms.

In an editorial (Streptococcus bovis: Causal or incidental involvement in cancer of the colon? in the International Journal of Cancer 119(9):xi-xii), Harald zur Hausen referring to this paper:

  Biarc J, Nguyen IS, Pini A, Gosse F, Richert S, Thierse D, van Dorsselaer A, Leize-Wagner E, Raul F, Klein JP, Scholler-Guinard M. (2004) Carcinogenic properties of proteins with proinflammatory activity from Streptococcus infantarius (formerly S. bovis). Carcinogenesis 25: 1477–84.

comments:

  ...used a partially purified S. bovis S300 fraction representing 12 different proteins and triggered the synthesis of proinflammatory proteins (human interleukin-8 and prostaglandin E2, correlated with the in vitro overexpression of cyclooxygenase-2 [Cox-2]) in human colon carcinoma cells (Caco-2) and in rat colonic mucosa. These data could point to a role of oxygen radicals in colon carcinogenesis induced by a chronic infection with S. bovis. The mechanism could be similar to the one suspected for the development of gastric carcinomas after persisting Helicobacter pylori infections. Presently it would still be important to know whether the increased presence of S. bovis in colonic cancers and polyps results from the preferential bacterial colonization of these cancers and their precursors or whether S. bovis represents a carcinogen that is causally involved in colon cancer.

The last sentence summarises the ongoing debate: does the bacterium promote the cancer, or does the cancer promote the bacterial infection?


It is probably Daddy Longlegs (Leiobunum vittatum)

this invert color image show the resemblance.

Source:
http://www.insectidentification.org/insect-description.asp?identification=Eastern-Harvestman

http://bugguide.net/node/view/840130

Might be eating a cockroach:

UPDATE:

OR

It might be Mitopus morio(modern harvestman)


Which DNA sequence will have higher melting temperature: CCCCCC... or GCGCGC...?

The dependence of melting temperature on different dinucleotide pairs was experimentally measured; the meting temperature calculator is based on those results. Based on these results, you would see that a GC dinucleotide pair would differ from GG and CC pairs. Possibly, this is because of steric effects and stacking conformations.

SantaLucia (1998; author of the nearest neighbour model) has referred to different experimental studies from which the values were obtained, in the Table-1 of the paper.


Do humans have enough biological differences to be grouped into races or subspecies?

Firstly, it's not true that you can't tell racial background from DNA. You most certainly can; it's quite possible to give fairly accurate phenotypic reconstruction of the features we choose as racial markers from DNA samples alone and also possible to identify real geographic ancestral populations from suitable markers.

The reason that human races aren't useful is that they're actually only looking at a couple of phenotypic markers and (a) these phenotypes don't map well to underlying genetics and (b) don't usefully model the underlying populations. The big thing that racial typing is based on is skin colour, but skin colour is controlled by only a small number of alleles. On the basis of skin colour you'd think the big division in human diversity is (and I simplify) between white Europeans and black Africans. However, there is vastly more genetic diversity within Africa than there is anywhere else. Two randomly chosen Africans will be, on average, more diverse from each other than two randomly chosen Europeans. What's more Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Africans are from each other.

This makes perfectly decent sense if you consider the deep roots of diversity within Africa (where humans originally evolved) to the more recent separation of Europeans from an African sub-population.

It's also worth noting that the phenotypic markers of race don't actually tell you much about underlying heredity; for example there's a famous photo of twin daughters one of whom is completely fair skinned, the other of whom is completely dark skinned; yet these two are sisters. This is, of course, an extreme example but it should tell you something about the usefulness of skin colour as a real genetic marker.


Parallel Autonomic regulation of Cough and Runny Nose

Skymninge mentioned opioidreceptors and the withdrawal symptom of opiods as a runny nose: codein binds to opioidreceptors.

I think now that the cough can trigger runny nose.
I breathed with empty nose some 15 minutes.
Then, I had a deep dry cough and right after it a stuffy nose.
I really felt this time the negative gradient at the level of kidneys and also posteriorly.
I do not know how this kind of pain was felt, I think, near or on the kidneys.
I do not understand the effects of deep dry coughs.
They seem to be linked to several processes and locations in the body.

After this deep dry cough, I did some abdominal breathes and this way massaging the lymphatic circulation systemically, the stuffy nose disappeared.
My thorax is opposite of astonic person (say if you remember the name in Propedeutics).
This can be a restricting factor in the circulation of the lymph.

My conjecture is that the people with big chests (opposite of astonic) need to concentrate more on abdominal breathing such that to keep out of stuffy noses.
Restricted lymphatic circulation causes less wastes returned to the blood circulation.
Thus, accumulation of bacteria in the larynges which increases the risk of a dry cough.
Good lymphatic circulation ensures that bacteria is not congested in the larynx.
So cough seems to be a mechanism to start a runny nose.

This all is finely regulated.
There are several receptors in the body.
The deep cough however seems to be linked to a reflex which causes a runny nose.

Some studies about opiates and respiratory activity

The effects of opiates on the respiratory activity of thoracic motoneurones in the anaesthetized and decerebrate rabbit.


What do different fermentation products have in common?

Although there is  no net oxidation or reduction in glycolysis, a constant supply of  NAD+ is (paradoxically) required in order for glycolysis to continue. Otherwise, the glyceraldyde-3-phosphate dehydrogenase reaction (GAPdh) could not generate 1,3-diphosphoglycerate.

So how is the NADH generated in the GAPdh reaction converted back to NAD+? Both alcohol and lactic acid fermentation regenerate NAD+ by reduction of the carbon skeleton that was oxidized in the GAPdh reaction, albeit at different 'points' in the glycolytic reaction sequence.

In alcohol fermentation, alcohol dehydrogenase acts as aldehyde reductase, reducing acetaldehyde to ethanol and NAD+.  In lactic acid fermentation, lactate dehydrogenase acts as a pyruvate reductase, reducing pyruvate to lactate and NAD+.

In both alcohol and lactic acid fermentation, there is no net oxidation or redution: glycolyis is the splitting of glucose.

Finally, we may note that the electron acceptor in both cases is 'internal'  Neither process requires an external electron acceptor such as oxygen.  The electrons removed from the carbon skeleton in the GAPdh reaction (generating NADH) are added back to the same carbon skeleton (but with different molecular arrangement) in both the ADH and LDH reactions.


Can ELISA be used to detect a plant enzyme? Creating assay for a new enzyme

I want to add something on top of Chris answer.

The production of an antibody it is usually a quite slow (and expensive) process, an alternative that worth to consider is phage display (https://en.wikipedia.org/wiki/Phage_display). Once you find the phage that effectively bind your protein of interest, you can use it instead of an antibody in what is called a Phage-ELISA assay.
However, mind that the ELISA (or Phage-ELISA) will give you information about the presence and the concentration of the enzyme, it will not give you any hint about its activity.


Why are vegetations in Infective endocarditis common on the atrial side?

With the bacterial IE, it would look like the vegetations tend to colonize the lower pressure sides of the valve structure (REF1). Something that was made clear that distinguishes the IE vegetations frm the Libman-Sacks vegetations was overall motility. Specifically, Libman-Sacks vegetations exhibit no independent motion and are largely sessile, whereas IE vegetations can be motile (REF2). In terms of where they attach I think this makes sense, the more motile vegetations colonize the less turbulent area, and the sessile vegetations seem to hold up in either scenario. Reference 1 also rather usefully points out that IE vegetations may be located anywhere on the valve structure as well, they just tend to be on the low-pressure side.

So being said i would argue that the motility of the organisms is a deciding factor.


Translation of Poly-U in the Nirenberg and Matthaei experiment

This is an intelligent question that highlights the ‘sleight of hand’ simplifications employed in many text books to make experimental science appear cleaner and more logical than is in fact the case. From what we now know about the requirement for an AUG initiation codon in protein biosynthesis these experiments should not have worked.

The reason they did was that they were performed at an unphysiologically high concentration of Mg2+ which overcomes the need for specific initiation (and, incidentally, allows other reactions of protein synthesis to proceed in an abnormal manner, particularly the codon-directed tRNA binding reaction used to finish the deciphering of the genetic code). You should also bear in mind that the efficiency of the reaction was probably much less than that within the cell, but this was of no concern as all that was required was that a product be synthesised.

Reference

I worked in this area in the late 60s/early 70s and the importance of magnesium concentration was just common knowledge in the field, so it is difficult to cite a reference to support my assertion. However a brief search brought up a contemporay paper on the effect of magnesium on initiation of protein synthesis in phage RNA, illustrating its importance. There are, no doubt, others.


What is the name of this plant (see pic)?

That looks like a member of genus Lupinus, flowering plants native to North and South America:

I couldn't find a good resource for species of Lupinus in Columbia so I can't help you with the species, unfortunately.


What is the most heat-tolerant organism?

Methanopyrus kandleri has been able to grow and proliferate at temperatures of up to 122°C when under around 20atm (Takai et. al. 2008).  This was achieved in the lab but the theory should hold true for deep sea thermal vents.  Another strain of M. kandleri survived incubation to 130°C however was unable to reproduce at this temperature.

One of the key adaptions for thermophiles is the selection towards an extremely thermo-stable copy of the enzyme DNA polymerase.  This allows DNA replication at high temperatures and is similar to the 'Taq' polymerase used in the polymer chain reaction in labs, derived from another thermophile, Thermus aquaticus.

References

 Takai K, Nakamura K, Toki T, Tsunogai U, Miyazaki M, Miyazaki J, Hirayama H, Nakagawa S, Nunoura T, Horikoshi K. 2008. Cell Proliferation at 122°C and Isotopically Heavy CH4 Production by a Hyperthermophilic Methanogen Under High-Pressure Cultivation. PNAS 105: 10949–10954.


Is this question about limiting factors answerable?

I think your thinking is fine, but you're being a bit pedantic about it. I don't think there is any typo.
The purpose of the question is for you to understand that there are two limiting factors here: light and CO2.
You can identify points in the graph where light is limiting because there is a slope with increasing light, and you can identify points in the graph where CO2 is limiting because light no longer increases the rate, and that the plateau level changes with different CO2 levels.
Yes, you are right, there could be other yet-unrevealed-to-you limiting factors here, but there is nothing in the graph to show this. You would need to see another set of lines where increasing CO2 further does not change the plateau level, and/or where the shape changes.
Chalk it up to Occam's razor. Without further information besides what is on this graph, if I asked you to draw your prediction about what the line would look like at 0.12% CO2, you should draw another line that follows the other and then plateaus at a third, higher level.


Has there been any observation of species adapting the evolution process?

Bacteria such as E. coli are known to increase their mutation rate (by switching to a more error prone polymerase among other things) when under stress. This can mean being placed in a medium where it's not adapted to grow (http://www.micab.umn.edu/courses/8002/Rosenberg.pdf) or when treated with antibiotics (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1088971/?tool=pmcentrez).


Does a non-extinct gliding species of bird exist?

There is a classification of birds called Soaring birds.
Soaring Birds

In definition, some land birds, such as vultures and certain hawks,
sustain flight for long periods without flapping their wings. They
take advantage of updrafts produced when the wind blows over hills and
mountain ridges or make use of rising columns of warm air called
"thermals."
Vultures stay within thermals by flying slowly in tight circles. They
have short, broad wings and a low wing loading (ratio of bird weight
to wing area) that allows them to remain aloft and to be highly
maneuverable at slow speeds. [1]

List of soaring birds

Birds of Prey

Buzzards
Condors
Eagles
Falcons
Harriers
Hawks
Kites
Osprey
Secretary Bird
Vultures

Passerine

Chough

Cranes

Sandhill

Sea birds

Albatrosses
Frigatebirds
Gulls
Herons
Pelicans
Petrels
Shearwaters
Storks
Terns

Extinct

Argentavis

Buzzard

Chough

Sandhill

Albatrosses

(source: scienceviews.com)
Argentavis[Extinct]

(source: mnn.com)
Update:
Most similar morphology to Archaeopteryx is found in Hoatzin (Opisthocomus hoazin) like claws as hands as they hold the branch when they are small.

(source: pbworks.com)
Source:
[1] Soaring Birds by Paul R. Ehrlich, David S. Dobkin, and Darryl Wheye.


What physical force attracts the anti-codon on tRNA to the codon on mRNA during translation?

As with many processes in cellular biology, nothing really moves anywhere, attracted by specific force. What that means, is that any molecule has a chance to interact with any other molecule, say, bind to it. Only force that is acted is electrical force of attraction of negative charges to positive ones.

Due to diffusion and temperature fluctuations, molecules wander around, bumping in each other. Sometimes, two complimentary molecules will bump into each other in a very desirable, energy-efficient orientation. Their atomic-scale interfaces (with tiny charges on it) will find each other as neat as hand finds glove of the right size/orientation neat and comfy. That is the way, for example, tRNA finds slot on ribosome/mRNA complex to plug into. just simple key-and-lock, or hand-and-glove model, that's all there is. And beauty is that you can try computationally calculate probability and energy of different interactions from molecular 3D structures.

Now, there are many tRNAs, but Glycine-tRNA will bind tightest to glycine-codon/ribosome complex. There is a chance that Alanine-tRNA will get in that spot, but that chance is very little compared to chance of proper interaction. Also, because interfaces of Ala-tRNA and Ala-codone don't match exactly, molecular vibration due to heat (temperature) will destroy this complex quickly. This allows specificity.


Aerobe or facultative anaerobe organism that metabolizes acetate?

You could try Paracoccus denitrificans.

Here is a study where acetate is used as the growth-limiting substrate: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.320.1692&rep=rep1&type=pdf

Here's the details of its version of acetate kinase: http://www.uniprot.org/uniprot/A1B9S8

I'd be happy to collaborate with you further on this.


What is the motivation behind fluorinated pharmaceuticals?

Fluorine has a combination of unique chemical properties, which makes it very useful in drug design :

It is small, such that replacing a C-H with a C-F is often possible, from a sterical point of view. Halogens, which share some of the other desirable properties of fluorine, are much larger.
It is very electronegative: it will attract electrons strongly, which allow polarising, stabilising or destabilising various moieties.
It is not found in natural products (except for trifluoroacetic acid), which means our metabolising apparatus, result of evolution by exposure to such products, can have difficulty dealing with it: thus ut makes drugs more resistant to degradation.

With these properties, you either start with fluorine in mind, to make  molecules that mimics transition state of reactions involving non-fluorinated compounds (thus, enzyme inhibitors), or mimic the peptide bond (but not cleavable as easily); or you add it later to a compound that already work for additional activity, or less clearance.

There are many good books and reviews, but you could start with this one.


There are, of course, many different deoxyribonucleases (DNase), but the question has other implicit problems. It assumes that there was a single event that resulted in the realization of the existence of a new enzymatic activity. As the Introduction to this paper by M. McCarty on the purification of one such enzyme in the Journal of General Physiology in 1946, science wasn’t (and still often isn’t) quite like that:

The enzyme which breaks down highly polymerized desoxyribonucleic (sic) acid
has been known for many years under various names. In 1903, Araki (3)
reported that crude preparations of trypsin and erepsin brought about
liquefaction of gels of a thymonucleate prepared according to the
method of Neumann (4) Although Araki interpreted the effect as being
proteolytic in nature, his experiments represent the first observations
on the enzymatic breakdown of this type of nucleic acid. Two years
later Sachs (5) demonstrated that liquefaction of the nucleate gel by
pancreatic extracts is caused by an enzyme distinct from trypsin, and
further presented evidence indicating that trypsin rapidly inactivates
the nuclease. De la Blanchardière (6) confirmed the findings of Sachs,
and made several unsuccessful attempts to separate the nuclease from
the inactivating tryptic enzymes. This writer also devised a more
quantitative method of measuring the nuclease activity by following the
fall in viscosity of a dilute solution of thymonucleate during
digestion with the enzyme.

Araki, T., Z. physiol. Chem.,1903,38, 84.

Sachs, F., Z. physiol. Chem.,1905,46, 337.

De la Blanchardière, P., Z. physiol. Chem., 1913, 87, 291

[desoxyribonucleic acid and thymonucleate are older terms for DNA and its ionized form]
Many scientists have subsequent been involved in identifying different types of DNase and their roles in DNA metabolism, and anyone wishing to know about a particular DNase would need to research the literature.


How to obtain a list of proteins sorted by the ~1400 unique protein folds?

If there is a simple way provided to do this it is very well hidden. The tedious and stupid way to do 1 (get a list of folds) would seem to involve rolling your own:

Go to http://scop.berkeley.edu/ver=2.07 (or whatever is the latest version).

Click on each of the 12 classes in turn. e.g. (a) all alpha proteins will take you to http://scop.berkeley.edu/sunid=46456 .

Save the source of each page as text.

Write and run your own parser to pull out the sunid () from the http://scop.berkeley.edu/sunid= and the description line if you wish. (This assumes you program.) I think this sunid is the fold id.

If you can than find some database or table that has PDB and sunid values in it, you can write another program to find the answer to 2.
Alternatively… (appended January 2021)

Download dir.cla.scope.2.07-stable.txt (or the latest version)
Save as a text file.
Open in Mircorsoft Excel. (Just dragging onto the app icon formatted it properly on my Mac. Your mileage may vary.)
You can just select the column with the ids, paste into another sheet, and then remove duplicates to get all the different fold ids. (Alternatively, you have about 276,000 entries to do with whatever you wish.)


Foveal ganglion cell density (Tay-Sachs Disease)

As you've already mentioned, cells near the primate macula tend to make one to one connections.  Due to this lack of convergence they can be somewhat smaller than normal cells (particularly in the size of their dendritic arbors) earning them the moniker "midget" ganglion and bipolar cells (also P cells).  By reducing the magnitude of photoreceptor convergence onto ganglion cells, the retina sacrifices luminal sensitivity for spatial acuity.  Or put another way, a downstream neuron in the LGN/V1 can be more "certain" about which photoreceptor is sending information when light is bright, but less certain that any information is being sent when light is dim.

The other side of the question you bring up is how the retinal ganglion cells themselves alter the image formed onto the photoreceptor layer.  For those that don't already know, photoreceptors are located at the very back of the retina.  Since they're the major light sensitive part of the retina, that means light has to go through the ganglion cells, bipolar cells, amacrine cells, and all of their associated processes before reaching the actual photosensitive part of the eye.  So, why not put photoreceptors at the front of the eye?  One major reason is metabolic, photoreceptors are tightly coupled with the retinal pigment epithelium which helps to re-process used photopigment as part of the retina's vitamin A cycle.

How can those two factors, a one to one correspondence and a decrease in thickness be present at the same time?  For reference, let's locate a cross section of a primate macula

Dark areas are cell nuclei.  The innermost layer of cells (bottom of the image) are ganglion cells, the next layer of cells up is bipolar cells (the inner nuclear layer) and the next layer up is photoreceptor cell bodies.  you can make out the cilial stalks of the photoreceptors pointing upwards toward the RPE.

From this image we can see a few transformations happening in the macula:

The photoreceptor layer is thicker, up to 7 or 8 cell bodies deep.  This means higher photoreceptor density.
The outer plexiform layer (photoreceptors to bipolar cell connections) is considerably thicker.  A single cone should connect to fewer bipolar cells in the retina, so how does this make sense?  We'll find the answer in #3.
The outer nuclear layer is only one cell thick.  This is the first layer that is actually thinner in the foveal region.  The cell bodies for photoreceptors from tis region have been displaced laterally, and the outer plexiform layer from #2 had to be larger to accommodate this lateral shift
The inner plexiform layer, connections between bipolar cells and ganglion cells, is nonexistent.  Also absent is the ganglion cell layer itself.

So how do these observations resolve your question?  Quite simply, the lateral movement of information from the foveal/macular photoreceptors happens predominantly in the outer plexiform layer.  That buys the inner plexiform layer considerably more space to further spread those signals laterally to ganglion cells, and avoids the problematic situation you suggested of having an extra-thick ring of ganglion cells immediately around the fovea.  The end result is that ganglion cells that respond to photoreceptors in the foveal region of space are even further out from the retina than the bipolar cells they connect to, which are themselves displaced.

As far as why a cherry red spot looks so large, that honestly depends on two factors: the disease or disorder in question and the zoom used.  Bear in mind that the red color comes from, as far as I know, the blood vessels in the choroid itself.  It would therefore not necessarily correspond exactly to the size of the macula, but instead to any area which is thinned in that vicinity.  I think you'll become more comfortable with that idea if you look back at the thickness of the total retina in the above figure and notice that even outside of the foveal region it is still growing thicker.

I think your question shows good instincts, because I believe that if the eye evolved to have a larger "true" fovea then you would get exactly what you describe: a large area of super high density vision surrounded by a region with non-linearly worse vision designed to support the central region.  Instead it appears that the primate macula is just large enough that we have a moderate sized central acute region and a (relatively) linear drop in spatial acuity moving out from it.


Here is a study of planarian worms, which are immortal in asexual reproduction and mortal in sexual reproduction.

Hydras also become mortal after they reproduce sexually.

Relevant to your question: Cells within planarian worm differ in expression of telomerase active subunit depending on body part. Immortal (asexual) worms have more expression in the area around the pharynx, those cells there are "the proliferative stem cells". There is a nice figure in the article.

I assume it is similar for hydra, that outer body coat has less expression than the cells inside. “Hydra is a bag of stem cells”

(Less relevant (a version of previous version of my answer. But does not answer the "every cell" inquiry well): In planarian worms "We demonstrate that this difference is reflected in the expression and alternate splicing of the protein subunit of the telomerase enzyme." The mentioned telomerase subunit was 1. comparatively more transcribed in immortal (asexual) worm and 2. within the resultant trancripts, there were possibilities of functional and non-functional isoforms due to alternate splicing. Immortal worms had higher ratio of functional isoforms. Summary: immortals have more transcripts and higher proportion of functional versions of them.)


DNA synthesis companies: cost per base, turn-around time, codon-optimization algorithms

Are you working in academia? It might be worthwhile to call the companies directly and see if there is a discounted rate for your institution (another lab or department may have already set something up).

You won't be able to get information on the different algorithms if they are proprietary.  However considering that codon usage data is public and shared knowledge, I can't imagine that the different algorithms are that much different. I think there are some tricks for choosing certain codons near the transcription start site in some organisms? From what I hear, the algorithms are constantly changing. I could tell you how my E. coli optimized gene from GenScript worked two years ago, but they'd probably design it differently now.

Okay - GenScript calls their algorithm "proprietary", so they are not sharing the details. DNA2.0 says their algorithm is patented, so it's out there for inspection. They published a PLOS paper on their E. coli algorithm: Welch et al..

Although, maybe all they do these days is spit out codon sequence randomly:

  The results obtained in this study indicate that the codon
  randomization method is a superior strategy for codon optimization. A
  significant improvement in protein expression was obtained for the
  largely established process of chymosin production, showing the power
  of this strategy to reduce production costs of industrial enzymes in
  microbial hosts. (Menzella 2011)

Stitching smaller synthesized fragments works well if you're pressed for time, but it's usually more expensive. However, sometimes these companies do special pricing on synthesis for <1kb, which makes stitching a great choice. Turnaround is generally faster for three 1kb fragments than one 3kb fragment.


Can two humans with 44 chromosomes produce viable offspring?

The article says "both his chromosome 14s are stuck to his chromosome 15s" - meaning both his mom and his dad (46,XX,rob(14,15) and 46,XY,rob(14,15) had a Robertsonian Translocation which doesn't really result in the loss of any genetic material. The very small chance occurred which one sperm carrying the translocation chromosome fused with an oocyte carrying the other translocation chromosome.

So the genotype of the dude is 44,XY,rob(14,15)(14,15), meaning he's normal because he technically has all the genomic information of a normal human.

If he mates with a normal woman (46,XX), then the resulting progeny will have an extra copy of chromosome 15, resulting in trisomy 15, which is non-viable.

If one such 44 chromosome individual mates with another person of the same chromosomal arrangement, then probably a viable fetus would be produced if a translocation chromosome ends up with the same translocation chromosome from the mother. I wouldn't call it a new species per se because it still contains the genetic material from a human. For example, there are many humans with chromosomal abnormalities (I.e trisomy 21, XXY, etc...). Also the background rate of translocations and chromosomal aberrations in somatic cells is notable, so I wouldn't use this as a new species definition.


How was birth control realized in ancient days?

The need for birth control has been a concept for thousands of years and remains an important issue for men and women today, the need for contraception helped humans to achieve control over our population and healthy sexual relationships without having the fear of pregnancy.
The medieval contraception methods mostly relies on plant based oral contraceptives and also plant based suppositories. There is always an element of myth in the usage of these medicines to control child birth, but due to the overusage of Silphion, the plant was gone extinct.

Silphion was a plant that grew in the hills near the Greek city-state of Cyrene located in North Africa. This plant was one example of an oral contraceptive in ancient times, based partly on Pliny's statement that it could be used "to promote the menstrual discharge" but since then has been harvested into extinction.
Reference

Asafoetida is widely used as a  contraceptive in medieval period, Asafoetida or asafetida is the dried latex exuded from the rhizome or tap root of several species of Ferula.

One of the earliest contraceptive pioneers was Soranus of Ephesus, a Greek physician of the 2nd century C.E. who practiced in Rome and wrote extensively on obstetrics, gynecology and pediatrics. Many of his texts exist to this day which describes plants that were recommended for use as oral contraceptives, suppositories and abortifacients: galbanum, silphium, opopanax, myrtle, rue, white pepper, cow parsnip and pomegranate.
Reference

Also condom is not a modern mechanism it was used in ancient times, but the usage was to protect oneself from sexually transmitted diseases, but an unknown chemical used  which is a spermicide and this resulted in contraception.

Records of condom use dates back to 3000 B.C. where King Minos of Crete, son of Zeus and Europa, utilized the bladders of goats to protect himself during intercourse.
In the 1500s, a syphilis epidemic spread across Europe. It was at this time that Gabriel Fallopius,created a linen
condom as a means to protect from the continuing spread of disease . This proved especially effective when soaked in an unknown chemical solution acting as a spermicide.
Reference

The medieval contraception methods includes,

Condoms
Female Barrier Methods
Herbs and Rituals
Intrauterine devices
Male methods
The Pill

These methods are widely described in this article.


This is a climbing plant from the Genus Mandevilla. It's a genus native to the Americas.

Here is a photo for comparisson:

However, since the Genus Mandevilla has more than 150 species (let alone cultivar and hybrids), narrowing it down to a particular species may be very difficult in your case.


Is the poison from Stink Bugs dangerous?

Apparently there are no poisonous species (see this website), and some species are even eaten (website). No worries.


Can the Staph streak method be used for culturing Neisseria on blood agar?

It depends on your species of Neisseria.

N. meningitidis grows on BAP (Blood Agar Plate), with colonies being grey and unpigmented on  appearing round, smooth, moist, glistening, and convex, with a clearly defined edge

You can read more about that here.

N. gonorrhoeae is known not to grow on BAP.
More on that here.


Do organs or any structure in the human body shrink/shorten if it's function is no longer useful?

First of all, our appendix isn't 'useless'. Their is a high concentration of lymph nodes (higher than anywhere else in your gut), so it might not be needed for digestion anymore, but it's function somewhat shifted to a more immunological role.
Secondly, yes there are other organs/body parts that shrink over time. In evolutionary time, look at our tailbone. In monkeys it's still a full tail, in apes it's almost nothing, and in humans it's still present in the skeleton, but not visible on the 'outside' anymore. Probably in a few (hundred/thousand/..) years it will be completely reduced until it is no longer present in the human skeleton (because since we don't have a tail anymore, it doesn't have any function anymore).
Over a much shorter timescale it is also possible. For example the thymus expands in puberty, and afterwards it shrinks until it is almost completely gone.


Deletion of codons at the start of a sequence in preparation for heterogeneous expression. Why?

The easiest answer would be to ask the authors of the patent.
Several other possibilities (see comments) were excluded, such as:

restriction sites which interfere with cloning
signal peptide
proteolytic cleavage

Although it's just a theory, removing part of the N-terminus might improve protein stability and half-life time because the first 30-40 amino acids lack an ordered structure (as judged by submitting the structure to Phyre). Those structures are known to aggregate and influence protein stability.

References:

The use of systematic N- and C-terminal deletions to promote production and structural studies of recombinant proteins.

Sequence composition of disordered regions fine-tunes protein half-life

Production of prone-to-aggregate proteins


How many different protein coding genes are in the Human Biome?

The Human Microbiome Project collected samples as shown in the image below from healthy volunteers:

They give an estimate of about 8 Million genes in the human microbiome, which is about 360x the number of genes in the human genome. See here for their press release with a lot of information. Additionally these two articles are as well interesting, if you want to dive deeper into the stuff:

A framework for human microbiome research
Structure, function and diversity of the healthy human microbiome


This paper gives a half-life of 26 hours for wild-type GFP expressed in mouse cells.


How does toluene inhalation damage the brain?

After crossing the blood-brain barrier, toluene, along with other volatile anesthetic agents, had been previously thought to inhibit neuronal transmission by causing a change in membrane or membrane protein conformation. Recent research has shown that interactions with several key brain neurotransmitters, mainly γ-aminobutyric acidA (GABA), to a lessor degree glycine, and possibly dopamine, are responsible for the clinical effects seen. Postmortem studies along with magnetic resonance imaging (MRI) findings have shown diffuse white matter demyelination and gliosis (solvent vapor/toluene leukoencephalopathy), which is postulated to be the end product by which chronic toxicity occurs, although the exact mechanism by which this occurs remains unclear

(McKeown at al. Toluene Toxicity).


Why telomere shortening slowing down cancer?

Think about the 24 different linear chromosomes in a diploid human XY cell.  In the absence of active telomerase enzyme to repair the chromosome ends following one round of cell division, then every time that cell divides each end of each chromosome will get a little bit shorter.

If the cell keeps dividing indefinitely, like a tumor cell, the chromosomes are effectively shrinking.  Eventually this chromosome shortening will result in deleting actual genes (at first, 24 chromosomes x 2 chromosome ends = 48 genes).   Not all of those genes are essential for cell viability; and the distance, or length, of DNA between the telomere and the first gene on that end will be variable.  But as soon as the chromosome shortening removes part of an essential gene, then that cell will quickly die.

It would be like erasing the words at both ends of a sentence, one letter at a time.  In the beginning, someone else would still be able to make sense out of your sentence, but eventually they would not be able to fully understand what information you were trying to convey.

Most of the terminally differentiated cells in an adult human are no longer actively dividing, so it is not a problem, they don’t need active telomerase.  However, cancer is a condition of unregulated cell division, and so all cancer cells have to have some mechanism of repairing the ends of their chromosomes.  Reactivation of TERT (Telomerase Reverse Transcriptase, the protein component of the telomerase enzyme) gene expression is extremely common in cancer cells.


What are these tiny, almost transparent, dots in my vision?

You are probably seeing floaters.

  Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent. At a young age, the vitreous is transparent, but as one ages, imperfections gradually develop

You might as well be seeing Scheerer's phenomenon

  The blue field entoptic phenomenon or Scheerer's phenomenon [..] is the appearance of tiny bright dots (nicknamed blue-sky sprites) moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky.

Please have a look at the wikipedia article for more information.

I only now realize that your question is a duplicate of Seeing strange things in light


What is the name of this spider and is it poisonous?

Ah, that would be the spiny orb weaver. You can see an almost exact same picture here. To make a guess on the species, its maybe Gasteracantha cancriformis as its said in that webpage I have tagged. They are generally harmless. Here's the wikipedia page.


What is the difference between Ostracodermi and Placodermi

If in reference to the prehistoric groups of fish of the respective classifications, ostracoderms would have had a bony head much like a shell, and placoderms had articulated plates covering the head/thoracic area. The differences are relatively straightforward, see the wikipedia pages for each:

https://en.wikipedia.org/wiki/Ostracoderm

https://en.wikipedia.org/wiki/Placodermi


What I can do in order to improve the folding of the protein?

If you have over-expressed an eukaryotic full length protein or the enzymatic part, then E. coli does not necessarily provide a good environment for its folding so you need to express it in the same system which the original protein came from, e.g. mammalian or Drosophila etc. E. coli over expression is mostly used to generate wast amounts of protein for the purposes of protein sequence based Ab generation amongst other things. Look at this review for some of the solutions it offers for proteins not folding correctly in E. coli when over-expressed (http://www.biomedcentral.com/1472-6750/4/32).

The remainder of your question is a duplicate of this question (Ni-NTA purification, problem with the chaperone protein), which I have provided an extensive answer/comments to!

In addition, since the lack of enzyme functionality is a potential indication of errors in its state/3D structure, it is however not a definitive reason. Could you provide some explanations as to what experiments you have conducted to reach that conclusion and how this second point about chaperone eluding with your protein relevant to the first and the last section of your question?


Definition of Linkage Desiquilibrium (LD)


Mutations occur spontaneously because all molecular processes are stochastic in nature: DNA replication is an imperfect process. However, certain external factors can increase the probability of a mutation to occur or even cause specific types of mutations.

Both spontaneous mutations and this kind of externally driven mutation contribute to the genetic variability that is the basis for evolution. It is sufficient that variation exist for evolution to be possible, no matter the origin of this variation. X-rays are probably not common in nature, but there is plenty UV on the surface of earth, and there probably exist chemical mutagens that are formed without human contribution.


What is the mass of a pigeon tail feather?

I just weighed a pigeon tail feather (~10 cm) long. The mass was 0.05 g. Although all tail feathers are not equal in length (and all pigeons are not equal in size), this is probably a good approximation.

Measuring the drag coefficient is going to be very challenging, because it will vary with the orientation of the oncoming airflow. A feather falling with its broad surface (in this feather ~1.2 cm in chord width) perpendicular to the flow will have a much high drag coefficient than a feather falling with the broad surface parallel to flow.